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Signaling responses after exposure to 5?-dihydrotestosterone or 17?-estradiol in norepinephrine-induced hypertrophy of neonatal rat ventricular myocytes  

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Androgens appear to enhance, whereas estrogens mitigate, cardiac hypertrophy. However, signaling pathways in cells for short (3 min) and longer term (48 h) treatment with 17?-estradiol (E2) or 5?-dihydrotestosterone (DHT) are understudied. We compared the effect of adrenergic stimulation by norepinephrine (NE; 1 ?M) alone or in combination with DHT (10 nM) or E2 (10 nM) treatment in neonatal rat ventricular myocytes (NRVMs) by cell area, protein synthesis, sarcomeric structure, gene expres...

Koshman, Yevgeniya E.; Piano, Mariann R.; Russell, Brenda; Schwertz, Dorie W.

2010-01-01

2

Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.  

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To determine the effects of chronic anemia on the functional and structural characteristics of the heart, 1-month-old male rats were fed a diet deficient in iron and copper, which led to a hemoglobin concentration of 4.63 g/dl, for 8 weeks. At sacrifice, under fentanyl citrate and droperidol anesthesia, systolic, diastolic, and mean arterial blood pressures were decreased, whereas differential pressure was increased. Left ventricular systolic pressure and the ventricular rate of pressure rise...

Olivetti, G.; Quaini, F.; Lagrasta, C.; Ricci, R.; Tiberti, G.; Capasso, J. M.; Anversa, P.

1992-01-01

3

Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased ß-adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased ß-adrenergic inotropic respo [...] nse. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of ß-adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. ß-Adrenergic receptor density was determined by [³H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 ± 0.28 vs 7.6 ± 0.32 pA/pF) and a 19% reduction in mean peak [Ca2+]i transients (0.13 ± 0.007 vs 0.16 ± 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 ± 4.3 vs 123.3 ± 0.9% in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. ß-Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 ± 20.22 vs 271.5 ± 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to ß-adrenergic stimulation was also reduced and was probably related to ß-adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.

R.M., Saraiva; N.G.B., Chedid; C.C., Quintero H.; L.E., Díaz G.; M.O., Masuda.

4

GENETICS OF LEFT VENTRICULAR HYPERTROPHY  

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High blood pressure makes the heart work harder and promotes enlargement of the left ventricle, left ventricular hypertrophy (LVH), which is an important risk factor for cardiovascular disease and death.

2012-01-01

5

Left ventricular hypertrophy in patients treated with regular hemodialyses  

Directory of Open Access Journals (Sweden)

Full Text Available Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

Petrovi? Dejan

2008-01-01

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TrpC3 Regulates Hypertrophy-Associated Gene Expression without Affecting Myocyte Beating or Cell Size  

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Pathological cardiac hypertrophy is associated with an increased risk of heart failure and cardiovascular mortality. Calcium (Ca2+) -regulated gene expression is essential for the induction of hypertrophy, but it is not known how myocytes distinguish between the Ca2+ signals that regulate contraction and those that lead to cardiac hypertrophy. We used in vitro neonatal rat ventricular myocytes to perform an RNA interference (RNAi) screen for ion channels that mediate Ca2+-dependent gene expre...

Brenner, Jacob S.; Dolmetsch, Ricardo E.

2007-01-01

7

Increased sarcolemmal Na+/H+ exchange activity in hypertrophied myocytes from dogs with chronic atrioventricular block  

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Full Text Available Dogs with compensated biventricular hypertrophy due to chronic atrioventricular block (cAVB, are more susceptible to develop drug-induced Torsade-de-Pointes arrhythmias and sudden cardiac death. It has been suggested that the increased Na+ influx in hypertrophied cAVB ventricular myocytes contribute to these lethal arrhythmias. The increased Na+ influx was not mediated by Na+ channels, in fact the Na+ current proved reduced in cAVB myocytes. Here we tested the hypothesis that increased activity of the Na+/H+ exchanger type 1 (NHE-1, commonly observed in hypertrophic hearts, causes the elevated Na+ influx. Cardiac acid-base transport was studied with a pH-sensitive fluorescent dye in ventricular myocytes isolated from control and hypertrophied cAVB hearts; the H+ equivalent flux through NHE-1, Na+-HCO3- cotransport (NBC, Cl-/OH- exchange (CHE and Cl-/HCO3- exchange (AE were determined and normalized per liter cell water and corrected for surface-to-volume ratio. In cAVB, sarcolemmal NHE-1 flux was increased by 65±6.3% in the pHi interval 6.3-7.2 and NBC, AE and CHE fluxes remained unchanged. Accordingly, at steady-state intracellular pH the total sarcolemmal Na+ influx by NHE-1+NBC increased from 8.5±1.5 amol/?m2/min in normal myocytes to 15±2.4 amol/?m2/min in hypertrophied cAVB myocytes. We conclude that compensated cardiac hypertrophy in cAVB dogs is accompanied with an increased sarcolemmal NHE-1 activity. This in conjunction with unchanged activity of the other acid-base transporters will raise the intracellular Na+ in hypertrophied cAVB myocytes.

JanHindrikRavesloot

2013-11-01

8

Heart rate variability in left ventricular hypertrophy.  

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BACKGROUND--Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM--To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS--36 controls and 154 patients with left ventricular hypertrophy (...

Mandawat, M. K.; Wallbridge, D. R.; Pringle, S. D.; Riyami, A. A.; Latif, S.; Macfarlane, P. W.; Lorimer, A. R.; Cobbe, S. M.

1995-01-01

9

Compensatory angiogenesis during progressive right ventricular hypertrophy.  

Science.gov (United States)

We investigated vascular adaptations occurring in progressive right ventricular hypertrophy (RVH) in adult mini pigs. Fourteen mini pigs had progressive RVH induced by implanting an inflatable cuff on the main pulmonary artery for 1-5 months and were compared to a control group (N = 11). RVH animals were divided into two groups, a moderate RVH (MH) that had RV/BW ratio increases of 20%-70% above controls and a severe hypertrophy group (SH) that had RV/BW ratio increase of 70%-117%. We measured coronary blood flow reserve (CBFR) with radiolabelled microspheres at maximal exercise and during adenosine vasodilation. Adenosine vasodilation did not decrease CBFR either regionally or transmurally in both the MH and SH groups. During exercise CBFR showed a small but significant decrease in the SH group. No intervention changed the endo/epi flow ratios. Morphometric studies showed that myocytes increased in cross sectional areas (CSA) in these hypertrophied hearts. The CSA of capillaries and arterioles and their numerical densities increased significantly in the endocardial and epicardial regions in both MH and SH groups. Capillary density showed a small but significant decrease in both MH and SH groups. We measured DNA synthesis in these hearts using tritiated thymidine labelling. We found a high labelling index in endothelial cells and a moderate labelling index in smooth muscle cells in early stages of hypertrophy. These data show that angiogenesis, observed in the morphometric studies and by DNA labelling, prevents CBFR changes during progressive RVH in the pig. Furthermore, angiogenesis is not uniform at different stages of progressive RVH. PMID:1378285

White, F C; Nakatani, Y; Nimmo, L; Bloor, C M

1992-01-01

10

Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy.  

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To determine whether IGF-1 opposes the stimulation of myocyte death in the surviving myocardium after infarction, transgenic mice overexpressing human IGF-1B in myocytes (FVB.Igf+/-) and wild-type littermates at 1.5 and 2.5 mo of age were subjected to coronary ligation and killed 7 d later. Myocardial infarction involved an average 50% of the left ventricle, and produced cardiac failure. In the region proximate to infarction, myocyte apoptosis increased 4. 2-fold and 2.1-fold in nontransgenic...

1997-01-01

11

Up-Regulation of AT1 and AT2 Receptors in Postinfarcted Hypertrophied Myocytes and Stretch-Mediated Apoptotic Cell Death  

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To determine whether up-regulation of AT1 and AT2 receptors occurred in hypertrophied myocytes after infarction and whether AT2 played a role in stretch-mediated apoptosis, left ventricular myocytes were dissociated from the surviving portion of the wall 8 days after coronary occlusion and cardiac failure in rats. Control cells were obtained from sham-operated animals. Myocytes were stretched in an equibiaxial stretch apparatus and angiotensin II (Ang II) formation and cell death were measure...

2000-01-01

12

Myocyte-restricted focal adhesion kinase deletion attenuates pressure overload-induced hypertrophy.  

Science.gov (United States)

Focal adhesion kinase (FAK) is a ubiquitously expressed cytoplasmic tyrosine kinase strongly activated by integrins and neurohumoral factors. Previous studies have shown that cardiac FAK activity is enhanced by hypertrophic stimuli before the onset of overt hypertrophy. Herein, we report that conditional deletion of FAK from the myocardium of adult mice did not affect basal cardiac performance, myocyte viability, or myofibrillar architecture. However, deletion of FAK abolished the increase in left ventricular posterior wall thickness, myocyte cross-sectional area, and hypertrophy-associated atrial natriuretic factor induction following pressure overload. Myocyte-restricted deletion of FAK attenuated the initial wave of extracellular signal-regulated kinase activation and cFos expression induced by adrenergic agonists and biomechanical stress. In addition, we found that persistent challenge of mice with myocyte-restricted FAK inactivation leads to enhanced cardiac fibrosis and cardiac dysfunction in comparison to challenged genetic controls. These studies show that loss of FAK impairs normal compensatory hypertrophic remodeling without a concomitant increase in apoptosis in response to cardiac pressure overload and highlight the possibility that FAK activation may be a common requirement for the initiation of this compensatory response. PMID:16902179

DiMichele, Laura A; Doherty, Jason T; Rojas, Mauricio; Beggs, Hilary E; Reichardt, Louis F; Mack, Christopher P; Taylor, Joan M

2006-09-15

13

Nonselective cation current in rabbit ventricular myocytes.  

Science.gov (United States)

Currents contributing repolarization in rabbit ventricular myocytes are very complex because the I(to.s) covers almost the whole repolarization phase of the action potential. The other components of repolarizing currents, such as I(Kr) and I(Ks), are small. In the present work, with whole-cell patch-clamp technique, a clear evidence was provided for the existence of a hitherto unreported, voltage-dependent, nonselective cation current (NSCC) in rabbit ventricular myocytes. Na(+), K(+), and Cs(+) can permeate through the nonselective cation channel and the NSCC can be blocked by Gd(3+). The channels are sensitive to Ca(2+), Mg(2+)-free, and insulin in bathing solution. Activation of NSCC may provide complex effects on action potential configuration depending on the basal conditions and the experimental situations. Considering the voltage dependence and rapid activation kinetics of this current, we speculate that this current can provide an important influence on all repolarization phases of the action potential as well as contribute to the resting membrane potential in rabbit ventricular myocytes. In addition, it is conceivable that, under certain pathophysiological conditions (e.g., ischemia or excessive mechanical stress), the sensitivity of the channels could be altered in such a way that the conductance opens even in the presence of physiological Ca(2+), Mg(2+), and insulin. It might be an important factor on the repolarization of the action potential. Changes in NSCC may lead to an induction or inhibition of arrhythmia. PMID:16179954

Song, Y-D; Yang, X-C; Liu, T-F; Gu, Z-W

2005-01-01

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Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.  

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Coronary artery narrowing, ranging from 19% to 61%, was induced in rats and ventricular performance, myocardial damage, and myocyte hypertrophy were examined 1 mo later. Animals were separated into two groups, exhibiting ventricular dysfunction and failure, respectively. Dysfunction consisted of a 2.4-fold increase in left ventricular end diastolic pressure (LVEDP), 15% decrease in left ventricular peak systolic pressure (LVPSP), 24% reduction in developed pressure (DP), and a 16% depression ...

1992-01-01

15

Clenbuterol induces cardiac myocyte hypertrophy via paracrine signalling and fibroblast-derived IGF-1.  

Science.gov (United States)

The ?(2)-selective adrenoreceptor agonist clenbuterol promotes both skeletal and cardiac muscle hypertrophy and is undergoing clinical trials in the treatment of muscle wasting and heart failure. We have previously demonstrated that clenbuterol induces a mild physiological ventricular hypertrophy in vivo with normal contractile function and without induction of ?-skeletal muscle actin (?SkA), a marker of pathological hypertrophy. The mechanisms of this response remain poorly defined. In this study, we examine the direct action of clenbuterol on cardiocyte cultures in vitro. Clenbuterol treatment resulted in increased cell size of cardiac myocytes with increased protein accumulation and myofibrillar organisation characteristic of hypertrophic growth. Real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) revealed elevated mRNA expression of ANP and brain natriuretic peptide (BNP) but without change in ?SkA, consistent with physiological hypertrophic growth. Clenbuterol-treated cultures also showed elevated insulin-like growth factor I (IGF-1) mRNA and activation of the protein kinase Akt. Addition of either IGF-1 receptor-blocking antibodies or LY294002 in order to inhibit phosphatidylinositol 3-kinase, a downstream effector of the IGF-1 receptor, inhibited the hypertrophic response indicating that IGF-1 signalling is required. IGF-1 expression localised primarily to the minor population of cardiac fibroblasts present in the cardiocyte cultures. Together these data show that clenbuterol acts to induce mild cardiac hypertrophy in cardiac myocytes via paracrine signalling involving fibroblast-derived IGF-1. PMID:20577844

Bhavsar, Pankaj K; Brand, Nigel J; Felkin, Leanne E; Luther, Pradeep K; Cullen, Martin E; Yacoub, Magdi H; Barton, Paul J R

2010-12-01

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Intense myocyte formation from cardiac stem cells in human cardiac hypertrophy  

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It is generally believed that increase in adult contractile cardiac mass can be accomplished only by hypertrophy of existing myocytes. Documentation of myocardial regeneration in acute stress has challenged this dogma and led to the proposition that myocyte renewal is fundamental to cardiac homeostasis. Here we report that in human aortic stenosis, increased cardiac mass results from a combination of myocyte hypertrophy and hyperplasia. Intense new myocyte formation re...

Urbanek, Konrad; Quaini, Federico; Tasca, Giordano; Torella, Daniele; Castaldo, Clotilde; Nadal-ginard, Bernardo; Leri, Annarosa; Kajstura, Jan; Quaini, Eugenio; Anversa, Piero

2003-01-01

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Stimulation of the p38 Mitogen-activated Protein Kinase Pathway in Neonatal Rat Ventricular Myocytes by the G Protein–coupled Receptor Agonists, Endothelin-1 and Phenylephrine: A Role in Cardiac Myocyte Hypertrophy?  

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We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein–coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiac myocytes from neonatal rat hearts. Both agonists increased the phosphorylation (activation) of p38-MAPK by ?12-fold. A p38-MAPK substrate, MAPK-activated protein kinase 2 (MAPKAPK2), was activated approximately fourfold and 10 ?M SB203580, a p38-MAPK inhibitor, abolished this activation. Ph...

1998-01-01

18

Left ventricular hypertrophy in patients treated with regular hemodialyses  

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Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- th...

Petrovi? Dejan; Stojimirovi? Biljana

2008-01-01

19

Intense myocyte formation from cardiac stem cells in human cardiac hypertrophy  

Science.gov (United States)

It is generally believed that increase in adult contractile cardiac mass can be accomplished only by hypertrophy of existing myocytes. Documentation of myocardial regeneration in acute stress has challenged this dogma and led to the proposition that myocyte renewal is fundamental to cardiac homeostasis. Here we report that in human aortic stenosis, increased cardiac mass results from a combination of myocyte hypertrophy and hyperplasia. Intense new myocyte formation results from the differentiation of stem-like cells committed to the myocyte lineage. These cells express stem cell markers and telomerase. Their number increased >13-fold in aortic stenosis. The finding of cell clusters with stem cells making the transition to cardiogenic and myocyte precursors, as well as very primitive myocytes that turn into terminally differentiated myocytes, provides a link between cardiac stem cells and myocyte differentiation. Growth and differentiation of these primitive cells was markedly enhanced in hypertrophy, consistent with activation of a restricted number of stem cells that, through symmetrical cell division, generate asynchronously differentiating progeny. These clusters strongly support the existence of cardiac stem cells that amplify and commit to the myocyte lineage in response to increased workload. Their presence is consistent with the notion that myocyte hyperplasia significantly contributes to cardiac hypertrophy and accounts for the subpopulation of cycling myocytes.

Urbanek, Konrad; Quaini, Federico; Tasca, Giordano; Torella, Daniele; Castaldo, Clotilde; Nadal-Ginard, Bernardo; Leri, Annarosa; Kajstura, Jan; Quaini, Eugenio; Anversa, Piero

2003-01-01

20

FGF23 induces left ventricular hypertrophy  

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Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, rac...

Faul, Christian; Amaral, Ansel P.; Oskouei, Behzad; Hu, Ming-chang; Sloan, Alexis; Isakova, Tamara; Gutie?rrez, Orlando M.; Aguillon-prada, Robier; Lincoln, Joy; Hare, Joshua M.; Mundel, Peter; Morales, Azorides; Scialla, Julia; Fischer, Michael; Soliman, Elsayed Z.

2011-01-01

 
 
 
 
21

Association between high grade ventricular arrhythmia and extent of left ventricular hypertrophy in hypertrophic cardiomyopathy.  

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The association between the extent of left ventricular (LV) hypertrophy and severity of ventricular or atrial arrhythmias are examined. Two-dimensional echocardiography and 24-h Holter electrocardiography monitoring were performed in 60 patients with hypertrophic cardiomyopathy (HCM). According to the distribution of the LV hypertrophy, the patients were divided into three groups: 1. Apical hypertrophy (APH), 2. Septal hypertrophy, and 3. Extensive hypertrophy. Ventricular arrhythmias were...

Cheng, Xiao-shu; Kusachi, Shozo; Urabe, Norio; Nogami, Kunio; Takemoto, Masao; Morishita, Naoya; Haraoka, Shoichi; Tsuji, Takao

1991-01-01

22

iNOS deficiency protects the heart from systolic overload induced ventricular hypertrophy and congestive heart failure  

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Inducible nitric oxide synthase (iNOS) protein is expressed in cardiac myocytes of patients and experimental animals with congestive heart failure (CHF). Here we show that iNOS expression plays a role in pressure overload induced myocardial chamber dilation and hypertrophy. In wild type mice, chronic transverse aortic constriction (TAC) resulted in myocardial iNOS expression, cardiac hypertrophy, ventricular dilation and dysfunction, and fibrosis, while iNOS deficient mice displayed much less...

Zhang, Ping; Xu, Xin; Hu, Xinli; Deel, Elza; Zhu, Guangshuo; Chen, Yingjie

2007-01-01

23

The mAKAP? Scaffold Regulates Cardiac Myocyte Hypertrophy via Recruitment of Activated Calcineurin  

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mAKAP? is the scaffold for a multimolecular signaling complex in cardiac myocytes that is required for the induction of neonatal myocyte hypertrophy. We now show that the pro-hypertrophic phosphatase calcineurin binds directly to a single site on mAKAP? that does not conform to any of the previously reported consensus binding sites. Calcineurin - mAKAP? complex formation is increased in the presence of Ca2+/calmodulin and in norepinephrine-stimulated primary cardiac myocytes. This binding ...

Li, Jinliang; Negro, Alejandra; Lopez, Johanna; Bauman, Andrea L.; Henson, Edward; Dodge-kafka, Kimberly; Kapiloff, Michael S.

2010-01-01

24

Effect of fosinopril on the transient outward potassium current of hypertrophied left ventricular myocardium in the spontaneously hypertensive rat.  

Science.gov (United States)

To investigate fosinopril's effect on the transient outward potassium current (Ito) of differing degrees of hypertrophied myocytes in the spontaneously hypertensive rat (SHR). Ten- and 24-week-old SHRs were used as models for cardiac hypertrophy. Hypertrophied ventricular myocytes were exposed to 1, 10, and 100 ?mol/L fosinopril; the whole-cell patch-clamp technique was used to study the effects on the transient outward potassium current. Ito current density was decreased in SHR myocytes relative to controls (14.17?±?0.31 and 11.62?±?0.08 pA/pF in 10- and 24-week-old SHR versus 16.73?±?0.15 pA/pF, p?myocytes compared with controls (14.92?±?0.14 and 15.27?±?0.13 pA/pF versus 14.17?±?0.31 pA/pF, p?myocytes at all doses (12.70?±?0.07, 13.74?±?0.10, and 14.53?±?0.13 versus 11.62?±?0.08 pA/pF for controls, p?hypertrophied myocytes in 24-week-old compared with 10-week-old SHR for each dose (1.08?±?0.09 versus 0.37?±?0.26 pA/pF, p?hypertrophied myocytes. This effect was more pronounced in myocytes with a greater degree of hypertrophy. PMID:24441766

Huang, Zhi-Bin; Fang, Chang; Lin, Mao-Huan; Yuan, Gui-Yi; Zhou, Shu-Xian; Wu, Wei

2014-05-01

25

BIOMARKERS OF LEFT VENTRICULAR HYPERTROPHY AND REMODELING IN BLACKS  

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Left ventricular hypertrophy, a marker for adverse cardiovascular events, is more common in blacks than non-Hispanic whites. Mechanisms leading to left ventricular hypertrophy and mediating its clinical sequelae in blacks are not fully understood. We investigated the associations of 39 candidate biomarkers in distinct biological pathways with left ventricular mass and geometry in blacks. Participants included 1193 blacks (63 ± 9 years, 72% women, 78% hypertensive) belonging to hypertensive s...

Coutinho, Thais; Al-omari, Malik; Mosley, Thomas H.; Kullo, Iftikhar J.

2011-01-01

26

A Mathematical Model of the Mouse Ventricular Myocyte Contraction  

Science.gov (United States)

Mathematical models of cardiac function at the cellular level include three major components, such as electrical activity, Ca2+ dynamics, and cellular shortening. We developed a model for mouse ventricular myocyte contraction which is based on our previously published comprehensive models of action potential and Ca2+ handling mechanisms. The model was verified with extensive experimental data on mouse myocyte contraction at room temperature. In the model, we implemented variable sarcomere length and indirect modulation of the tropomyosin transition rates by Ca2+ and troponin. The resulting model described well steady-state force-calcium relationships, dependence of the contraction force on the sarcomere length, time course of the contraction force and myocyte shortening, frequency dependence of the contraction force and cellular contraction, and experimentally measured derivatives of the myocyte length variation. We emphasized the importance of the inclusion of variable sarcomere length into a model for ventricular myocyte contraction. Differences in contraction force and cell shortening for epicardial and endocardial ventricular myocytes were investigated. Model applicability for the experimental studies and model limitations were discussed.

Mullins, Paula D.; Bondarenko, Vladimir E.

2013-01-01

27

FGF23 induces left ventricular hypertrophy.  

Science.gov (United States)

Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF23 levels and LVH. In an established animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change in blood pressure was observed. These results unveil a klotho-independent, causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD. PMID:21985788

Faul, Christian; Amaral, Ansel P; Oskouei, Behzad; Hu, Ming-Chang; Sloan, Alexis; Isakova, Tamara; Gutiérrez, Orlando M; Aguillon-Prada, Robier; Lincoln, Joy; Hare, Joshua M; Mundel, Peter; Morales, Azorides; Scialla, Julia; Fischer, Michael; Soliman, Elsayed Z; Chen, Jing; Go, Alan S; Rosas, Sylvia E; Nessel, Lisa; Townsend, Raymond R; Feldman, Harold I; St John Sutton, Martin; Ojo, Akinlolu; Gadegbeku, Crystal; Di Marco, Giovana Seno; Reuter, Stefan; Kentrup, Dominik; Tiemann, Klaus; Brand, Marcus; Hill, Joseph A; Moe, Orson W; Kuro-O, Makoto; Kusek, John W; Keane, Martin G; Wolf, Myles

2011-11-01

28

Up-Regulation of AT1 and AT2 Receptors in Postinfarcted Hypertrophied Myocytes and Stretch-Mediated Apoptotic Cell Death  

Science.gov (United States)

To determine whether up-regulation of AT1 and AT2 receptors occurred in hypertrophied myocytes after infarction and whether AT2 played a role in stretch-mediated apoptosis, left ventricular myocytes were dissociated from the surviving portion of the wall 8 days after coronary occlusion and cardiac failure in rats. Control cells were obtained from sham-operated animals. Myocytes were stretched in an equibiaxial stretch apparatus and angiotensin II (Ang II) formation and cell death were measured 3 and 12 hours later. AT1 and AT2 proteins were evaluated in freshly isolated myocytes and after stretch. The effects of AT1 and AT2 antagonists on stretch-induced Ang II synthesis and apoptosis were also established. Myocardial infarction increased AT1 and AT2 in myocytes and stretch further up-regulated these receptors. Ang II levels were higher in postinfarcted myocytes and this peptide increased with the duration of stretch in both groups of cells. Similarly, apoptosis increased with time in control and postinfarcted myocytes. Absolute values of Ang II and apoptosis were greater in myocytes from infarcted hearts at 3 and 12 hours after stretch. Addition of AT1 blocker to cultures inhibited stretch-activated apoptosis in both myocyte populations as well as the generation of Ang II in postinfarcted myocytes. In contrast, AT2 antagonists had no impact on these cellular events. In conclusion, Ang II stimulated cell death through AT1 receptor activation, whereas ligand binding to AT2 receptor did not alter Ang II concentration and apoptosis in normal and postinfarcted hypertrophied myocytes.

Leri, Annarosa; Liu, Yu; Li, Baosheng; Fiordaliso, Fabio; Malhotra, Ashwani; Latini, Roberto; Kajstura, Jan; Anversa, Piero

2000-01-01

29

CALCIUM-INDEPENDENT PHOSPHOLIPASE A2 IN RABBIT VENTRICULAR MYOCYTES  

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We have previously reported that the majority of phospholipase A2 (PLA2) activity in rabbit ventricular myocytes is membrane-associated, calcium-independent (iPLA2), selective for arachidonylated plasmalogen phospholipids and inhibited by the iPLA2-selective inhibitor bromoenol lactone (BEL). Here, we identified the presence of iPLA2 in rabbit ventricular myocytes, determined the full length sequences for rabbit iPLA2? and iPLA2? and compared their homology to the human isoforms. Rabbit iPL...

Beckett, Caroline S.; Mchowat, Jane

2008-01-01

30

Association between high grade ventricular arrhythmia and extent of left ventricular hypertrophy in hypertrophic cardiomyopathy.  

Directory of Open Access Journals (Sweden)

Full Text Available The association between the extent of left ventricular (LV hypertrophy and severity of ventricular or atrial arrhythmias are examined. Two-dimensional echocardiography and 24-h Holter electrocardiography monitoring were performed in 60 patients with hypertrophic cardiomyopathy (HCM. According to the distribution of the LV hypertrophy, the patients were divided into three groups: 1. Apical hypertrophy (APH, 2. Septal hypertrophy, and 3. Extensive hypertrophy. Ventricular arrhythmias were found in 82% of the patients and supraventricular arrhythmias were detected in 70% of the patients. Lown grade III and IV arrhythmias occurred significantly more frequently in patients with extensive than with septal hypertrophy. Lown grade III to IV arrhythmias did not occur in patients with APH. Present results show a significant association between the extent of LV hypertrophy and the severity of ventricular arrhythmias in HCM.

Cheng,Xiao-shu

1991-06-01

31

Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy  

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Cardiac hypertrophy is controlled by a complex signal transduction and gene regulatory network, containing multiple layers of crosstalk and feedback. While numerous individual components of this network have been identified, understanding how these elements are coordinated to regulate heart growth remains a challenge. Past approaches to measure cardiac myocyte hypertrophy have been manual and often qualitative, hindering the ability to systematically characterize the network's higher-order co...

2012-01-01

32

Ecto-5'-nucleotidase deficiency exacerbates pressure-overload induced left ventricular hypertrophy and dysfunction  

Science.gov (United States)

This study examined whether endogenous extracellular adenosine acts to facilitate the adaptive response of the heart to chronic systolic overload. To examine whether endogenous extracellular adenosine can protect the heart against pressure overload induced heart failure, transverse aortic constriction (TAC) was performed on mice deficient in extracellular adenosine production as the result of genetic deletion of CD73. While there was no difference in left ventricular (LV) size or function between CD73 deficient mice (KO mice) and wild type (WT) mice under unstressed conditions, aortic constriction for 2 or 4 weeks induced significantly more myocardial hypertrophy, LV dilation and LV dysfunction in KO mice compared to WT mice. Thus, after 2 weeks of TAC, LV fractional shortening decreased to 27.4±2.5% and 21.9±1.7% in WT and KO mice respectively (p<0.05). Consistent with a role of adenosine in reducing tissue remodeling, KO mice displayed increased myocardial fibrosis and myocyte hypertrophy compared to WT mice. Furthermore, adenosine treatment reduced phenylephrine induced cardiac myocyte hypertrophy and collagen production in cultured neonatal rat cardiac myocytes and cardiac fibroblasts, respectively. Consistent with a role for adenosine in modulating cardiomyocyte hypertrophy, KO mice demonstrated increased activation of mTOR signaling, accompanied by higher expression of the hypertrophy marker atrial natriuretic peptide (ANP). Conversely, the adenosine analogue 2-chloro-adenosine significantly reduced cell size, mTOR/p70S6K activation, and ANP expression in cultured neonatal cardiomyocytes. These data demonstrate that CD73 helps to preserve cardiac function during chronic systolic overload by preventing maladaptive tissue remodeling.

Xu, Xin; Fassett, John; Hu, Xinli; Zhu, Guangshuo; Lu, Zhongbing; Li, Yunfang; Schnermann, Jurgen; Bache, Robert J.; Chen, Yingjie

2008-01-01

33

An analysis of electrocardiographic criteria for determining left ventricular hypertrophy  

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OBJECTIVE: To determine the most sensitive criterion for the detection of left ventricular hypertrophy according to echocardiographically defined left ventricular mass. METHODS: The Sokolow-Lyon voltage, Sokolow-Lyon-Rappaport, Cornell voltage duration product, White-Bock, and Romhilt-Estes point scoring criteria were compared with left ventricular mass index, corrected for body surface, obtained from the echocardiograms of 306 outpatients (176 females, 130 males), of all age groups. RESULTS:...

Gasperin Carlos Alberto; Germiniani Helio; Facin Carlos Roberto; Souza Admar Moraes de; Cunha Cláudio Leinig Pereira da

2002-01-01

34

Impaired left ventricular filling in hypertensive left ventricular hypertrophy as a marker of the presence of an arrhythmogenic substrate.  

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OBJECTIVE--To assess the prevalence of ventricular late potentials and ventricular tachycardia in hypertensive subjects with left ventricular hypertrophy and to study their relation to clinical characteristics. SETTING--Teaching and general hospital in Padua. METHODS--107 hypertensive subjects with echocardiographic signs of left ventricular hypertrophy were studied with signal averaged electrocardiography and 24 hour Holter monitoring. Signal averaged electrocardiogram analysis was performed...

Palatini, P.; Maraglino, G.; Accurso, V.; Sturaro, M.; Toniolo, G.; Dovigo, P.; Baccillieri, S.

1995-01-01

35

Patterns of diastolic dysfunction in left ventricular hypertrophy.  

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The relative sensitivities of and interrelations between different measurements of diastolic function were studied in 50 patients with left ventricular hypertrophy diagnosed on anatomical grounds. Isovolumic relaxation time, the interval from minimum cavity dimension to mitral valve opening and relative dimension increase during this period, and the peak rate of dimension increase and wall thinning during rapid ventricular filling were measured by digitised M mode echocardiography. The relati...

Shapiro, L. M.; Gibson, D. G.

1988-01-01

36

Electrocardiographic Criteria for Left Ventricular Hypertrophy in Children  

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Previous studies to determine the sensitivity of the electrocardiogram (ECG) for left ventricular hypertrophy (LVH) in children had their imperfections: they were not done on an unselected hospital population, several criteria used in adults were not applied to children, and obsolete limits of normal for the ECG parameters were used. Furthermore, left ventricular mass (LVM) was taken as the reference standard for LVH, with no regard for other clinical evidence. The study population consisted ...

Rijnbeek, Peter R.; Herpen, Gerard; Kapusta, Livia; Ten Harkel, A. Derk Jan; Witsenburg, Maarten; Kors, Jan A.

2008-01-01

37

["Genes for mitochondria" in arterial hypertension and left ventricular hypertrophy].  

Science.gov (United States)

Study is devoted to "genes for mitochondria"--genes of mitochondrial genome and mitochondrial DNA polymerase gamma gene (POLG1). We compared frequencies of polymorphisms in mitochondrial DNA and in POLG1 between healthy individuals and patients with arterial hypertension, as well as between patients with and without left ventricular hypertrophy. We did not discover significant differences of distribution of C allele of MspI-polymorphism in POLG1 in studied group. We have shown higher prevalence of mitochondrial haplogroup H of mtDNA in patients without left ventricle hypertrophy (OR = 0.42; 95% CI 0.17-0.98; p = 0.043), while compared with patients having this complication. Haplogroup T was more frequently detected in patients with left ventricle hypertrophy (OR = 6.16; 95% CI 1.17-9.74; p = 0.018). This result suggest implication of mitochondrial DNA in hypertension-induced left venticular hypertrophy. PMID:20198856

Bu?kin, S V; Golubenko, M V; Puzyrev, V P

2010-01-01

38

Mitochondrial metabolic adaptation in right ventricular hypertrophy and failure  

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Right ventricular failure (RVF) is the leading cause of death in pulmonary arterial hypertension (PAH). Some patients with pulmonary hypertension are adaptive remodelers and develop RV hypertrophy (RVH) but retain RV function; others are maladaptive remodelers and rapidly develop RVF. The cause of RVF is unclear and understudied and most PAH therapies focus on regressing pulmonary vascular disease. Studies in animal models and human RVH suggest that there is reduced glucose oxidation and incr...

Piao, Lin; Marsboom, Glenn; Archer, Stephen L.

2010-01-01

39

Left ventricular hypertrophy and the insulin resistance syndrome  

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Left ventricular hypertrophy (LVH) and the insulin resistance syndrome are common conditions associated with a markedly increased cardiovascular risk. In a fairly large prospective longitudinal study of men from the general population, we found that an unfavorable serum fatty acid profile and components of the insulin resistance syndrome such as dyslipidemia, obesity and hypertension at age 50 predicted the prevalence of LVH at age 70. In cross-sectional analyses at age 70, several components...

Sundstro?m, Johan

2001-01-01

40

Unexplained left ventricular hypertrophy: consider a diagnosis of Fabry's disease  

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Lysosomal storage disorders are a group of disorders characterised by the deficiency of a specific lysosomal hydrolase. These diseases are rare, with only a few hundred patients in the Netherlands. Fabry's disease, an X-linked lysosomal storage disorder, is caused by a deficiency of the lysosomal enzyme ?-galactosidase A which results in, among other things, left ventricular hypertrophy, renal failure and cerebrovascular events. Patients with Fabry's disease, especially males, have a decreas...

Linthorst, G. E.; Vedder, A. C.; Bouma, B. J.; Dekker, L. R. C.; Hollak, C. E. M.

2006-01-01

 
 
 
 
41

Inhibition of Angiotensin II-Induced Cardiac Hypertrophy and Associated Ventricular Arrhythmias by a p21 Activated Kinase 1 Bioactive Peptide  

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Cardiac hypertrophy increases the risk of morbidity and mortality of cardiovascular disease and thus inhibiting such hypertrophy is beneficial. In the present study, we explored the effect of a bioactive peptide (PAP) on angiotensin II (Ang II)-induced hypertrophy and associated ventricular arrhythmias in in vitro and in vivo models. PAP enhances p21 activated kinase 1 (Pak1) activity by increasing the level of phosphorylated Pak1 in cultured neonatal rat ventricular myocytes (NRVMs). Such PAP-induced Pak1 activation is associated with a significant reduction of Ang II-induced hypertrophy in NRVMs and C57BL/6 mice, in vitro and in vivo, respectively. Furthermore, PAP antagonizes ventricular arrhythmias associated with Ang II-induced hypertrophy in mice. Its antiarrhythmic effect is likely to be involved in multiple mechanisms to affect both substrate and trigger of ventricular arrhythmogenesis. Thus our results suggest that Pak1 activation achieved by specific bioactive peptide represents a potential novel therapeutic strategy for cardiac hypertrophy and associated ventricular arrhythmias.

Lin, Wee K.; Zhang, Yanmin; Liu, Wei; Huang, Kai; Terrar, Derek A.; Solaro, R. John; Wang, Xin; Ke, Yunbo; Lei, Ming

2014-01-01

42

Telmisartan regresses left ventricular hypertrophy in caveolin-1-deficient mice.  

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The role of angiotensin II (Ang II) in promoting cardiac hypertrophy is well known; however, its role in a spontaneous model of hypertrophy in mice lacking the protein caveolin-1 (Cav-1 KO) has not been explored. In this study, WT and Cav-1 KO mice were treated with angiotensin receptor blocker (ARB), telmisartan (Telm), and cardiac function was assessed by echocardiography. Treatment of Cav-1 KO mice with Telm significantly improved cardiac function compared with age-matched vehicle-treated Cav-1 KO mice, whereas Telm did not affect cardiac function in WT mice. Both left ventricular (LV) weight to body weight ratios and LV to tibial length ratios were also reverted by Telm in Cav-1 KO but not in WT mice. LV hypertrophy was associated with increased expression of natriuretic peptides A and B, ?-myosin heavy chain and TGF-?, and Telm treatment normalized the expression of these genes. Telm reduced the expression of collagen genes (Col1A and Col3A) and associated perivascular fibrosis in intramyocardial vessels in Cav-1 KO mice. In conclusion, Telm treatment reduces indexes of cardiac hypertrophy in this unique genetic model of spontaneous LV hypertrophy. PMID:20585312

Krieger, Marta H; Di Lorenzo, Annarita; Teutsch, Christine; Kauser, Katalin; Sessa, William C

2010-11-01

43

Telmisartan regresses left ventricular hypertrophy in caveolin-1 deficient mice  

Science.gov (United States)

The role of angiotensin II (Ang II) in promoting cardiac hypertrophy is well known, however the role of the Ang II in a spontaneous model of hypertrophy in mice lacking the protein caveolin-1 (Cav- KO) has not been explored. In this study, WT and Cav-1 KO mice were treated with angiotensin receptor blocker (ARB), telmisartan, and cardiac function assessed by echocardiography. Treatment of Cav-1 KO mice with telmisartan significantly improved cardiac function compared to age-matched, vehicle treated Cav-1 KO mice, while telmisartan did not affected cardiac function in WT mice. Both left ventricular (LV) weight to body weight ratios and LV to tibial length ratios were also reverted by telmisartan in Cav-1 KO but not WT mice. LV hypertrophy was associated with increased expression of natriuretic peptides-A and –B, ?-myosin heavy chain and TGF-? and telmisartan treatment normalized the expression of these genes. Telmisartan reduced the expression of collagen genes (Col1A and Col3A) and associated perivascular fibrosis in intramyocardial vessels in Cav-1 KO mice. In conclusion, telmisartan treatment reduces indexes of cardiac hypertrophy in this unique genetic model of spontaneous LV hypertrophy.

Kreiger, Marta H; Di Lorenzo, Annarita; Teutsch, Christine; Kauser, Katalin; Sessa, William C.

2011-01-01

44

An analysis of electrocardiographic criteria for determining left ventricular hypertrophy  

Directory of Open Access Journals (Sweden)

Full Text Available OBJECTIVE: To determine the most sensitive criterion for the detection of left ventricular hypertrophy according to echocardiographically defined left ventricular mass. METHODS: The Sokolow-Lyon voltage, Sokolow-Lyon-Rappaport, Cornell voltage duration product, White-Bock, and Romhilt-Estes point scoring criteria were compared with left ventricular mass index, corrected for body surface, obtained from the echocardiograms of 306 outpatients (176 females, 130 males, of all age groups. RESULTS: The Cornell voltage duration product criteria index had the greatest sensitivity in women (54.90%, and the Sokolow-Lyon-Rappaport index was most sensitive in men (73.53%. When applied to men at the same voltage amplitude (20mm as that in women, the Cornell index showed increased sensitivity relative to the conventional index (28mm of 67.65% (P<=0.01 and a sensitivity similar to that of the Sokolow-Lyon-Rappaport index, with higher specificity (P<=0.01. The White-Bock and Romhilt-Estes criteria were the least sensitive in men and women, despite their high specificity. The electrocardiographic criteria were more efficient when dilatation predominated over left ventricular hypertrophy. CONCLUSION: The Cornell index had greater sensitivity in women, and the Sokolow-Lyon-Rappaport index was more sensitive in men. When applied to men at the same voltage amplitude as that of women, the Cornell index had an increase in sensitivity similar to that of the Sokolow-Lyon-Rappaport index.

Carlos Alberto Gasperin

2002-01-01

45

YY1 Protects Cardiac Myocytes from Pathologic Hypertrophy by Interacting with HDAC5  

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YY1 is a transcription factor that can repress or activate the transcription of a variety of genes. Here, we show that the function of YY1 as a repressor in cardiac myocytes is tightly dependent on its ability to interact with histone deacetylase 5 (HDAC5). YY1 interacts with HDAC5, and overexpression of YY1 prevents HDAC5 nuclear export in response to hypertrophic stimuli and the increase in cell size and re-expression of fetal genes that accompany pathological cardiac hypertrophy. Knockdown...

Sucharov, Carmen C.; Dockstader, Karen; Mckinsey, Timothy A.

2008-01-01

46

PKC translocation and ERK1/2 activation in compensated right ventricular hypertrophy secondary to chronic emphysema.  

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Full Text Available Abstract Background Right ventricular hypertrophy (RVH is an important complication of chronic lung disease. However, the signal transduction pathways involved as well as the physiological changes to the right ventricle have not been investigated. Emphysema was produced in male, Syrian Golden hamsters by intra-tracheal instillation of 250 IU/kg elastase (Emp, n = 17. Saline treated animals served as controls (Con, n = 15. Results Nine months later, Emp hamsters had 75% greater lung volume, and evidence of RVH at the gross and myocyte level (RV:tibia length Emp 6.84 ± 1.18 vs. Con 5.14 ± 1.11 mg/mm; myocyte cross sectional area Emp 3737 vs. Con 2695 ?m2, but not left ventricular hypertrophy. Serial echocardiographic analysis from baseline to nine months after induction of emphysema revealed increasing right ventricular internal dimension and decreased pulmonary artery acceleration time only in Emp hamsters. There was an increase in translocation of PKC ?I and PKC ? from cytosolic to membranous cell fractions in RV of Emp hamsters. Phosphorylation of PKC ? was unchanged. Translocation of PKC ? and ?II were unchanged. Emp animals had a 22% increase in phospho-ERK 1/2, but no change in levels of total ERK 1/2 compared to Con. Conclusion These data suggest that PKC ?I, ? and ERK 1/2 may play a role in mediating compensated RVH secondary to emphysema and may have clinical relevance in the pathogenesis of RVH.

Litwin Sheldon E

2005-05-01

47

An analysis of electrocardiographic criteria for determining left ventricular hypertrophy  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english OBJECTIVE: To determine the most sensitive criterion for the detection of left ventricular hypertrophy according to echocardiographically defined left ventricular mass. METHODS: The Sokolow-Lyon voltage, Sokolow-Lyon-Rappaport, Cornell voltage duration product, White-Bock, and Romhilt-Estes point sc [...] oring criteria were compared with left ventricular mass index, corrected for body surface, obtained from the echocardiograms of 306 outpatients (176 females, 130 males), of all age groups. RESULTS: The Cornell voltage duration product criteria index had the greatest sensitivity in women (54.90%), and the Sokolow-Lyon-Rappaport index was most sensitive in men (73.53%). When applied to men at the same voltage amplitude (20mm) as that in women, the Cornell index showed increased sensitivity relative to the conventional index (28mm) of 67.65% (P

Gasperin, Carlos Alberto; Germiniani, Helio; Facin, Carlos Roberto; Souza, Admar Moraes de; Cunha, Cláudio Leinig Pereira da.

48

Chlorogenic acid prevents isoproterenol-induced hypertrophy in neonatal rat myocytes.  

Science.gov (United States)

Cardiac hypertrophy is an independent risk factor for cardiovascular disease and its subsequent progression to heart failure represents a major cause of morbidity and mortality in the world. CGA is an important component of Chinese herbal medicine, acting as an antioxidant, scavenging free radicals and preventing inflammation. This study found that with the pre-treatment of chlorogenic acid in Iso-induced neonatal rat myocytes, the levels of the hypertrophic markers, ANP, BNP and ?-MHC decreased. The nuclear translocation of NF-?B was blocked, whereas NF-?BIA, an inhibitor of NF-?B, was upregulated accordingly. And the level of the intracellular ROS was also reduced. These data reveal that chlorogenic acid may inhibit Iso-induced cardiac hypertrophy by attenuating NF-?B signaling pathway and suppressing ROS. PMID:24583048

Li, Yanfei; Shen, Dan; Tang, Xiaomei; Li, Xin; Wo, Da; Yan, Hongwei; Song, Rui; Feng, Jian; Li, Ping; Zhang, Jie; Li, Jue

2014-05-01

49

Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress  

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Mechanical stretch and oxidative stress have been shown to prolong action potential duration (APD) and produce early afterdepolarizations (EADs). Here, we developed a simulation model to study the role of stretch-activated channel (SAC) currents in triggering EADs in ventricular myocytes under oxidative stress. We adapted our coupling clamp circuit so that a model ionic current representing the actual SAC current was injected into ventricular myocytes and added as a real-time current. This cu...

Wang, Yanggan; Joyner, Ronald W.; Wagner, Mary B.; Cheng, Jun; Lai, Dongwu; Crawford, Brian H.

2009-01-01

50

NADPH oxidase-derived superoxide impairs calcium transients and contraction in aged murine ventricular myocytes  

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Abstract Since aging increases oxidative stress, we analyzed the contribution of reactive oxygen species (ROS) to the contractile dysfunction of aged ventricular myocytes and investigated whether short-term interference with ROS formation could normalize contractile performance. Isolated ventricular myocytes from young (2-4months) and aged (24-26months) male mice (C57BL/6) were used. We analyzed sarcomere shortening and calcium transients (Indo-1 fluorescence) of voltage...

2010-01-01

51

Induction of the skeletal alpha-actin gene in alpha 1-adrenoceptor-mediated hypertrophy of rat cardiac myocytes.  

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Myocardial hypertrophy in vivo is associated with reexpression of contractile protein isogenes characteristic of fetal and neonatal development. The molecular signals for hypertrophy and isogene switching are unknown. We studied alpha (sarcomeric)-actin messenger RNA (mRNA) expression in cultured cardiac myocytes from the neonatal rat. In the cultured cells, as in the adult heart in vivo, expression of cardiac alpha-actin (cACT) predominated over that of skeletal alpha-actin (sACT) mRNA, the ...

Bishopric, N. H.; Simpson, P. C.; Ordahl, C. P.

1987-01-01

52

Indo-1 binding to protein in permeabilized ventricular myocytes alters its spectral and Ca binding properties.  

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We have examined the binding of the fluorescent Ca indicator indo-1 to cellular protein in permeabilized ventricular myocytes and also to soluble and particulate myocyte protein. Using either a filtration technique or equilibrium dialysis, and conditions similar to those in a cardiac myocyte patch clamped with 100 microM indo-1 in the patch pipette, we found that 72% of the total indo-1 was bound to myocyte protein at a protein concentration of 100 mg/ml. This corresponds to a binding of 3.8 ...

1992-01-01

53

The Association of Growth Differentiation Factor-15 with Left Ventricular Hypertrophy in Hypertensive Patients  

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Growth differentiation factor-15 (GDF-15) has been identified as an endogenous anti-hypertrophy effect. However, the association of plasma GDF-15 levels with left ventricular hypertrophy (LVH) in hypertension is poorly understood. We investigate the effect of plasma GDF-15 levels on left ventricular hypertrophy (LVH) in hypertension. We measured the plasma levels of GDF-15 in 299 untreated hypertensive patients which consisted of 99 with LVH and 200 without LVH using immunoradiometric assay. ...

Xue, Hao; Fu, Zhenhong; Chen, Yundai; Xing, Youhong; Liu, Jie; Zhu, Hang; Zhou, Xiao

2012-01-01

54

IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-2 and NF-ATc1  

Science.gov (United States)

Localized synthesis of insulin-like growth factors (IGFs) has been broadly implicated in skeletal muscle growth, hypertrophy and regeneration. Virally delivered IGF-1 genes induce local skeletal muscle hypertrophy and attenuate age-related skeletal muscle atrophy, restoring and improving muscle mass and strength in mice. Here we show that the molecular pathways underlying the hypertrophic action of IGF-1 in skeletal muscle are similar to those responsible for cardiac hypertrophy. Transfected IGF-1 gene expression in postmitotic skeletal myocytes activates calcineurin-mediated calcium signalling by inducing calcineurin transcripts and nuclear localization of calcineurin protein. Expression of activated calcineurin mimics the effects of IGF-1, whereas expression of a dominant-negative calcineurin mutant or addition of cyclosporin, a calcineurin inhibitor, represses myocyte differentiation and hypertrophy. Either IGF-1 or activated calcineurin induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signalling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs.

Musaro, A.; McCullagh, K. J.; Naya, F. J.; Olson, E. N.; Rosenthal, N.

1999-01-01

55

Association between routine and standardized blood pressure measurements and left ventricular hypertrophy among patients on hemodialysis  

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Abstract Background Left ventricular (LV) hypertrophy is common among patients on hemodialysis. While a relationship between blood pressure (BP) and LV hypertrophy has been established, it is unclear which BP measurement method is the strongest correlate of LV hypertrophy. We sought to determine agreement between various blood pressure measurement methods, as well as identify which method was the strongest correlate of LV hypertrophy among patients on hemodialysis. Met...

2010-01-01

56

Cardiac arrhythmias and left ventricular hypertrophy in systemic hypertension  

International Nuclear Information System (INIS)

Background: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. Objective was to investigate the prevalence of cardiac arrhythmias and LVH in systemic hypertension. Methods: In all subjects blood pressure was measured, electrocardiography and echocardiography was done. Holter monitoring and exercise test perform in certain cases. There were 500 hypertensive patients, 156 (31.2%) men and 344 (69%) women >30 years of age in the study. Among them 177 (35.4%) were diabetic, 224 (45%) were dyslipidemia, 188 (37.6%) were smokers, and 14 (3%) had homocysteinemia. Mean systolic BP (SBP) was 180 +- 20 mm Hg and diastolic BP (DBP) was 95 +- 12 in male and female patients. Left ventricular mass index (LVMI) was 119.2 +- 30 2 2gm/m in male while 103 +- 22 gm/m in female patients. Palpitation was seen in 126 (25%) male and 299 (59.8%) female patients. Atrial fibrillation was noted in 108 (21.6%) male and 125 (25%) female patients, 30 (6%) male and 82 (16.4%) female patients had atrial flutter. Ventricular tachycardia was noted in 37 (7.4%) male and 59 (11.8%) female patients. Holter monitoring showed significant premature ventricular contractions (PVC'S) in 109 (21.8%) male and 128 (25.69%) female patients while Holter showed atrial arrhythmias (APC'S) in 89 (17.8%) males and 119 (23.8%) females. Angiography findings diagnosed coronary artery disease in 119 (23.8%) with CAD male and 225 (45%) without CAD while 47 (9.4%) females presented with CAD and 109 (21.8%) without CAD. Conclusion: A significant association has been demonstrated between hypertension and arrhythmias. Diastolic dysfunction of the left ventricle, left atrial size and function, as well as LVH have been suggested as the underlying risk factors for supraventricular, ventricular arrhythmias and sudden death in hypertensives with LVH. (author)

2010-01-01

57

Modeling CICR in rat ventricular myocytes: voltage clamp studies  

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Full Text Available Abstract Background The past thirty-five years have seen an intense search for the molecular mechanisms underlying calcium-induced calcium-release (CICR in cardiac myocytes, with voltage clamp (VC studies being the leading tool employed. Several VC protocols including lowering of extracellular calcium to affect Ca2+ loading of the sarcoplasmic reticulum (SR, and administration of blockers caffeine and thapsigargin have been utilized to probe the phenomena surrounding SR Ca2+ release. Here, we develop a deterministic mathematical model of a rat ventricular myocyte under VC conditions, to better understand mechanisms underlying the response of an isolated cell to calcium perturbation. Motivation for the study was to pinpoint key control variables influencing CICR and examine the role of CICR in the context of a physiological control system regulating cytosolic Ca2+ concentration ([Ca2+]myo. Methods The cell model consists of an electrical-equivalent model for the cell membrane and a fluid-compartment model describing the flux of ionic species between the extracellular and several intracellular compartments (cell cytosol, SR and the dyadic coupling unit (DCU, in which resides the mechanistic basis of CICR. The DCU is described as a controller-actuator mechanism, internally stabilized by negative feedback control of the unit's two diametrically-opposed Ca2+ channels (trigger-channel and release-channel. It releases Ca2+ flux into the cyto-plasm and is in turn enclosed within a negative feedback loop involving the SERCA pump, regulating[Ca2+]myo. Results Our model reproduces measured VC data published by several laboratories, and generates graded Ca2+ release at high Ca2+ gain in a homeostatically-controlled environment where [Ca2+]myo is precisely regulated. We elucidate the importance of the DCU elements in this process, particularly the role of the ryanodine receptor in controlling SR Ca2+ release, its activation by trigger Ca2+, and its refractory characteristics mediated by the luminal SR Ca2+ sensor. Proper functioning of the DCU, sodium-calcium exchangers and SERCA pump are important in achieving negative feedback control and hence Ca2+ homeostasis. Conclusions We examine the role of the above Ca2+ regulating mechanisms in handling various types of induced disturbances in Ca2+ levels by quantifying cellular Ca2+ balance. Our model provides biophysically-based explanations of phenomena associated with CICR generating useful and testable hypotheses.

Palade Philip T

2010-11-01

58

Scoring technique for diagnosis of ventricular hypertrophy from three orthogonal lead electrocardiogram.  

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A prospective study for the development of scoring techniques for the diagnosis of ventricular hypertrophy from the three orthogonal lead electrocardiogram was undertaken. A total of 51 hearts was examined at necropsy in a training group on which the scoring techniques were developed and a test group of a further 82 hearts was studied to assess the sensitivity and specificity of the method. The hearts were classified as being normal or having left ventricular hypertrophy, right ventricular hy...

Macfarlane, P. W.; Chen, C. Y.; Boyce, B.; Fraser, R. S.

1981-01-01

59

How reliable is the electrocardiogram in detecting left ventricular hypertrophy in hypertension?  

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This paper assesses the sensitivity and specificity of the electrocardiogram in detecting left ventricular hypertrophy in 75 hypertensive patients. Each patient underwent a 12 lead electrocardiogram and echocardiogram. Left ventricular mass index, using echocardiogram, was calculated according to the Penn convention and left ventricular hypertrophy was assessed by standard electrocardiographic criteria. The electrocardiogram was found to be very specific but insensitive in the detection of le...

Vijan, S. G.; Manning, G.; Millar-craig, M. W.

1991-01-01

60

Left ventricular hypertrophy, geometric patterns and clinical correlates among treated hypertensive Nigerians  

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Full Text Available BACKGROUND: Left ventricular hypertrophy can be due to various reasons including hypertension. It constitutes an increased cardiovascular risk . Various left ventricular geometric patterns occur in hypertension and may affect the cardiovascular risk profile of hypertensive subjects. METHODS: One hundred and eighty eight hypertensive subjects participated in this study. Left ventricular hypertrophy was diagnosed by echocardiography. Relative wall thickness was derived by 2 x PWTLVIDd. Subjects were arbitrarily categorized according to the duration of hypertension. Statistical analysis was done using SPSS 15.0. RESULTS:The mean age of the study population was 55.95 plus or minus 10.71 years. Subjects who had hypertension for more than 5 years were more likely to be older and had a lower ejection fraction , larger left ventricular diastolic internal dimension than those with duration of hypertension less than 5 years. Concentric remodelling was the commonest left ventricular geometric pattern among the hypertensive subjects closely followed by normal left ventricular geometry. Concentric hypertrophy and eccentric hypertrophy were rare among the study population.Left ventricular geometry was associated mainly with left ventricular chamber and wall dimensions. CONCLUSION: Concentric remodelling is the commonest pattern of left ventricular geometric pattern of the left ventricle among hypertensive subjects. Left ventricular geometry is associated with the chamber and wall dimensions. Eccentric hypertrophy is associated with the lowest left ventricular systolic function and therefore possibly an herald to progressive systolic impairment

Olayinka Akinwusi

2010-03-01

 
 
 
 
61

Left Ventricular Hypertrophy is Prevalent in Sprague-Dawley Rats  

Science.gov (United States)

Unrecognized cardiovascular abnormalities may confound the interpretation of research data collected using rats. However, although SPF rat colonies are screened for microbes and kept under standardized environmental conditions, their cardiovascular status is largely unknown. We recently performed surgery on anesthetized 80-d-old Sprague–Dawley rats and observed a high mortality that could not be attributed to the procedures or preceding treatments. Upon necropsy, cardiomyopathy was readily apparent in a substantial proportion of these rats. To further evaluate the nature of this condition, we evaluated the histology and morphology of hearts from both Sprague–Dawley and Lewis rats. Compared with Lewis rats, Sprague–Dawley rats had greater left ventricular wall thickness and larger cardiomyocyte cell size. Severe left ventricle hypertrophy was present in 38% of young adult Sprague–Dawley rats. These findings may have implications for research models that use Sprague–Dawley rats.

McAdams, Ryan M; McPherson, Ronald J; Dabestani, Nazila M; Gleason, Christine A; Juul, Sandra E

2010-01-01

62

Unusual localization and translocation of TRPV4 protein in cultured ventricular myocytes of the neonatal rat  

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Full Text Available TRPV4 protein forms a Ca2+-permeable channel that is sensitive to osmotic and mechanical stimuli and responds to warm temperatures, and expresses widely in various kinds of tissues. As for cardiac myocytes, TRPV4 has been detected only at the mRNA level and there were few reports about subcellular localization of the protein. The purpose of the present study was to investigate the expression profile of TRPV4 protein in cultured neonatal rat ventricular myocytes. Using Western blots, immunofluorescence, confocal microscopy and immuno-electron microscopy, we have shown that TRPV4 protein was predominantly located in the nucleus of cultured neonatal myocytes. Furthermore, cardiac myocytes responded to hypotonic stimulation by translocating TRPV4 protein out of the nucleus. The significance and mechanism concerning the unusual distribution and translocation of TRPV4 protein in cardiac myocytes remain to be clarified.

W. Wang

2012-07-01

63

Subcellular heterogeneity of ryanodine receptor properties in ventricular myocytes with low T-tubule density  

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Rationale: In ventricular myocytes of large mammals, not all ryanodine receptor (RyR) clusters are associated with T-tubules (TTs); this fraction increases with cellular remodeling after myocardial infarction (MI). Objective: To characterize RyR functional properties in relation to TT proximity, at baseline and after MI. Methods: Myocytes were isolated from left ventricle of healthy pigs (CTRL) or from the area adjacent to a myocardial infarction ...

Rota, M.; Biesmans, L.; Macquaide, N.; Heinzel, F. R.; Bito, V.; Smith, G. L.; Sipido, K. R.

2011-01-01

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Conditional cardiac overexpression of S100A6 attenuates myocyte hypertrophy and apoptosis following myocardial infarction.  

Science.gov (United States)

S100A6, a 20 kDa, Ca2+ - binding dimer with low basal cardiac expression, is upregulated in the rat heart following infarction and forced expression of S100A6 in rat neonatal cardiac myocyte cultures, inhibited the induction of ? myosin heavy chain (MHC), skeletal ? actin (skACT) and myocyte apoptosis in response to diverse stimuli including tumor necrosis factor ?. To define a role for S100A6 in vivo, we generated cardiac myocyte-specific transgenic mice by placing the human S100A6 cDNA downstream of a promoter responsive to a doxycycline (DOX)-regulated transcriptional activator (tTA) and breeding this line with one harboring cardiac myocyte-restricted (?MHC) expression of tTA (?MHC-tTA). We compared S100A6-?MHC-tTA mice 35 days post-myocardial infarction (MI) produced by coronary artery ligation with similar matched sham-operated controls on (S100A6 transgene overexpressed) or off (S100A6 transgene silenced) DOX. There were no differences between the sham groups on or off DOX. Thirty five days post-MI, myocardial S100A6 levels increased 12.5-fold in S100A6-?-MHC-tTA mice off DOX compared with S100A6-?-MHC-tTA mice on DOX. Hemodynamic studies, echocardiography and postmortem examination indicated that S100A6-?MHC-tTA mice on DOX 35 days post-MI mounted a hypertrophic response (20-22.5 % increase) accompanied by a program of fetal gene re-expression, fibrosis and myocardial apoptosis. Whereas the S100A6-?-MHC-tTA mice off DOX showed an attenuated myocyte hypertrophic response, less fibrosis and apoptosis which was beneficial to preservation of cardiac function. Therefore, S100A6 is a potential therapeutic target for modulation of adverse left ventricular remodeling in the early post infarct period. PMID:23844739

Tsoporis, James T; Izhar, Shehla; Desjardins, Jean-Francois; Leong-Poi, Howard; Parker, Thomas G

2014-01-01

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Arritmias ventriculares e hipertrofia ventricular esquerda na cardiomiopatia hipertrófica / Ventricular arrhythmias and left ventricular hypertrophy in hypertrophic cardiomyopathy  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: Portuguese Abstract in portuguese FUNDAMENTO: Na Cardiomiopatia Hipertrófica (CMH), o grau de Hipertrofia Ventricular Esquerda (HVE) poderia influenciar o desenvolvimento de arritmias ventriculares. OBJETIVO: Analisar, na CMH, a associação entre a ocorrência de arritmias ventriculares no eletrocardiograma-Holter (ECG-Holter) e o gra [...] u de HVE determinado ao ecocardiograma pela espessura parietal máxima (EPM) e Índice de Massa (IM). MÉTODOS: Cinquenta e quatro pacientes consecutivos com CMH realizaram ECG-Holter de 24 horas e ecocardiograma para avaliação do grau de HVE através da EPM e IM. Foram estabelecidos dois níveis para a ocorrência de arritmias ventriculares: I - extrassístoles isoladas ou pareadas e II - Taquicardia Ventricular Não Sustentada (TVNS). RESULTADOS: Nos 13 pacientes (24%) com TVNS (nível II), houve maior frequência de EPM do ventrículo esquerdo (VE) > 21 mm (n = 10, 77%; 25 ± 4 mm) e IMVE > 144 g/m² (n = 10, 77%; 200 ± 30 g/m²), em relação àqueles que apresentavam apenas arritmia extrassistólica (nível I) (n = 41, 76%), em que essas medidas foram identificadas em, respectivamente, 37% (n = 15, 23 ± 1 mm), p = 0,023, e 39% (n = 16, 192 ± 53 g/m²) dos casos, p = 0,026. Os citados valores de corte foram determinados por curva ROC com intervalo de confiança de 95%. O registro de TVNS foi mais comum em pacientes com EPMVE > 21 mm e IMVE > 144 g/m² (8 de 13; 62%), do que naqueles com uma (4 de 13; 31%) ou nenhuma (1 de 13; 8%) variável ecocardiográfica acima dos valores de corte, p = 0,04. CONCLUSÃO: A ocorrência de arritmias ventriculares no Holter associou-se, na CMH, ao grau de HVE, avaliado pelo ecocardiograma através da respectiva EPM e IM. Abstract in english BACKGROUND: In hypertrophic cardiomyopathy (HCM), the degree of left ventricular hypertrophy (LVH) could influence the development of ventricular arrhythmias. OBJECTIVE: In HCM, analyze the association between the occurrence of ventricular arrhythmias determined by Holter electrocardiogram (ECG-Holt [...] er) and the degree of LVH determined by maximum wall thickness (MWT) in echocardiography and body mass index (BMI). METHODS: Fifty-four consecutive patients with HCM underwent 24-hour ECG-Holter and echocardiography for assessment of level of LVH through MWT and BMI. Two levels were established for the occurrence of Ventricular Arrhythmias: I - alone or paired extrasystoles and II - Non- Sustained Ventricular Tachycardia (NSVT). RESULTS: In 13 patients (24%) with NSVT (level II), there was a higher frequency of MWT of the left ventricle (LV) > 21 mm (n = 10, 77%, 25 ± 4 mm) and LLLV = 144 g/m² (n = 10, 77%, 200 ± 30 g/m²), in comparison with those presenting with extrasystole arrhythmias (level I) (n = 41, 76%), in which these measures were identified in, respectively, 37 % (n= 15, 23 ± 1 mm), p = 0.023, and 39% (n = 16, 192 ± 53 g / m²) of the cases (p = 0.026). The cut-off values mentioned were determined by the ROC curve with a confidence interval of 95%. NSVT was more common in patients with MWTLV > 21 mm and LLLV > 144 g/m² (8 of 13, 62%) than in those with (4 of 13, 31%) or without (1 of 13; 8%) echocardiographic variables above cut-off values (p = 0.04). CONCLUSION: In HCM, occurrence of ventricular arrhythmias by Holter was associated with the degree of LVH assessed by echocardiography through MWT and BMI.

Beatriz Piva e, Mattos; Marco Antonio Rodrigues, Torres; Valéria Centeno de, Freitas; Fernando Luís, Scolari; Melina Silva de, Loreto.

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Electrocardiographic Criteria for Left Ventricular Hypertrophy in Children  

Science.gov (United States)

Previous studies to determine the sensitivity of the electrocardiogram (ECG) for left ventricular hypertrophy (LVH) in children had their imperfections: they were not done on an unselected hospital population, several criteria used in adults were not applied to children, and obsolete limits of normal for the ECG parameters were used. Furthermore, left ventricular mass (LVM) was taken as the reference standard for LVH, with no regard for other clinical evidence. The study population consisted of 832 children from whom a 12-lead ECG and an M-mode echocardiogram were taken on the same day. The validity of the ECG criteria was judged on the basis of an abnormal LVM index, either alone or in combination with other clinical evidence. The ECG criteria were based on recently established age-dependent normal limits. At 95% specificity, the ECG criteria have low sensitivities (<25%) when an elevated LVM index is taken as the reference for LVH. When clinical evidence is also taken into account, the sensitivity improved considerably (<43%). Sensitivities could be further improved when ECG parameters were combined. The sensitivity of the pediatric ECG in detecting LVH is low but depends strongly on the definition of the reference used for validation.

van Herpen, Gerard; Kapusta, Livia; ten Harkel, A. Derk Jan; Witsenburg, Maarten; Kors, Jan A.

2008-01-01

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Evaluation of myocardial function in the presence of left ventricular hypertrophy in athletes and hypertensive patients  

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Introduction Myocardial hypertrophy of the left ventricle may be of physiological or pathological nature. Distinction of these two types of hypertrophy is sometimes not easy and represents a diagnostic challenge. The aim of the study was to assess global diastolic and regional systolic and diastolic myocardial function in the presence of left ventricular hypertrophy in athletes and hypertensive patients. Material and methods In 18 male hypertensive patients and 14 male athletes global diastol...

Deljanin-Ili? Marina; Ili? Stevan; ?or?evi? Dragan; Zdravkovi? Marija; Ili? Vladimir

2008-01-01

68

Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension.  

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Digitised M mode echocardiography was used to determine the relation between the degree of left ventricular hypertrophy and abnormalities of isovolumic relaxation and diastolic function. Fifty six patients with varying severity of non-malignant systemic hypertension without evidence of ischaemic heart disease, left ventricular dilation, or clinical heart failure were studied. In addition, 10 athletes with hypertrophy and 20 normal subjects were studied. Athletes and patients with moderate (sy...

1984-01-01

69

Renal Transplantation Is Not Associated with Regression of Left Ventricular Hypertrophy: A Magnetic Resonance Study  

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Background and objectives: Patients with end-stage renal failure (ESRD) have an increased risk of premature cardiovascular (CV) disease. Left ventricular hypertrophy is an independent risk factor for CV events and death in ESRD. Renal transplantation has been associated with reduction in CV risk and echocardiographic regression of left ventricular hypertrophy. However, echocardiography overestimates LV mass in ESRD patients. Cardiac magnetic resonance (CMR) provides more detailed, volume-inde...

Patel, Rajan K.; Mark, Patrick B.; Johnston, Nicola; Mcgregor, Ellon; Dargie, Henry J.; Jardine, Alan G.

2008-01-01

70

Suppression of aldosterone mediates regression of left ventricular hypertrophy in patients with hypertension  

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BACKGROUND: High circulating aldosterone levels stimulate myocardial fibrosis and left ventricular hypertrophy (LVH). However, it is not clear whether suppression of aldosterone directly contributes to LVH regression in hypertensive patients. METHODS: The Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial randomised 465 hypertensive overweight subjects with LVH to the direct renin inhibitor aliskiren 300 mg, losartan 100 mg or the combination and followed patients for 9 months. All patie...

Pouleur, Anne-catherine; Uno, H.; Prescott, M. F.; Desai, A.; Appelbaum, E.; Lukashevich, V.; Smith, B. A.; Dahlof, B.; Solomon, S. D.

2011-01-01

71

Reduction of Left Ventricular Hypertrophy by Sirolimus in Kidney Transplant Recipients: A Nonrandomized Clinical Trial  

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Background: Persistence of left ventricular hypertrophy (LVH) in renal transplant recipients is associated with unfavorable outcomes. Calcineurin-inhibitor (CNI) nephrotoxicity is a major cause of morbidity and mortality after kidney transplantation. In this study we compared sirolimus (SRL) with calcineurin-inhibitor as primary immunosuppressants for the attenuation of left ventricular hypertrophy in renal transplantation recipients. Methods: In this prospective cohort study done in Shariati...

Sedghipour M; Sah, Tabatabaei; Sadadi F; Kamal Hedayat D; Nikdoost F; Sate H; Ghorbani Yekta B

2012-01-01

72

Numerical analysis of the effect of T-tubule location on calcium transient in ventricular myocytes.  

Science.gov (United States)

Intracellular calcium (Ca2+) signaling in cardiac myocytes is vital for proper functioning of the heart. Understanding the intracellular Ca2+ dynamics would give an insight into the functions of normal and diseased hearts. In the current study, spatiotemporal Ca2+ dynamics is investigated in ventricular myocytes by considering Ca2+ release and re-uptake via sarcolemma and transverse tubules (T-tubules), Ca2+ diffusion and buffering in the cytosol, and the blockade of Ca2+ activities associated with the sarcoplasmic reticulum. This study is carried out using a three dimensional (3D) geometric model of a branch of T-tubule extracted from the electron microscopy (EM) images of a partial ventricular myocyte. Mathematical modeling is done by using a system of partial differential equations involving Ca2+, buffers, and membrane channels. Numerical simulation results suggest that a lack of T-tubule structure at the vicinity of the cell surface could increase the peak time of Ca2+ concentration in myocytes. The results also show that T-tubules and mobile buffers play an important role in the regulation of Ca2+ transient in ventricular myocytes. PMID:24212025

George, Uduak Z; Wang, Jun; Yu, Zeyun

2014-01-01

73

Metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes  

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Repeated administration of MDMA (ecstasy) produces eccentric left ventricular (LV) dilation and diastolic dysfunction. While the mechanism(s) underlying this toxicity are unknown; oxidative stress plays an important role. MDMA is metabolized into redox cycling metabolites that produce superoxide. In this study, we demonstrated that metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes. Metabolites of MDMA used in this study included: al...

2009-01-01

74

BP control and left ventricular hypertrophy regression in children with CKD.  

Science.gov (United States)

In adult patients with CKD, hypertension is linked to the development of left ventricular hypertrophy, but whether this association exists in children with CKD has not been determined conclusively. To assess the relationship between BP and left ventricular hypertrophy, we prospectively analyzed data from the Chronic Kidney Disease in Children cohort. In total, 478 subjects were enrolled, and 435, 321, and 142 subjects remained enrolled at years 1, 3, and 5, respectively. Echocardiograms were obtained 1 year after study entry and then every 2 years; BP was measured annually. A linear mixed model was used to assess the effect of BP on left ventricular mass index, which was measured at three different visits, and a mixed logistic model was used to assess left ventricular hypertrophy. These models were part of a joint longitudinal and survival model to adjust for informative dropout. Predictors of left ventricular mass index included systolic BP, anemia, and use of antihypertensive medications other than angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Predictors of left ventricular hypertrophy included systolic BP, female sex, anemia, and use of other antihypertensive medications. Over 4 years, the adjusted prevalence of left ventricular hypertrophy decreased from 15.3% to 12.6% in a systolic BP model and from 15.1% to 12.6% in a diastolic BP model. These results indicate that a decline in BP may predict a decline in left ventricular hypertrophy in children with CKD and suggest additional factors that warrant additional investigation as predictors of left ventricular hypertrophy in these patients. PMID:24071004

Kupferman, Juan C; Aronson Friedman, Lisa; Cox, Christopher; Flynn, Joseph; Furth, Susan; Warady, Bradley; Mitsnefes, Mark

2014-01-01

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Left Ventricular Hypertrophy Evaluation in Obese Hypertensive Patients: Effect of Left Ventricular Mass Index Criteria  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english PURPOSE: To evaluate left ventricular mass (LVM) index in hypertensive and normotensive obese individuals. METHODS: Using M mode echocardiography, 544 essential hypertensive and 106 normotensive patients were evaluated, and LVM was indexed for body surface area (LVM/BSA) and for height² (LVM/h²). Th [...] e 2 indexes were then compared in both populations, in subgroups stratified according to body mass index (BMI): or = 30kg/m². RESULTS: The BSA index does not allow identification of significant differences between BMI subgroups. Indexing by height² provides significantly increased values for high BMI subgroups in normotensive and hypertensive populations. CONCLUSION: Left ventricular hypertrophy (LVH) has been underestimated in the obese with the use of LVM/BSA because this index considers obesity as a physiological variable. Indexing by height² allows differences between BMI subgroups to become apparent and seems to be more appropriate for detecting LVH in obese populations.

Rosa, Eduardo Cantoni; Moysés, Valdir Ambrósio; Sesso, Ricardo Cintra; Plavnik, Frida Liane; Ribeiro, Fernando Flexa; Kohlmann, Nárcia E. B.; Ribeiro, Artur Beltrame; Zanella, Maria Tereza; Kohlmann Jr., Osvaldo.

76

Left Ventricular Hypertrophy Evaluation in Obese Hypertensive Patients: Effect of Left Ventricular Mass Index Criteria  

Directory of Open Access Journals (Sweden)

Full Text Available PURPOSE: To evaluate left ventricular mass (LVM index in hypertensive and normotensive obese individuals. METHODS: Using M mode echocardiography, 544 essential hypertensive and 106 normotensive patients were evaluated, and LVM was indexed for body surface area (LVM/BSA and for height² (LVM/h². The 2 indexes were then compared in both populations, in subgroups stratified according to body mass index (BMI: or = 30kg/m². RESULTS: The BSA index does not allow identification of significant differences between BMI subgroups. Indexing by height² provides significantly increased values for high BMI subgroups in normotensive and hypertensive populations. CONCLUSION: Left ventricular hypertrophy (LVH has been underestimated in the obese with the use of LVM/BSA because this index considers obesity as a physiological variable. Indexing by height² allows differences between BMI subgroups to become apparent and seems to be more appropriate for detecting LVH in obese populations.

Eduardo Cantoni Rosa

2002-04-01

77

Effect of ethanol on action potential and ionic membrane currents in rat ventricular myocytes.  

Czech Academy of Sciences Publication Activity Database

rat ventricular myocyteKód oboru RIV: BO - BiofyzikaImpakt faktor: 3.138, rok: 2010http://apps.isiknowledge.com/full_record.do?product=UA&search_mode=GeneralSearch&qid=15&SID=Y1pmpi@7k2HPEc8ehEE&page=1&doc=1&colname=WOS

Bébarová, M.; Matejovi?, P.; Pásek, Michal; Ohlídalová, D.; Jansová, D.; Šimurdová, M.; Šimurda, J.

78

Echocardiographic assessment of inappropriate left ventricular mass and left ventricular hypertrophy in patients with diastolic dysfunction  

Science.gov (United States)

Background: Early diagnosis of left ventricular mass (LVM) inappropriateness and left ventricular hypertrophy (LVH) can result in preventing diastolic left ventricular dysfunction and its related morbidity and mortality. This study was performed to determine if diastolic dysfunction is associated with LVH and inappropriate LVM. Materials and Methods: One hundred and twenty five uncomplicated hypertension from Isfahan Healthy Heart Program underwent two-dimensional echocardiography. Inappropriate LVM was defined as an LVM index greater than 88 g/m2 of body-surface area in women and greater than 102 g/m2 in men. LVH-defined septal and posterior wall thickness greater than 0/9 cm in women and greater than 1 cm in men, respectively. Echocardiographic parameters, including early diastolic peak velocity (E)/late diastolic peak velocity (A), deceleration time (DT), and E/early mitral annulus velocity (E?) were measured. Results: The mean systolic and diastolic blood pressure at the patients’ admission day were 142.87 ± 18.12 and 88.45 ± 9.18 mmHg, respectively. Totally, 21.7% of subjects had inappropriate LV mass that moderate and severe abnormal LV mass was revealed in 5.6% and 5.6%, respectively. The mean of age and BMI was significantly higher in patients with moderate left ventricular hypertrophy (P 0.05). Spearman's Rank test was used to test the correlation between diastolic dysfunction and LV mass (P = 0.025). Conclusion: LVH is correlated with the severity of diastolic dysfunction manifested by the E/A value and deceleration time, but inappropriate LVM can slightly predict diastolic dysfunction severity in uncomplicated hypertension.

Shemirani, Hasan; Hemmati, Rohola; Khosravi, Alireza; Gharipour, Mojgan; Jozan, Mahnaz

2012-01-01

79

Functional subcellular distribution of ?1- and ?2-adrenergic receptors in rat ventricular cardiac myocytes  

Science.gov (United States)

?-adrenergic stimulation is a key regulator of cardiac function. The localization of major cardiac adrenergic receptors (?1 and ?2) has been investigated using biochemical and biophysical approaches and has led to contradictory results. This study investigates the functional subcellular localization of ?1- and ?2-adrenergic receptors in rat ventricular myocytes using a physiological approach. Ventricular myocytes were isolated from the hearts of rat and detubulated using formamide. Physiological cardiac function was measured as Ca2+ transient using Fura-2-AM and cell shortening. Selective activation of ?1- and ?2-adrenergic receptors was induced with isoproterenol (0.1 ?mol/L) and ICI-118,551 (0.1 ?mol/L); and with salbutamol (10 ?mol/L) and atenolol (1 ?mol/L), respectively. ?1- and ?2-adrenergic stimulations induced a significant increase in Ca2+ transient amplitude and cell shortening in intact rat ventricular myocytes (i.e., surface sarcolemma and t-tubules) and in detubulated cells (depleted from t-tubules, surface sarcolemma only). Both ?1- and ?2-adrenergic receptors stimulation caused a greater effect on Ca2+ transient and cell shortening in detubulated myocytes than in control myocytes. Quantitative analysis indicates that ?1-adrenergic stimulation is ?3 times more effective at surface sarcolemma compared to t-tubules, whereas ?2- adrenergic stimulation occurs almost exclusively at surface sarcolemma (?100 times more effective). These physiological data demonstrate that in rat ventricular myocytes, ?1-adrenergic receptors are functionally present at surface sarcolemma and t-tubules, while ?2-adrenergic receptors stimulation occurs only at surface sarcolemma of cardiac cells.

Cros, Caroline; Brette, Fabien

2013-01-01

80

Functional subcellular distribution of ?1- and ?2-adrenergic receptors in rat ventricular cardiac myocytes.  

Science.gov (United States)

?-adrenergic stimulation is a key regulator of cardiac function. The localization of major cardiac adrenergic receptors (?1 and ?2) has been investigated using biochemical and biophysical approaches and has led to contradictory results. This study investigates the functional subcellular localization of ?1- and ?2-adrenergic receptors in rat ventricular myocytes using a physiological approach. Ventricular myocytes were isolated from the hearts of rat and detubulated using formamide. Physiological cardiac function was measured as Ca(2+) transient using Fura-2-AM and cell shortening. Selective activation of ?1- and ?2-adrenergic receptors was induced with isoproterenol (0.1 ?mol/L) and ICI-118,551 (0.1 ?mol/L); and with salbutamol (10 ?mol/L) and atenolol (1 ?mol/L), respectively. ?1- and ?2-adrenergic stimulations induced a significant increase in Ca(2+) transient amplitude and cell shortening in intact rat ventricular myocytes (i.e., surface sarcolemma and t-tubules) and in detubulated cells (depleted from t-tubules, surface sarcolemma only). Both ?1- and ?2-adrenergic receptors stimulation caused a greater effect on Ca(2+) transient and cell shortening in detubulated myocytes than in control myocytes. Quantitative analysis indicates that ?1-adrenergic stimulation is ?3 times more effective at surface sarcolemma compared to t-tubules, whereas ?2- adrenergic stimulation occurs almost exclusively at surface sarcolemma (?100 times more effective). These physiological data demonstrate that in rat ventricular myocytes, ?1-adrenergic receptors are functionally present at surface sarcolemma and t-tubules, while ?2-adrenergic receptors stimulation occurs only at surface sarcolemma of cardiac cells. PMID:24303124

Cros, Caroline; Brette, Fabien

2013-08-01

 
 
 
 
81

Dispersion of the QT interval and autonomic modulation of heart rate in hypertensive men with and without left ventricular hypertrophy.  

Science.gov (United States)

Left ventricular hypertrophy is an independent risk factor for sudden cardiac death in hypertension, but the mechanisms of electrical instability associated with hypertrophy are not well known. We studied dispersion of the QT interval, an index of inhomogeneity of repolarization, and heart rate variability, a measure of cardiac autonomic modulation, in a randomly selected population of 162 men with systemic hypertension and made comparisons between the patients with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index > or = 131 g/m2, n = 44) and those without hypertrophy (left ventricular mass index corrected QT dispersion (67 +/- 37 versus 53 +/- 21 milliseconds, P QT apex dispersion (55 +/- 22 versus 44 +/- 16 milliseconds, P left ventricular hypertrophy than in those without hypertrophy. Thirteen of the 44 patients (30%) with hypertrophy versus 7 of the 118 patients (6%) without hypertrophy had an abnormally long QT apex dispersion ( > 70 milliseconds) (P left ventricular hypertrophy. The measures of heart rate variability were not related to QT dispersion or left ventricular mass index but had a negative correlation with blood pressure values (eg, r = -.30 between the low-frequency component of heart rate variability and systolic pressure, P mass index, antihypertensive medication, and the other demographic variables were similar between the groups, but the patients with left ventricular hypertrophy had higher systolic (P Left ventricular hypertrophy in hypertensive men is associated with inhomogeneity of the early phase of ventricular repolarization, favoring susceptibility to reentrant ventricular tachyarrhythmias. Abnormalities in cardiac autonomic function, which may trigger a spontaneous onset of arrhythmias, are related to elevated blood pressure but not specifically to left ventricular hypertrophy. PMID:8675257

Perkiömäki, J S; Ikäheimo, M J; Pikkujämsä, S M; Rantala, A; Lilja, M; Kesäniemi, Y A; Huikuri, H V

1996-07-01

82

Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the spontaneously hypertensive rat.  

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To determine whether chronic antihypertensive therapy prevents the progression of cardiac hypertrophy and the deterioration in cardiac performance observed in spontaneously hypertensive rats (SHR) with long-term hypertension, 14-month-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 months with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/liter of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-month-old SHR (un...

Pfeffer, J. M.; Pfeffer, M. A.; Mirsky, I.; Braunwald, E.

1982-01-01

83

Molecular phenotype of right ventricular hypertrophy in human tetralogy of Fallot  

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In 1888 the French physician Etienne-Louis Arthur Fallot described a “tetrad” of congenital anatomical defects in a heart, which are now collectively referred to as tetralogy of Fallot (TF). TF is characterized by a (sub)valvular pulmonary stenosis, a ventricular septal defect (VSD), dextroposition of the aorta (overriding the VSD) and concomitant right ventricular hypertrophy (RVH) (Fig. 1.1). The right ventricular (RV) outflowtract obstruction can be more or less severe, ...

Peters, T. H. F.

2003-01-01

84

Modeling CICR in rat ventricular myocytes: voltage clamp studies  

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Abstract Background The past thirty-five years have seen an intense search for the molecular mechanisms underlying calcium-induced calcium-release (CICR) in cardiac myocytes, with voltage clamp (VC) studies being the leading tool employed. Several VC protocols including lowering of extracellular calcium to affect Ca2+ loading of the sarcoplasmic reticulum (SR), and administration of blockers caffeine and thapsigargin have been utilized to probe the phenome...

2010-01-01

85

Left Ventricular Hypertrophy May Be Transient in the Emergency Department  

Directory of Open Access Journals (Sweden)

Full Text Available Background: While research has established that the bedside electrocardiogram (ECG is an insensitive test for the presence or absence of left ventricular hypertrophy (LVH, the finding, when present, is thought to be reproducible.Objective: To assess the reproducibility of serial ECGs done in the emergency department (ED with regard to the presence or absence of LVH.Method: A prospective study on consecutive patients admitted to an ED-run cardiac observation unit. A single reviewer collected and scored ECGs for the presence of LVH, using three established criteria (Cornell, Sokolow-Lyon and Romhilt-Estes. Demographic and medical history was also collected.Results: Over a three-year time period, 295 patients were enrolled; 132 males and 163 females with a mean age of 54.4 years (range, 19-89 years. The prevalence of LVH ranged from 11-14% and the agreement among all three criteria was fair (kappa = 0.325. Using the Cornell criteria, 33 patients had ECG#1 consistent with LVH. Of the patients meeting LVH criteria on ECG #1, only 15 retained their diagnosis of LVH on ECG#2 (i.e. 55% of the LVH identified in ECG#1 was not seen in ECG#2. Additionally, nine patients developed an ECG diagnosis of LVH between ECG#1 and ECG#2. In total, 27 (nine percent of the total had ECG measurements that changed between ECG#1 and ECG#2. We made similar findings with the Sokolow-Lyon and Romhilt-Estes criteria. The results were not modified by gender, blood pressure or medication use.Conclusion: The finding of LVH on ECG was not very reproducible during serial measurements on the same person during a single 24-hour observation period.[WestJEM. 2009;10:140-143

Shoenberger, Jan M

2009-08-01

86

Prevalencia de hipertrofia ventricular izquierda en pacientes diabéticos / Prevalence of left ventricular hypertrophy in diabetic patients  

Scientific Electronic Library Online (English)

Full Text Available SciELO Public Health | Language: Spanish Abstract in spanish Con el objetivo de establecer la prevalencia de hipertrofia ventricular izquierda (HVI) en pacientes con diabetes mellitus tipo 2 (DM), se realizó un estudio transversal en estos pacientes, estableciendo sus características antropométricas, presión arterial y control metabólico. Para evaluar la pres [...] encia de HVI se empleó ecocardiografía transtorácica. El estudio incluyó 91 pacientes, en los cuales la prevalencia de HVI fue de 63,7%, siendo más frecuente en mujeres que en varones (p=0,001). Adicionalmente, se encontró un 46,2% de pacientes con disfunción diastólica del ventrículo izquierdo. Se concluye que existe una importante prevalencia de HVI en pacientes diabéticos sin antecedentes de causas definidas de hipertrofia. No se encontró relación con sexo, control metabólico, IMC y tiempo de diagnóstico Abstract in english In order to establish the prevalence of left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus, (DM) a cross-sectional study was conducted in these patients studying their anthropometric characteristics, blood pressure and metabolic control. To evaluate the presence of LVH, a t [...] rans-thoracic echocardiogram was used. The study included 91 patients, finding a 63.7% prevalence of HVI, with women being more affected than men (p=0.001). Additionally, 46.2% of patients were found to have diastolic dysfunction of the left ventricle. We conclude that there is an important prevalence of LVH in diabetic patients without defined causes of hypertrophy. There was no association with sex, metabolic control, BMI and time of diagnosis

Valarezo-Sevilla, Diego; Pazmiño-Martínez, Armín; Morales-Mora, Nidya.

87

Prevalencia de hipertrofia ventricular izquierda en pacientes diabéticos / Prevalence of left ventricular hypertrophy in diabetic patients  

Scientific Electronic Library Online (English)

Full Text Available SciELO Peru | Language: Spanish Abstract in spanish Con el objetivo de establecer la prevalencia de hipertrofia ventricular izquierda (HVI) en pacientes con diabetes mellitus tipo 2 (DM), se realizó un estudio transversal en estos pacientes, estableciendo sus características antropométricas, presión arterial y control metabólico. Para evaluar la pres [...] encia de HVI se empleó ecocardiografía transtorácica. El estudio incluyó 91 pacientes, en los cuales la prevalencia de HVI fue de 63,7%, siendo más frecuente en mujeres que en varones (p=0,001). Adicionalmente, se encontró un 46,2% de pacientes con disfunción diastólica del ventrículo izquierdo. Se concluye que existe una importante prevalencia de HVI en pacientes diabéticos sin antecedentes de causas definidas de hipertrofia. No se encontró relación con sexo, control metabólico, IMC y tiempo de diagnóstico Abstract in english In order to establish the prevalence of left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus, (DM) a cross-sectional study was conducted in these patients studying their anthropometric characteristics, blood pressure and metabolic control. To evaluate the presence of LVH, a t [...] rans-thoracic echocardiogram was used. The study included 91 patients, finding a 63.7% prevalence of HVI, with women being more affected than men (p=0.001). Additionally, 46.2% of patients were found to have diastolic dysfunction of the left ventricle. We conclude that there is an important prevalence of LVH in diabetic patients without defined causes of hypertrophy. There was no association with sex, metabolic control, BMI and time of diagnosis

Valarezo-Sevilla, Diego; Pazmiño-Martínez, Armín; Morales-Mora, Nidya.

88

Mechanical Effects on KATP Channel Gating in Rat Ventricular Myocytes  

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Cardiac KATP channels link metabolism with electrical activity. They are implicated in arrhythmias, secretion of atrial natriuretic peptide and protection of the heart from hypertrophy and failure. These processes may involve mechanosensitivity. KATP channels can be activated by mechanical stimulation and disrupting the cortical actin increases the activity. We propose that KATP channels are modulated by local bilayer tension and this tension is affected by cortical F-actin. Here we measured ...

Huang, Haixia; Liang, Lifang; Liu, Ping; Wei, Hua; Sachs, Frederick; Niu, Weizhen; Wang, Wei

2013-01-01

89

Inotropic response of rabbit ventricular myocytes to endothelin-1: difference from isolated papillary muscles.  

Science.gov (United States)

Endothelin-1 (ET-1) increased cell shortening and Ca2+ transients over the concentration of 3 x 10(-11) M to 10(-9) M with EC50 of 8.3 x 10(-11) M in rabbit single ventricular myocytes. Thus ET-1 was approximately 60 times more potent in single myocytes than in papillary muscles (EC50 = 5.1 x 10(-9) M) of the same species. In single myocytes, ET-1 at 10(-8) M elicited an inhibitory response that counteracted the facilitatory response: the concentration-response curve (CRC) for ET-1 was bell shaped. The ET(A)-receptor antagonist BQ-485 shifted CRC for ET-1 to the right in parallel; however, the facilitatory response to 10(-8) M ET-1 was markedly enhanced by BQ-485 and also by the ET(B) antagonist BQ-788. The ET(A)/ET(B) antagonist TAK-044 abolished the ET-1-induced response. These findings indicate that the response to ET-1 of single myocytes is different from that of papillary muscles in concentration dependence, characteristics of the response, and susceptibility to ET-receptor antagonists. Anomalous pharmacological characteristics of ET-1-induced response in rabbit papillary muscles may be due to integrated regulatory mechanisms that may involve also various types of noncardiac cell in ventricular myocardium. PMID:11454562

Talukder, M A; Norota, I; Sakurai, K; Endoh, M

2001-08-01

90

Stretch Current-induced Abnormal Impulses in CaMKII? Knockout Mouse Ventricular Myocytes  

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Background CaMKII activation is pro-arrhythmic in heart failure where myocardium is stretched. However, the arrhythmogenic role of CaMKII in stretched ventricle has not been well understood. Objective We tested abnormal impulse inducibility by stretch current in myocytes isolated from CaMKII? knockout (KO) mouse left ventricle (LV) where CaMKII activity is reduced by ? 62%. Methods and Results Action potentials (APs) were recorded by whole-cell patch clamp, and abnormal impulses were induced in LV myocytes by a simulation of stretch-activated-channel (SAC) current. SAC activation failed to induce abnormal impulses in wild type (WT) myocytes but steadily produced early afterdepolarizations (EADs) and automaticity in KO myocytes in which an increase in L-type calcium channel (LTCC) current (ICa) and a reduction of sarcoplasmic reticulum (SR) Ca2+ leak and action potential duration (APD) were observed. The abnormal impulses were not suppressed by CaMKII inhibitor AIP whereas a low concentration of nifedipine eliminated abnormal impulses without shortening APD, implicating ICa in promoting stretch-induced abnormal impulses. In addition, APD prolongation by LTCC opener S(?)Bay K 8644 or isoproterenol facilitated abnormal impulse induction in WT ventricular myocytes even in the presence of CaMKII inhibitor AIP, whereas APD prolongation by K+ channel blocker 4-aminopyridine promoted abnormal impulses in KO myocytes but not in WT myocytes. Conclusion ICa activation plays a central role in stretch-induced abnormal impulses and APD prolongation is arrhythmogenic only when ICa is highly activated. At increased ICa activation, CaMKII inhibition cannot suppress abnormal impulse induction.

Lai, Dongwu; Xu, Lin; Cheng, Jun; Guilbert, Arnaud B.; Lim, Hyun Joung; Fu, Guosheng; Wang, Yanggan

2012-01-01

91

In situ calibration of fura-2 and BCECF fluorescence in adult rat ventricular myocytes  

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Quantitation of Ca+ and H+ activities within cells using presently available fluorescent probes is optimal when the fluorescence signal is calibrated in situ after each experiment. Fura-2 and 2',7'-bis(2-carboxy-ethyl)-5,6-carboxyfluoroscein (BCECF) are difficult to calibrate in freshly dissociated adult cardiac myocytes because calibration procedures produce cellular hypercontracture. In situ calibration was accomplished in rat ventricular cells by saturating fura-2 with La3+, an agent known...

1990-01-01

92

Phorbol ester activation of chloride current in guinea-pig ventricular myocytes.  

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1. Although earlier studies with phorbol esters indicate that protein kinase C (PKC) may be an important regulator of Cl- current (Icl) in cardiac cells, there is a need for additional quantitative data and investigation of conflicting findings. Our objectives were to measure the magnitude, time course, and concentration-dependence of Icl activated in guinea-pig ventricular myocytes by phorbol 12-myristate 13-acetate (PMA), evaluate its PKC dependence, and examine its modification by external...

1996-01-01

93

Model of Excitation-Contraction Coupling of Rat Neonatal Ventricular Myocytes  

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The neonatal rat ventricular myocyte culture is one of the most popular experimental cardiac cell models. To our knowledge, the excitation-contraction coupling (ECC) of these cells, i.e., the process linking the electrical activity to the cytosolic Ca2+ transient and contraction, has not been previously analyzed, nor has it been presented as a complete system in detail. Neonatal cardiomyocytes are in the postnatal developmental stage, and therefore, the features of their ECC differ vastly fro...

Korhonen, Topi; Ha?nninen, Sandra L.; Tavi, Pasi

2009-01-01

94

Swelling-activated Gd3+-sensitive Cation Current and Cell Volume Regulation in Rabbit Ventricular Myocytes  

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The role of swelling-activated currents in cell volume regulation is unclear. Currents elicited by swelling rabbit ventricular myocytes in solutions with 0.6–0.9× normal osmolarity were studied using amphotericin perforated patch clamp techniques, and cell volume was examined concurrently by digital video microscopy. Graded swelling caused graded activation of an inwardly rectifying, time-independent cation current (ICir,swell) that was reversibly blocked by Gd3+, but ICir,swell was not...

1997-01-01

95

Fetal right-ventricular hypertrophy with pericardial effusion and maternal untreated hyperthyroidism.  

Science.gov (United States)

Uncontrolled/untreated maternal hyperthyroidism has been associated with fetal tachycardia. We report a case of right-ventricular (RV) hypertrophy with pericardial effusion related to untreated maternal Graves' disease. A 33-year-old G4P1021 woman with uncontrolled Graves' disease presented at 29 weeks gestation with abdominal pain and vaginal bleeding. Fetal echocardiogram showed severe RV hypertrophy and a pericardial effusion. The infant was born prematurely, and initial transthoracic echocardiogram showed severe RV hypertrophy and a small pericardial effusion. The infant had clinical findings consistent with congenital thyrotoxicosis and was treated for this. Follow-up imaging at 4 weeks showed improvement of the cardiac hypertrophy and pericardial effusion. This article describes the presentation of fetal RV hypertrophy with congenital thyrotoxicosis and underscores the importance of screening for this prenatally in mothers with uncontrolled or untreated hyperthyroidism. PMID:23179424

Kwon, Elena N; Kambalapalli, Mamatha; Francis, Gary; Donofrio, Mary T

2013-12-01

96

Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure  

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MicroRNAs (miRs) are small, noncoding RNAs that are emerging as crucial regulators of cardiac remodeling in left ventricular hypertrophy (LVH) and failure (LVF). However, there are no data on their role in right ventricular hypertrophy (RVH) and failure (RVF). This is a critical question given that the RV is uniquely at risk in patients with congenital right-sided obstructive lesions and in those with systemic RVs. We have developed a murine model of RVH and RVF using pulmonary artery constri...

Reddy, Sushma; Zhao, Mingming; Hu, Dong-qing; Fajardo, Giovanni; Hu, Shijun; Ghosh, Zhumur; Rajagopalan, Viswanathan; Wu, Joseph C.; Bernstein, Daniel

2012-01-01

97

Telmisartan regresses left ventricular hypertrophy in caveolin-1 deficient mice  

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The role of angiotensin II (Ang II) in promoting cardiac hypertrophy is well known, however the role of the Ang II in a spontaneous model of hypertrophy in mice lacking the protein caveolin-1 (Cav- KO) has not been explored. In this study, WT and Cav-1 KO mice were treated with angiotensin receptor blocker (ARB), telmisartan, and cardiac function assessed by echocardiography. Treatment of Cav-1 KO mice with telmisartan significantly improved cardiac function compared to age-matched, vehicle t...

Kreiger, Marta H.; Di Lorenzo, Annarita; Teutsch, Christine; Kauser, Katalin; Sessa, William C.

2010-01-01

98

Echocardiography-based left ventricular mass estimation. How should we define hypertrophy?  

Directory of Open Access Journals (Sweden)

Full Text Available Abstract Left ventricular hypertrophy is an important risk factor in cardiovascular disease and echocardiography has been widely used for diagnosis. Although an adequate methodologic standardization exists currently, differences in measurement and interpreting data is present in most of the older clinical studies. Variability in border limits criteria, left ventricular mass formulas, body size indexing and other adjustments affects the comparability among these studies and may influence both the clinical and epidemiologic use of echocardiography in the investigation of the left ventricular structure. We are going to review the most common measures that have been employed in left ventricular hypertrophy evaluation in the light of some recent population based echocardiographic studies, intending to show that echocardiography will remain a relatively inexpensive and accurate tool diagnostic tool.

Rohde Luis EP

2005-06-01

99

Aliskiren limits abdominal aortic aneurysm, ventricular hypertrophy and atherosclerosis in an apolipoprotein-E-deficient mouse model.  

Science.gov (United States)

Aliskiren is a direct renin inhibitor developed to treat hypertension. Several clinical studies have suggested that aliskiren has beneficial effects on cardiovascular diseases beyond its antihypertensive effect. In the present study, we examined whether aliskiren limits the progression of AAA (abdominal aortic aneurysm), VH (ventricular hypertrophy) and atherosclerosis in an AngII (angiotensin II)-infused mouse model. ApoE-/- (apolipoprotein-E-deficient) mice were infused subcutaneously with AngII (1000 ng/kg of body weight per day; 4 weeks) to induce AAA and VH. At the completion of the AngII infusion, mice were randomly allocated to three groups to receive vehicle control, low-dose aliskiren (10 mg/kg of body weight per day) or high-dose aliskiren (50 mg/kg of body weight per day) for 4 weeks. Suprarenal aortic diameter assessed by ultrasound was significantly smaller in mice administered aliskiren at days 42 and 56. Aliskiren also significantly reduced the normalized heart weight, ventricular myocyte cell width and aortic arch atherosclerosis. Aliskiren lowered PRR (pro-renin receptor) expression and MAPK (mitogen-activated protein kinase) activity in the suprarenal aorta and heart. Aortic infiltration of T-lymphocytes and macrophages was reduced by aliskiren. In conclusion, aliskiren limits the progression of AAA, VH and atherosclerosis in an AngII-infused mouse model. PMID:24476071

Seto, Sai-Wang; Krishna, Smriti M; Moran, Corey S; Liu, David; Golledge, Jonathan

2014-07-01

100

Organic Nitrates Favor Regression of Left Ventricular Hypertrophy in Hypertensive Patients on Chronic Peritoneal Dialysis  

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The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH) in hypertensive patients on chronic peritoneal dialysis (PD). Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group) took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group) took other antihypertensive drugs. Blood pressure (BP), left ventricular mass index (...

Han Li; Shixiang Wang

2013-01-01

 
 
 
 
101

Hypertension and hyperparathyroidism are associated with left ventricular hypertrophy in patients on hemodialysis  

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Conflicting data for association between left ventricular hypertrophy (LVH) and secondary hyperparathyroidism has been reported previously among dialysis patients. The present study was conducted to evaluate the association of hyperparathyroidism and hypertension with LVH. Charts of 130 patients on hemodialysis for at least six months were reviewed. All were subjected to M-mode echocardiography. Left ventricular mass (LVM) was calculated by Devereux's formula. LVM Index (LVMI) was calculated ...

Al-hilali, N.; Hussain, N.; Ataia, A. I.; Al-azmi, M.; Al-helal, B.; Johny, K. V.

2009-01-01

102

Echocardiography-based left ventricular mass estimation. How should we define hypertrophy?  

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Abstract Left ventricular hypertrophy is an important risk factor in cardiovascular disease and echocardiography has been widely used for diagnosis. Although an adequate methodologic standardization exists currently, differences in measurement and interpreting data is present in most of the older clinical studies. Variability in border limits criteria, left ventricular mass formulas, body size indexing and other adjustments affects the comparability among these studies and may influ...

Foppa Murilo; Duncan Bruce B; Ep, Rohde Luis

2005-01-01

103

Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study.  

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We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) ...

Veglio, Franco

2011-01-01

104

QT interval dispersion in chronic heart failure and left ventricular hypertrophy: relation to autonomic nervous system and Holter tape abnormalities.  

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OBJECTIVE--To study QT dispersion in left ventricular hypertrophy and chronic heart failure and to determine the relation to ventricular arrhythmias. SETTING--Investigational laboratory of a tertiary referral centre. STUDY DESIGN--Patients with left ventricular hypertrophy and normal systolic function (n = 14) and patients with chronic heart failure (n = 18) were matched with controls (n = 17). The QT dispersion was examined in relation to abnormalities in resting mechanical and autonomic fun...

Davey, P. P.; Bateman, J.; Mulligan, I. P.; Forfar, C.; Barlow, C.; Hart, G.

1994-01-01

105

Cardiomyocyte-Specific Overexpression of HEXIM1 Prevents Right Ventricular Hypertrophy in Hypoxia-Induced Pulmonary Hypertension in Mice  

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Right ventricular hypertrophy (RVH) and right ventricular (RV) contractile dysfunction are major determinants of prognosis in pulmonary arterial hypertension (PAH) and PAH remains a severe disease. Recently, direct interruption of left ventricular hypertrophy has been suggested to decrease the risk of left-sided heart failure. Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) is a negative regulator of positive transcription elongation factor b (P-TEFb), which activates RNA polymerase ...

Yoshikawa, Noritada; Shimizu, Noriaki; Maruyama, Takako; Sano, Motoaki; Matsuhashi, Tomohiro; Fukuda, Keiichi; Kataoka, Masaharu; Satoh, Toru; Ojima, Hidenori; Sawai, Takashi; Morimoto, Chikao; Kuribara, Akiko; Hosono, Osamu; Tanaka, Hirotoshi

2012-01-01

106

Adult ECG criteria for left ventricular hypertrophy in young competitive athletes.  

Science.gov (United States)

Time-tested data indicate that ECG diagnosis of left ventricular hypertrophy in young athletes is challenging due to low sensitivity of the commonly used criteria. We sought to establish whether adult ECG criteria can be appropriate to make diagnosis of both common and uncommon patterns of left ventricular hypertrophy in young trained athletes. A total of 122 athletes, ages 16.2±3.8 years, training at least 5?h per week, were studied with Sokolow-Lyon voltage, Romhilt-Estes, Cornell voltage, Cornell Product, Perugia and Framingham scores. Garson Criteria were also investigated in athletes under 16. Participants were divided into 2 groups based on the presence (group-A, n=56) or absence (group-B, n=66) of at least one positive ECG score. Test performance was calculated with respect to accurate echocardiographic diagnosis of left ventricular hypertrophy. There were no inter-group differences regarding physical characteristics and training burden. 9 athletes from group-A (16%) and 2 from group-B (3%) were found to have left ventricular hypertrophy, likely to be pathological in 2 cases from group-A. Criteria gathering both QRS voltages and ST-T anomalies, like Perugia-score, best identified this subgroup and should be preferred to those based on QRS voltage analysis alone. PMID:23900896

Speranza, G; Magaudda, L; de Gregorio, C

2014-03-01

107

Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo  

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Signaling events controlled by calcineurin promote cardiac hypertrophy, but the degree to which such pathways are required to transduce the effects of various hypertrophic stimuli remains uncertain. In particular, the administration of immunosuppressive drugs that inhibit calcineurin has inconsistent effects in blocking cardiac hypertrophy in various animal models. As an alternative approach to inhibiting calcineurin in the hearts of intact animals, transgenic mice ...

Rothermel, Beverly A.; Mckinsey, Timothy A.; Vega, Rick B.; Nicol, Rebekka L.; Mammen, Pradeep; Yang, John; Antos, Christopher L.; Shelton, John M.; Bassel-duby, Rhonda; Olson, Eric N.; Williams, R. Sanders

2001-01-01

108

Rescue of cardiomyocyte dysfunction by phospholamban ablation does not prevent ventricular failure in genetic hypertrophy  

Science.gov (United States)

Cardiac hypertrophy, either compensated or decompensated, is associated with cardiomyocyte contractile dysfunction from depressed sarcoplasmic reticulum (SR) Ca2+ cycling. Normalization of Ca2+ cycling by ablation or inhibition of the SR inhibitor phospholamban (PLN) has prevented cardiac failure in experimental dilated cardiomyopathy and is a promising therapeutic approach for human heart failure. However, the potential benefits of restoring SR function on primary cardiac hypertrophy, a common antecedent of human heart failure, are unknown. We therefore tested the efficacy of PLN ablation to correct hypertrophy and contractile dysfunction in two well-characterized and highly relevant genetic mouse models of hypertrophy and cardiac failure, G?q overexpression and human familial hypertrophic cardiomyopathy mutant myosin binding protein C (MyBP-CMUT) expression. In both models, PLN ablation normalized the characteristically prolonged cardiomyocyte Ca2+ transients and enhanced unloaded fractional shortening with no change in SR Ca2+ pump content. However, there was no parallel improvement in in vivo cardiac function or hypertrophy in either model. Likewise, the activation of JNK and calcineurin associated with G?q overexpression was not affected. Thus, PLN ablation normalized contractility in isolated myocytes, but failed to rescue the cardiomyopathic phenotype elicited by activation of the G?q pathway or MyBP-C mutations.

Song, Qiujing; Schmidt, Albrecht G.; Hahn, Harvey S.; Carr, Andrew N.; Frank, Beate; Pater, Luke; Gerst, Mike; Young, Karen; Hoit, Brian D.; McConnell, Bradley K.; Haghighi, Kobra; Seidman, Christine E.; Seidman, Jonathan G.; Dorn, Gerald W.; Kranias, Evangelia G.

2003-01-01

109

Left ventricular hypertrophy in Turner syndrome : a prospective echocardiographic study  

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Cardiovascular risk stratification in Turner syndrome (TS) is difficult. Increased left ventricular mass associates with an adverse prognosis in several settings, and this study aimed to elucidate this risk marker in relation to metabolic and cardiovascular status in TS.

Mortensen, Kristian Havmand; Gravholt, Claus Højbjerg

2012-01-01

110

Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study  

DEFF Research Database (Denmark)

In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload Udgivelsesdato: 2008/7

Chinali, M.; Simone, G. de

2008-01-01

111

Validation of an in vitro contractility assay using canine ventricular myocytes  

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Measurement of cardiac contractility is a logical part of pre-clinical safety assessment in a drug discovery project, particularly if a risk has been identified or is suspected based on the primary- or non-target pharmacology. However, there are limited validated assays available that can be used to screen several compounds in order to identify and eliminate inotropic liability from a chemical series. We have therefore sought to develop an in vitro model with sufficient throughput for this purpose. Dog ventricular myocytes were isolated using a collagenase perfusion technique and placed in a perfused recording chamber on the stage of a microscope at ? 36 °C. Myocytes were stimulated to contract at a pacing frequency of 1 Hz and a digital, cell geometry measurement system (IonOptix™) was used to measure sarcomere shortening in single myocytes. After perfusion with vehicle (0.1% DMSO), concentration–effect curves were constructed for each compound in 4–30 myocytes taken from 1 or 2 dog hearts. The validation test-set was 22 negative and 8 positive inotropes, and 21 inactive compounds, as defined by their effect in dog, cynolomolgous monkey or humans. By comparing the outcome of the assay to the known in vivo contractility effects, the assay sensitivity was 81%, specificity was 75%, and accuracy was 78%. With a throughput of 6–8 compounds/week from 1 cell isolation, this assay may be of value to drug discovery projects to screen for direct contractility effects and, if a hazard is identified, help identify inactive compounds. -- Highlights: ? Cardiac contractility is an important physiological function of the heart. ? Assessment of contractility is a logical part of pre-clinical drug safety testing. ? There are limited validated assays that predict effects of compounds on contractility. ? Using dog myocytes, we have developed an in vitro cardiac contractility assay. ? The assay predicted the in vivo contractility with a good level of accuracy.

Harmer, A.R., E-mail: alex.harmer@astrazeneca.com; Abi-Gerges, N.; Morton, M.J.; Pullen, G.F.; Valentin, J.P.; Pollard, C.E.

2012-04-15

112

Regulation of sarcoplasmic reticulum Ca(2+) release by cytosolic glutathione in rabbit ventricular myocytes.  

Science.gov (United States)

Of the major cellular antioxidant defenses, glutathione (GSH) is particularly important in maintaining the cytosolic redox potential. Whereas the healthy myocardium is maintained at a highly reduced redox state, it has been proposed that oxidation of GSH can affect the dynamics of Ca(2+)-induced Ca(2+) release. In this study, we used multiple approaches to define the effects of oxidized glutathione (GSSG) on ryanodine receptor (RyR)-mediated Ca(2+) release in rabbit ventricular myocytes. To investigate the role of GSSG on sarcoplasmic reticulum (SR) Ca(2+) release induced by the action potential, we used the thiol-specific oxidant diamide to increase intracellular GSSG in intact myocytes. To more directly assess the effect of GSSG on RyR activity, we introduced GSSG within the cytosol of permeabilized myocytes. RyR-mediated Ca(2+) release from the SR was significantly enhanced in the presence of GSSG. This resulted in decreased steady-state diastolic [Ca(2+)]SR, increased SR Ca(2+) fractional release, and increased spark- and non-spark-mediated SR Ca(2+) leak. Single-channel recordings from RyR's incorporated into lipid bilayers revealed that GSSG significantly increased RyR activity. Moreover, oxidation of RyR in the form of intersubunit crosslinking was present in intact myocytes treated with diamide and permeabilized myocytes treated with GSSG. Blocking RyR crosslinking with the alkylating agent N-ethylmaleimide prevented depletion of SR Ca(2+) load induced by diamide. These findings suggest that elevated cytosolic GSSG enhances SR Ca(2+) leak due to redox-dependent intersubunit RyR crosslinking. This effect can contribute to abnormal SR Ca(2+) handling during periods of oxidative stress. PMID:24334252

Mazurek, Stefan R; Bovo, Elisa; Zima, Aleksey V

2014-03-01

113

Influence of left ventricular hypertrophy on infarct size and left ventricular ejection fraction in ST-elevation myocardial infarction  

International Nuclear Information System (INIS)

Background: Left ventricular hypertrophy (LVH) predisposes to larger infarct size, which may be underestimated by the left ventricular ejection fraction (LVEF) due to supranormal systolic performance often present in patients with LVH. The aim of the study was to compare infarct size and LVEF in patients with ST-segment elevation myocardial infarction (STEMI) and increased left ventricular mass on cardiac magnetic resonance (CMR). Methods: The study included unselected group of 52 patients (61 ± 11 years, 69% male) with first STEMI who had CMR after median 5 days from the onset of the event. Left ventricular hypertrophy (LVH) was defined as left ventricular mass index exceeding 95th percentile of references values for age and gender. Infarct size was assessed with means of late gadolinium enhancement (LGE). Results: LVH was found in 16 patients (31%). In comparison to the rest of the group, patients with LVH had higher absolute and relative infarct mass (p = 0.002 and p = 0.02, respectively). LVH was related to higher prevalence of microvascular obstruction and myocardial haemorrhage and higher number of LV segments with transmural necrosis (p = 0.02, p = 0.01 and p = 0.01, respectively). Despite marked difference in the infarct size between both studied subgroups there was no difference in LVEF and mean number of dysfunctional LV segments. Conclusions: Patients with LVH undergoing STEMI have larger infarct size underestimated by the LV systolic performance in comparison to patients without LVH.

2012-03-01

114

LabHEART: an interactive computer model of rabbit ventricular myocyte ion channels and Ca transport  

Science.gov (United States)

An interactive computer program, LabHEART, was developed to simulate the action potential (AP), ionic currents, and Ca handling mechanisms in a rabbit ventricular myocyte. User-oriented, its design allows switching between voltage and current clamp and easy on-line manipulation of key parameters to change the original formulation. The model reproduces normal rabbit ventricular myocyte currents, Ca transients, and APs. We also changed parameters to simulate data from heart failure (HF) myocytes, including reduced transient outward (I(to)) and inward rectifying K currents (I(K1)), enhanced Na/Ca exchange expression, and reduced sarcoplasmic reticulum Ca-ATPase function, but unaltered Ca current density. These changes caused reduced Ca transient amplitude and increased AP duration (especially at lower frequency) as observed experimentally. The model shows that the increased Na/Ca exchange current (I(NaCa)) in HF lowers the intracellular [Ca] threshold for a triggered AP from 800 to 540 nM. Similarly, the decrease in I(K1) reduces the threshold to 600 nM. Changes in I(to) have no effect. Combining enhanced Na/Ca exchange with reduced I(K1) (as in HF) lowers the threshold to trigger an AP to 380 nM. These changes reproduce experimental results in HF, where the contributions of different factors are not readily distinguishable. We conclude that the triggered APs that contribute to nonreentrant ventricular tachycardia in HF are due approximately equally (and nearly additively) to alterations in I(NaCa) and I(K1). A free copy of this software can be obtained at http://www.meddean.luc.edu/lumen/DeptWebs/physio/bers.html.

Puglisi, J. L.; Bers, D. M.

2001-01-01

115

Body size adjustments for left ventricular mass by cardiovascular magnetic resonance and their impact on left ventricular hypertrophy classification  

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Methods to index left ventricular (LV) mass, measured by cardiovascular magnetic resonance (CMR), for body size have not been investigated. The purposes of this study were to develop allometric indices for LV mass measured by CMR and compare estimates of the prevalence and predictive value of LV hypertrophy defined by a new allometric height-weight index, LV mass/body surface area (BSA), height indices (a new allometric height index; and previously derived indices from echocardiographic measu...

Brumback, Lyndia C.; Kronmal, Richard; Heckbert, Susan R.; Ni, Hanyu; Hundley, W. Gregory; Lima, Joa?o A.; Bluemke, David A.

2010-01-01

116

Gap junctional conductance between pairs of ventricular myocytes is modulated synergistically by H+ and Ca++  

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Gap junctional conductance (gj) between cardiac ventricular myocyte pairs is rapidly, substantially, and reversibly reduced by sarcoplasmic acidification with CO2 when extracellular calcium activity is near physiological levels (1.0 mM CaCl2 added; 470 microM Ca++). Intracellular calcium concentration (Cai), measured by fura-2 fluorescence in cell suspensions, was 148 +/- 39 nM (+/- SEM, n = 6) and intracellular pH (pHi), measured with intracellular ion-selective microelectrodes, was 7.05 +/-...

1990-01-01

117

Effects of propafenone on calcium currents in single ventricular myocytes of guinea-pig.  

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1. The effects of propafenone on the inward calcium current (ICa) were investigated in isolated single ventricular myocytes of the guinea-pig by the whole-cell clamp method. Propafenone inhibited ICa in a dose-dependent manner at concentrations of propafenone ranging from 1 x 10(-8) to 1 x 10(-3) M and half maximal block of ICa occurred at a propafenone concentration of 1.5 x 10(-6) M. Propafenone did not change the current-voltage relation of ICa other than a reduction in amplitude and showe...

1993-01-01

118

Effects of propafenone on calcium current in guinea-pig ventricular myocytes.  

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1. The modulation of L-type voltage-sensitive calcium channels in guinea-pig isolated ventricular myocytes by propafenone was examined by the whole cell voltage-clamp technique. 2. Propafenone, 10(-7) -5 x 10(-5) M, produced a concentration-dependent inhibition of Ca current (ICa) without any significant change in the current-voltage relation. Half-blocking concentration (IC50) of propafenone for the peak ICa at +10 mV was 5 x 10(-6) M. 3. The voltage-dependence of ICa inactivation was shifte...

1993-01-01

119

Metabolic Inhibition Strongly Inhibits Na+-Dependent Mg2+ Efflux in Rat Ventricular Myocytes  

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We measured intracellular Mg2+ concentration ([Mg2+]i) in rat ventricular myocytes using the fluorescent indicator furaptra (25°C). In normally energized cells loaded with Mg2+, the introduction of extracellular Na+ induced a rapid decrease in [Mg2+]i: the initial rate of decrease in [Mg2+]i (initial ?[Mg2+]i/?t) is thought to represent the rate of Na+-dependent Mg2+ efflux (putative Na+/Mg2+ exchange). To determine whether Mg2+ efflux depends directly on energy derived from cellular metab...

Tashiro, Michiko; Inoue, Hana; Konishi, Masato

2009-01-01

120

Pathophysiologic assessment of left ventricular hypertrophy and strain in asymptomatic patients with essential hypertension  

International Nuclear Information System (INIS)

To investigate the significance of the electrocardiographic (ECG) pattern of left ventricular hypertrophy and strain, two groups of asymptomatic patients with essential hypertension were compared. The patients were similar in terms of age, smoking habit, serum cholesterol and blood pressure levels, but differed in the presence (Group I, n = 23) or absence (Group II, n = 23) of the ECG pattern of left ventricular hypertrophy and strain. Group I patients had significantly more episodes of exercise-induced ST segment depression (14 versus 4, p less than 0.05) and reversible thallium perfusion abnormalities (11 of 23 versus 3 of 23, p less than 0.05) despite similar exercise capacity and absence of chest pain. Nonsustained ventricular tachycardia was detected on 24 h ambulatory ECG monitoring in two patients in Group I, but no patient in Group II. Coronary arteriography performed in 20 Group I patients demonstrated significant coronary artery disease in 8 patients. This study has shown that there is a subgroup of hypertensive patients with ECG left ventricular hypertrophy and strain who have covert coronary artery disease. This can be detected by thallium perfusion scintigraphy, and may contribute to the increased risk known to be associated with this ECG abnormality

1989-01-01

 
 
 
 
121

Effects of nifedipine on left ventricular systolic and diastolic functions in patients with left ventricular hypertrophy  

International Nuclear Information System (INIS)

The effect of nifedpine on left ventricular (LV) systolic and diastolic function was studied in 10 patients with hypertrophic cadiomyopathy(HCM), 8 patients with hypertensive hypertrophy(HT) and 9 normal subjects. Multigated cardiac blood pool imaging with Tc-99m were obtained at 40-degree left anterior oblique position before and after nifedipine administration (10 mg, sublingually). As systolic indices, we obtained LV ejection fraction and mean first third ejection rate. And as diastolic indices, mean filling rate during first third of diastole (1/3 FRsub(mean)) and diastolic maximal filling rate were calculated. Before nifedipine, systolic indices were significantly superior in HCM group than in other 2 groups, and diastolic indices were significantly lower in HCM and HT groups than in normal. After nifedipine, systolic indices improved in HT group but they did not change in other 2 groups. Diastolic indices improved significantly in HCM and HT groups after nifedpine. In HCM group, 1/3 FRsub(mean) improved more markedly in symptomatic patients than in asymptomatic patients. The ratio of diastolic function to systolic function (1/3 FRsub(mean)/1/3 ERsub(mean)) did not change in normal and HT groups but it increased significantly in HCM group. There we a slight increase in heart rate (HR) and decrease in systemic arterial pressure (BP). The increase in HR was similar among 3 groups but the decrease in BP was significantly greater in HT group in whom control BP was significantly higher than other groups. LV end-diastolic volume did not change in 3 groups by nifedipine administration. These data suggested that abnormal diastolic function in HCM and HT was faborably modified by nifedipine, but their mechanisms were different. In HT, it was considered to relate with improved systolic function due to LV afterload reduction, while in HCM, it was not related to the peripheral hemodynamic effects nor improved systolic function. (author)

1984-01-01

122

Effects of nifedipine on left ventricular systolic and diastolic functions in patients with left ventricular hypertrophy  

Energy Technology Data Exchange (ETDEWEB)

The effect of nifedpine on left ventricular (LV) systolic and diastolic function was studied in 10 patients with hypertrophic cadiomyopathy(HCM), 8 patients with hypertensive hypertrophy(HT) and 9 normal subjects. Multigated cardiac blood pool imaging with Tc-99m were obtained at 40-degree left anterior oblique position before and after nifedipine administration (10 mg, sublingually). As systolic indices, we obtained LV ejection fraction and mean first third ejection rate. And as diastolic indices, mean filling rate during first third of diastole (1/3 FRsub(mean)) and diastolic maximal filling rate were calculated. Before nifedipine, systolic indices were significantly superior in HCM group than in other 2 groups, and diastolic indices were significantly lower in HCM and HT groups than in normal. After nifedipine, systolic indices improved in HT group but they did not change in other 2 groups. Diastolic indices improved significantly in HCM and HT groups after nifedpine. In HCM group, 1/3 FRsub(mean) improved more markedly in symptomatic patients than in asymptomatic patients. The ratio of diastolic function to systolic function (1/3 FRsub(mean)/1/3 ERsub(mean)) did not change in normal and HT groups but it increased significantly in HCM group. There we a slight increase in heart rate (HR) and decrease in systemic arterial pressure (BP). The increase in HR was similar among 3 groups but the decrease in BP was significantly greater in HT group in whom control BP was significantly higher than other groups. LV end-diastolic volume did not change in 3 groups by nifedipine administration. These data suggested that abnormal diastolic function in HCM and HT was faborably modified by nifedipine, but their mechanisms were different. In HT, it was considered to relate with improved systolic function due to LV afterload reduction, while in HCM, it was not related to the peripheral hemodynamic effects nor improved systolic function.

Narita, Michihiro; Kurihara, Tadashi; Murano, Kenichi; Usami, Masahisa; Honda, Minoru; Kanao, Keisuke (Sumitomo Hospital, Osaka (Japan))

1984-10-01

123

Validation of an in vitro contractility assay using canine ventricular myocytes.  

Science.gov (United States)

Measurement of cardiac contractility is a logical part of pre-clinical safety assessment in a drug discovery project, particularly if a risk has been identified or is suspected based on the primary- or non-target pharmacology. However, there are limited validated assays available that can be used to screen several compounds in order to identify and eliminate inotropic liability from a chemical series. We have therefore sought to develop an in vitro model with sufficient throughput for this purpose. Dog ventricular myocytes were isolated using a collagenase perfusion technique and placed in a perfused recording chamber on the stage of a microscope at ~36 °C. Myocytes were stimulated to contract at a pacing frequency of 1 Hz and a digital, cell geometry measurement system (IonOptix™) was used to measure sarcomere shortening in single myocytes. After perfusion with vehicle (0.1% DMSO), concentration-effect curves were constructed for each compound in 4-30 myocytes taken from 1 or 2 dog hearts. The validation test-set was 22 negative and 8 positive inotropes, and 21 inactive compounds, as defined by their effect in dog, cynolomolgous monkey or humans. By comparing the outcome of the assay to the known in vivo contractility effects, the assay sensitivity was 81%, specificity was 75%, and accuracy was 78%. With a throughput of 6-8 compounds/week from 1 cell isolation, this assay may be of value to drug discovery projects to screen for direct contractility effects and, if a hazard is identified, help identify inactive compounds. PMID:22373797

Harmer, A R; Abi-Gerges, N; Morton, M J; Pullen, G F; Valentin, J P; Pollard, C E

2012-04-15

124

Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan  

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OBJECTIVE: To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses. METHODS: Patients of both sexes with moderate hypertension confirmed by ambulatory monitoring of arte-rial blood pressure and with left ventricular hypertrophy on echocardiogram were assigned to three groups: enalapril (35 mg/day, n=15), losartan (175 mg/day, n=15) and enalapril+losartan (15 mg+100 mg/day...

Avanza Jr Antônio Carlos; El Aouar Lilian Mameri; Mill José Geraldo

2000-01-01

125

Calcium alternans in a couplon network model of ventricular myocytes: role of sarcoplasmic reticulum load.  

Science.gov (United States)

Intracellular calcium (Ca) alternans in cardiac myocytes have been shown in many experimental studies, and the mechanisms remain incompletely understood. We recently developed a "3R theory" that links Ca sparks to whole cell Ca alternans through three critical properties: randomness of Ca sparks; recruitment of a Ca spark by neighboring Ca sparks; and refractoriness of Ca release units. In this study, we used computer simulation of a physiologically detailed mathematical model of a ventricular myocyte couplon network to study how sarcoplasmic reticulum (SR) Ca load and other physiological parameters, such as ryanodine receptor sensitivity, SR uptake rate, Na-Ca exchange strength, and Ca buffer levels affect Ca alternans in the context of 3R theory. We developed a method to calculate the parameters used in the 3R theory (i.e., the primary spark rate and the recruitment rate) from the physiologically detailed Ca cycling model and paced the model periodically to elicit Ca alternans. We show that alternans only occurs for an intermediate range of the SR Ca load, and the underlying mechanism can be explained via its effects on the 3Rs. Furthermore, we show that altering the physiological parameters not only directly changes the 3Rs but also alters the SR Ca load, having an indirect effect on the 3Rs as well. Therefore, our present study links the SR Ca load and other physiological parameters to whole cell Ca alternans through the framework of the 3R theory, providing a general mechanistic understanding of Ca alternans in ventricular myocytes. PMID:22661509

Nivala, Michael; Qu, Zhilin

2012-08-01

126

Left ventricular hypertrophy is associated with diastolic filling alterations in normotensive offspring of hypertensive nigerians.  

Science.gov (United States)

Contribution of left ventricular diastolic dysfunction to adverse events in patients with cardiovascular diseases is increasingly being recognized and individuals with pedigree for hypertension are thought to exhibit anatomic and or functional changes in their left ventricle before they become hypertensive. This study aimed at characterizing left ventricular diastolic function in normotensive offspring of hypertensive Nigerians. Sixty-five offspring of hypertensive parents aged 15-25 years (subjects) with 65-age and sex-matched offspring of normotensive parents (controls) were studied for early makers of hypertensive cardiovascular disease using Doppler echocardiogram. Mean mitral E velocity was reduced (P = 0.01) in the subjects (73.3 ± 12.6?cm/s) compared with the controls (80.2 ± 22.5?cm/s). Similarly, mean S velocity of pulmonary venous flow was lower (P = 0.01) in the subjects than in the controls. Left atrial dimension and mitral E/A ratio in the subjects with left ventricular hypertrophy were higher (P = 0.002, 0.004 respectively) than in the subjects without this abnormality. We concluded that normotensive offspring of hypertensive Nigerians showed early alterations in indexes of left ventricular diastolic filling and these abnormalities were exaggerated in the presence of left ventricular hypertrophy. PMID:23193485

Kolo, P M; Sanya, E O; Omotoso, A B; Soladoye, A; Ogunmodede, J A

2012-01-01

127

Refinement of total 12-lead QRS voltage criteria for diagnosing left ventricular hypertrophy  

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Objective: We sought to test the hypothesis that the total QRS voltage without either set of the limb leads (I, II, III) or (R, L, F) may be a better indicator of LVH as compared to the total QRS voltage. Background: The total 12 lead QRS voltage has been a validated electrocardiographic criterion for left ventricular hypertrophy (LVH), with an upper limit of175 mm. However, there is some redundancy in this measurement as...

Deepti Kumar; Rishi Bajaj; Lovely Chhabra; Spodick, David H.

2013-01-01

128

Left ventricular hypertrophy are associated with increased ostial pulmonary vein diameter  

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Atrial fibrillation (AF), which is called as a global epidemic disease, frequently found in hypertensive patients with left ventricular hypertrophy (LVH). Pulmonary vein (PV), which is known to have an important role in AF initiation and maintenance, increases in its diameter during AF. We sought to investigate PVs diameter changes in LVH with sinus rhythm. Of 70 hypertensive patients with sinus rhythm, 42 subjects demonstrated LVH. The mean ostial diameter of patient with and without LVH,...

2006-01-01

129

Therapeutic inhibition of fatty acid oxidation in right ventricular hypertrophy: exploiting Randle’s cycle  

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Right ventricular hypertrophy (RVH) and RV failure are major determinants of prognosis in pulmonary hypertension and congenital heart disease. In RVH, there is a metabolic shift from glucose oxidation (GO) to glycolysis. Directly increasing GO improves RV function, demonstrating the susceptibility of RVH to metabolic intervention. However, the effects of RVH on fatty acid oxidation (FAO), the main energy source in adult myocardium, are unknown. We hypothesized that partial inhibitors of FAO (...

Fang, Yong-hu; Piao, Lin; Hong, Zhigang; Toth, Peter T.; Marsboom, Glenn; Bache-wiig, Peter; Rehman, Jalees; Archer, Stephen L.

2012-01-01

130

Potential Impact of Carbohydrate and Fat Intake on Pathological Left Ventricular Hypertrophy  

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Currently, a high carbohydrate/low fat diet is recommended for patients with hypertension; however, the potentially important role that the composition of dietary fat and carbohydrate plays in hypertension and the development of pathological left ventricular hypertrophy (LVH) has not been well characterized. Recent studies demonstrate that LVH can also be triggered by activation of insulin signaling pathways, altered adipokine levels, or the activity of peroxisome proliferator-activated recep...

2007-01-01

131

Anti-Hypertensive Drugs Have Different Effects on Ventricular Hypertrophy Regression  

Science.gov (United States)

OBJECTIVES: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. METHODS: The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. RESULTS: The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective ?1 receptor antagonist) with respect to LVH regression. CONCLUSION: The anti-hypertensive drugs induced various degrees of hypertrophic regression.

Filho, Celso Ferreira; de Abreu, Luiz Carlos; Valenti, Vitor E.; Ferreira, Marcelo; Meneghini, Adriano; Silveira, Jose Alexandre; Perez Riera, Andres R.; Colombari, Eduardo; Murad, Neif; Santos-Silva, Paulo Roberto; da Silva, Lovian Jose Henrique Pereira; Vanderlei, Luiz Carlos Marques; Carvalho, Tatiana D.; Ferreira, Celso

2010-01-01

132

Effect of antipsychotic drug perphenazine on fast sodium current and transient outward potassium current in rat ventricular myocytes.  

Czech Academy of Sciences Publication Activity Database

rat ventricular myocytesKód oboru RIV: ED - FyziologieImpakt faktor: 2.631, rok: 2009http://apps.isiknowledge.com/full_record.do?product=UA&search_mode=GeneralSearch&qid=1&SID=T1JpdjJ8PNNeAL7D3il&page=1&doc=3&colname=WOS

Bébarová, M.; Matejovi?, P.; Pásek, Michal; Jansová, D.; Šimurdová, M.; Nováková, M.; Šimurda, J.

133

Study of Huoxue Qianyang Granules in revising the left ventricular hypertrophy of spontaneous hypertension rats  

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Full Text Available Objective: To study the mechanism of Huoxue Qianyang Granule (HXQYG, a traditional Chinese compound medicine, in revising the left ventricular hypertrophy of hypertension. Methods: Spontaneous hypertension rats (SHR were randomly divided into seven groups: untreated group, Songling Xuemaikang (SLXMK-treated group, captopril-treated group, high-, medium- and low-dose HXQYG-treated groups, and normal control group. The systolic blood pressure (SBP and left ventricular mass index (LVMI were measured. The content of angiotensin ? (Ang? in left ventricular tissue was determined by radioimmunoassay. The expressions of angiotensin converting enzyme (ACE protein and mRNA in left ventricular tissue were analyzed separately by immunohistochemical method and RT-PCR. Results: (1 SBP and LVMI were higher in the untreated group than those in the normal control group, and they were lower in the high- and medium-dose HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. (2 The content of Ang? and expressions of ACE protein and mRNA in the left ventricular tissue in the untreated group were higher than those in the normal control group, and they were lower in the HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. Conclusion: HXQYG can reverse the left ventricular hypertrophy of SHR, which may be due to decreasing the amount of Ang? and expressions of ACE protein and mRNA in the left ventricular tissue.

Duan ZHOU

2006-11-01

134

IP3 receptor-dependent Ca2+ release modulates excitation-contraction coupling in rabbit ventricular myocytes.  

Science.gov (United States)

Inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R)-dependent Ca(2+) signaling exerts positive inotropic, but also arrhythmogenic, effects on excitation-contraction coupling (ECC) in the atrial myocardium. The role of IP(3)R-dependent sarcoplasmic reticulum (SR) Ca(2+) release in ECC in the ventricular myocardium remains controversial. Here we investigated the role of this signaling pathway during ECC in isolated rabbit ventricular myocytes. Immunoblotting of proteins from ventricular myocytes showed expression of both type 2 and type 3 IP(3)R at levels approximately 3.5-fold less than in atrial myocytes. In permeabilized myocytes, direct application of IP(3) (10 microM) produced a transient 21% increase in the frequency of Ca(2+) sparks (P < 0.05). This increase was accompanied by a 13% decrease in spark amplitude (P < 0.05) and a 7% decrease in SR Ca(2+) load (P < 0.05) and was inhibited by IP(3)R antagonists 2-aminoethoxydiphenylborate (2-APB; 20 microM) and heparin (0.5 mg/ml). In intact myocytes endothelin-1 (100 nM) was used to stimulate IP(3) production and caused a 38% (P < 0.05) increase in the amplitude of action potential-induced (0.5 Hz, field stimulation) Ca(2+) transients. This effect was abolished by the IP(3)R antagonist 2-APB (2 microM) or by using adenoviral expression of an IP(3) affinity trap that buffers cellular IP(3). Together, these data suggest that in rabbit ventricular myocytes IP(3)R-dependent Ca(2+) release has positive inotropic effects on ECC by facilitating Ca(2+) release through ryanodine receptor clusters. PMID:18055509

Domeier, Timothy L; Zima, Aleksey V; Maxwell, Joshua T; Huke, Sabine; Mignery, Gregory A; Blatter, Lothar A

2008-02-01

135

Left Ventricular Hypertrophy: An allometric comparative analysis of different ECG markers  

International Nuclear Information System (INIS)

Allometry, in general biology, measures the relative growth of a part in relation to the whole living organism. Left ventricular hypertrophy (LVH) is the heart adaptation to excessive load (systolic or diastolic). The increase in left ventricular mass leads to an increase in the electrocardiographic voltages. Based on clinical data, we compared the allometric behavior of three different ECG markers of LVH. To do this, the allometric fit AECG ? + ? (VM) relating left ventricular mass (estimated from ecocardiographic data) and ECG amplitudes (expressed as the Cornell-Voltage, Sokolow and the ECG overall voltage indexes) were compared. Besides, sensitivity and specificity for each index were analyzed. The more sensitive the ECG criteria, the better the allometric fit. In conclusion: The allometric paradigm should be regarded as the way to design new and more sensitive ECG-based LVH markers.

2011-12-23

136

Ca(2+) homeostasis in sealed t-tubules of mouse ventricular myocytes.  

Science.gov (United States)

We have recently shown that in mouse ventricular myocytes, t-tubules can be quickly and tightly sealed during the resolution of hyposmotic shock of physiologically relevant magnitude. Sealing of t-tubules is associated with trapping extracellular solution inside the myocytes but the ionic homeostasis of sealed t-tubules and the consequences of potential transtubular ion fluxes remain unknown. In this study we investigated the dynamics of Ca(2+) movements associated with sealing of t-tubules. The data show that under normal conditions sealed t-tubules contain Ca(2+) at concentrations below 100?M. However, blockade of voltage-dependent Ca(2+) channels with 10?M nicardipine, or increasing extracellular concentration of K(+) from 5.4mM to 20mM led to several fold increase in concentration of t-tubular Ca(2+). Alternatively, the release of Ca(2+) from sarcoplasmic reticulum using 10mM caffeine led to the restoration of t-tubular Ca(2+) towards extracellular levels within few seconds. Sealing of t-tubules in the presence of extracellular 1.5mM Ca(2+) and 5.4mM extracellular K(+) led to occasional and sporadic intracellular Ca(2+) transients. In contrast, sealing of t-tubules in the presence of 10mM caffeine was characterized by a significant long lasting increase in intracellular Ca(2+). The effect was completely abolished in the absence of extracellular Ca(2+) and significantly reduced in pre-detubulated myocytes but was essentially preserved in the presence of mitochondrial decoupler dinitrophenol. This study shows that sealed t-tubules are capable of highly regulated transport of Ca(2+) and present a major route for Ca(2+) influx into the cytosol during sealing process. PMID:24787472

Moench, I; Lopatin, A N

2014-07-01

137

G?q-mediated Activation of GRK2 by Mechanical Stretch in Cardiac Myocytes: THE ROLE OF PROTEIN KINASE C*  

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G protein-coupled receptor kinase-2 (GRK2) is a critical regulator of ?-adrenergic receptor (?-AR) signaling and cardiac function. We studied the effects of mechanical stretch, a potent stimulus for cardiac myocyte hypertrophy, on GRK2 activity and ?-AR signaling. To eliminate neurohormonal influences, neonatal rat ventricular myocytes were subjected to cyclical equi-biaxial stretch. A hypertrophic response was confirmed by “fetal” gene up-regulation. GRK2 activity in cardiac myocytes ...

Malhotra, Ricky; D Souza, Karen M.; Staron, Michelle L.; Birukov, Konstantin G.; Bodi, Ilona; Akhter, Shahab A.

2010-01-01

138

Direct analysis of beta-adrenergic receptor subtypes on intact adult ventricular myocytes of the rat  

International Nuclear Information System (INIS)

beta 1- and beta 2-Adrenergic receptors co-exist in the adult rat ventricle. Radioligand binding and cell purification techniques have been employed to determine the cellular origin of these receptors. The beta-adrenergic antagonist ligand (+/-)-[125I] iodocyanopindolol binds to 2 X 10(5) receptors per purified adult rat cardiomyocyte, with a dissociation constant of 70 pM. The subtype-selective antagonists betaxolol (beta 1), practolol (beta 1), and zinterol (beta 2) compete for [125I]iodocyanopindolol-binding sites on intact myocytes in monophasic manners with dissociation constants of 46, 845, and 923 nM, respectively. [125I]iodocyanopindolol binding to membranes prepared from nonmyocyte elements of rat ventricle occurs with a dissociation constant of 43 pM and a capacity of 88 fmol/mg membrane protein. Computer analysis of competition of [125I]iodocyanopindolol binding by betaxolol, practolol, and zinterol in nonmyocyte membranes demonstrates biphasic curves that comprise binding to both beta 1- and beta 2-receptors. These data demonstrate that purified adult ventricular myocytes possess only beta 1-receptors, and that the beta 2-receptors found in rat ventricle are located on nonmyocyte cell types

1985-01-01

139

Accumulation of slowly activating delayed rectifier potassium current (IKs) in canine ventricular myocytes  

DEFF Research Database (Denmark)

In guinea-pig ventricular myocytes, in which the deactivation of slowly activating delayed rectifier potassium current (IKs) is slow, IKs can be increased by rapid pacing as a result of incomplete deactivation and subsequent current accumulation. Whether accumulation of IKs occurs in dogs, in which the deactivation is much faster, is still unclear. In this study the conditions under which accumulation occurs in canine ventricular myocytes were studied with regard to its physiological relevance in controlling action potential duration (APD). At baseline, square pulse voltage clamp experiments revealed that the accumulation of canine IKs could occur, but only at rather short interpulse intervals (<100 ms). With action potential (AP) clamp commands of constant duration (originally recorded at rate of 2 Hz), an accumulation was only found at interpulse intervals close to 0 ms. Transmembrane potential recordings with high-resistance microelectrodes revealed, however, that at the fastest stimulation rates with normally captured APs (5 Hz) the interpulse interval exceeded 50 ms. This suggested that no IKs accumulation occurs, which was supported by the lack of effect of an IKs blocker, HMR 1556 (500 nM), on APD. In the presence of the beta-adrenergic receptor agonist isoproterenol (isoprenaline, 100 nM) the accumulation with AP clamp commands of constant duration was much more pronounced and a significant accumulating current was found at a relevant interpulse interval of 100 ms. HMR 1556 prolonged APD, but this lengthening was reverse rate dependent. AP clamp experiments in a physiologically relevant setting (short, high rate APs delivered at a corresponding rate) revealed a limited accumulation of IKs in the presence of isoproterenol. In conclusion, a physiologically relevant accumulation of IKs was only observed in the presence of isoproterenol. Block of IKs, however, led to a reverse rate-dependent prolongation of APD indicating that IKs does not have a dominant role at short cycle lengths.

Stengl, Milan; Volders, Paul G A

2003-01-01

140

Apoptosis in severe, compensated pressure overload predominates in nonmyocytes and is related to the hypertrophy but not function  

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It is widely held that myocyte apoptosis in left ventricular hypertrophy (LVH) contributes to left ventricle (LV) dysfunction and heart failure. The main goal of this investigation was to determine if there is a statistical relationship among LV hypertrophy, apoptosis and LV function, and importantly whether the apoptosis occurs in myocytes or nonmyocytes in the heart. We used both rat and canine models of severe LVH induced by chronic thoracic aortic banding with resultant LV-aortic pressure...

Gelpi, Ricardo J.; Park, Misun; Gao, Shumin; Dhar, Sunil; Vatner, Dorothy E.; Vatner, Stephen F.

2011-01-01

 
 
 
 
141

123I-MIBG myocardial imaging in hypertensive patients. Abnormality progresses with left ventricular hypertrophy  

International Nuclear Information System (INIS)

Twenty-seven patients with essential hypertension were prospectively studied with 123I-labeled metaiodobenzyl-guanidine (123I-MIBG) to assess the presence and location of impaired sympathetic innervation in hypertrophied myocardium. Thirteen patients had left ventricular hypertrophy on echocardiography, and 14 had normal echocardiograms. The wash-out ratio of 123I-MIBG in these two groups did not differ significantly (35.3±6.1 and 35.4±5.1) but was higher than in control subjects (29.4±6.7). The delayed heart-to-mediastinum count ratio was lower in the patients with hypertrophy than in the patients without hypertrophy (1.93±0.28 and 2.22±0.21; p<0.05) and the control subjects (1.93±0.28 and 2.33±0.25; p<0.05). On SPECT imaging, abnormalities in segmental uptake were frequent at the posterior and postero-lateral wall in both groups, although the hypertrophic group had more significant impairment. Our results lead to the hypothesis that hypertension in more advanced stages may be associated not only with hypertrophic changes but also with more advanced regional impairment of cardiac sympathetic innervation. (author)

1996-08-01

142

Swelling-activated Gd3+-sensitive cation current and cell volume regulation in rabbit ventricular myocytes.  

Science.gov (United States)

The role of swelling-activated currents in cell volume regulation is unclear. Currents elicited by swelling rabbit ventricular myocytes in solutions with 0.6-0.9x normal osmolarity were studied using amphotericin perforated patch clamp techniques, and cell volume was examined concurrently by digital video microscopy. Graded swelling caused graded activation of an inwardly rectifying, time-independent cation current (ICir,swell) that was reversibly blocked by Gd3+, but ICir,swell was not detected in isotonic or hypertonic media. This current was not related to IK1 because it was insensitive to Ba2+. The PK/PNa ratio for ICir,swell was 5.9 +/- 0.3, implying that inward current is largely Na+ under physiological conditions. Increasing bath K+ increased gCir,swell but decreased rectification. Gd3+ block was fitted with a K0.5 of 1.7 +/- 0.3 microM and Hill coefficient, n, of 1.7 +/- 0.4. Exposure to Gd3+ also reduced hypotonic swelling by up to approximately 30%, and block of current preceded the volume change by approximately 1 min. Gd3+-induced cell shrinkage was proportional to ICir,swell when ICir,swell was varied by graded swelling or Gd3+ concentration and was voltage dependent, reflecting the voltage dependence of ICir,swell. Integrating the blocked ion flux and calculating the resulting change in osmolarity suggested that ICir,swell was sufficient to explain the majority of the volume change at -80 mV. In addition, swelling activated an outwardly rectifying Cl- current, ICl,swell. This current was absent after Cl- replacement, reversed at ECl, and was blocked by 1 mM 9-anthracene carboxylic acid. Block of ICl,swell provoked a 28% increase in swelling in hypotonic media. Thus, both cation and anion swelling-activated currents modulated the volume of ventricular myocytes. Besides its effects on cell volume, ICir,swell is expected to cause diastolic depolarization. Activation of ICir, swell also is likely to affect contraction and other physiological processes in myocytes. PMID:9276755

Clemo, H F; Baumgarten, C M

1997-09-01

143

Evaluation of left ventricular eccentric hypertrophy by /sup 201/Tl-myocardial scintigraphy  

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In order to elucidate the mechanism of left ventricular eccentric hypertrophy in conditions of volume overload, Tl-201 myocardial scintigraphy was performed in patients with aortic valve regurgitation and mitral valve regurgitation. There was a good relationship between the severity of Tl-defects, as determined by Tl-201 myocardial scintigraphy, and the changes in the T wave on the ECG on the one hand and the NYHA functional classification of heart diseases. In 17 of 18 patients where LVDd increased with increasing severity of Tl-defects and the defects were moderate to severe, LVDd was 65 mm or larger. There was a significant negative correlation between the washout rate for the whole circumference of the left ventricle, as determined by exercise Tl-201 SPECT, and LVDd (r=-0.603, p<0.01). The phenomenon of redistribution as determined by exercise Tl-201 myocardial scintigraphy was observed relatively early. Our results suggest that mechanical volume overload and ischemic changes are involved in left ventricular wall damage in left ventricular eccentric hypertrophy. For patients with moderate to severe Tl-defects valve replacement is indicated, no matter whether they may have heart failure or arrhythmia.

Yamazaki, Junichi; Kawamura, Yasuaki; Okuzumi, Ichio; Morishita, Takeshi; Koyama, Nobuya; Komatsu, Hisashi; Ohsawa, Hidefumi; Yabe, Yoshimasa

1989-03-01

144

Fabry disease presenting as apical left ventricular hypertrophy in a patient carrying the missense mutation R118C.  

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Anderson-Fabry disease is an X-linked lysosomal storage disorder caused by abnormalities of the GLA gene, which encodes the enzyme ?-galactosidase A. A deficiency of this enzyme leads to the lysosomal accumulation of glycosphingolipids, which may cause left ventricular hypertrophy that is typically concentric and symmetric. We present the case of a 60-year-old woman with symptoms of dyspnea, atypical chest pain and palpitations, in whom a transthoracic echocardiogram revealed an apical variant of hypertrophic cardiomyopathy. Analysis of specific sarcomeric genetic mutations was negative. The patient underwent a screening protocol for Anderson-Fabry disease, using a dried blood spot test, which was standard at our institution for patients with left ventricular hypertrophy. The enzymatic activity assay revealed reduced ?-galactosidase A enzymatic activity. Molecular analysis identified a missense point mutation in the GLA gene (p.R118C). This case report shows that Anderson-Fabry disease may cause an apical form of left ventricular hypertrophy. The diagnosis was only achieved because of systematic screening, which highlights the importance of screening for Anderson-Fabry disease in patients with unexplained left ventricular hypertrophy, including those presenting with more unusual patterns, such as apical variants of left ventricular hypertrophy. This case also supports the idea that the missense mutation R118C is indeed a true pathogenic mutation of Anderson-Fabry disease. PMID:24661928

Caetano, Francisca; Botelho, Ana; Mota, Paula; Silva, Joana; Leitão Marques, António

2014-03-01

145

Amiodarone Kyusei Toyo Ga Ieusagi Tanri Shinshitsukin Saibo Ni Oyobosu Denki Seirigakuteki Sayo (Effects of Perfusion of Amiodarone on Electrophysiological Properties in Single Rabbit Ventricular Myocytes).  

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The acute administration of amiodarone, an antiarrhythmic agent, was studied and the data was compared with chronic administration. The ventricular myocytes were isolated from rabbit hearts, perfusated with perfusate containing amiodarone, and action pote...

K. Kamiya J. Cheng I. Kodama J. Toyama

1993-01-01

146

Total ginsenosides inhibit the right ventricular hypertrophy induced by monocrotaline in rats.  

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Ginsenosides have been reported to release nitric oxide (NO) and decrease intracellular free Ca(2+) in cardiovascular system, which play important roles in antihypertrophic effect. This study investigated the potential inhibitory effect of total ginsenosides (TG) on right ventricular hypertrophy induced by monocrotaline (MCT, 60 mg/kg/d) and examined the possible antihypertrophic mechanism in male Sprague Dawley rats. MCT-intoxicated animals were treated with TG (20, 40, 60 mg/kg/d) for 18 d. TG treatment ameliorated MCT-induced elevations in right ventricular peak systolic pressure, right ventricular hypertrophy and the expression of atrial natriuretic peptide; N(G)-nitro-L-arginine-methyl ester (L-NAME), an NO synthase (NOS) inhibitor, had no influence on these inhibitory effects of TG 40 mg/kg/d, and TG at this dose had no any effect on the eNOS mRNA expression, suggesting the limited rule of NO in TG's effects. To further examine the mechanisms of the protection, the expression of calcineurin and its catalytic subunit CnA, as well as extracellular signal-regulated kinase-1 (ERK-1) and mitogen-activated protein kinase (MAPK) Phosphatase-1 (MKP-1) was examined. TG treatment significantly suppressed MCT-induced elevations of these signaling pathways in a dose-dependent manner. In summary, TG is effective in protecting against MCT-induced right ventricle hypertrophy, possibly through lowering pulmonary hypertension. Multiple molecular mechanisms appeared to be involved in this protection, such as the suppression of MCT-activated calcineurin and ERK signaling pathways. PMID:18670084

Qin, Na; Gong, Qi-Hai; Wei, Li-Wei; Wu, Qin; Huang, Xie-Nan

2008-08-01

147

Left Ventricular Hypertrophy and Insulin Resistance in Adults from an Urban Community in the Gambia: Cross-Sectional Study  

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Objective To determine the association between left ventricular hypertrophy and insulin resistance in Gambians. Design Cross-sectional study. Setting Outpatient clinics of Royal Victoria Teaching Hospital and Medical Research Council Laboratories in Banjul. Participants Three hundred and sixteen consecutive patients were enrolled from outpatient clinics. The data of 275 participants (89 males) were included in the analysis with a mean (± standard deviation) age of 53.7 (±11.9) years. Interventions A questionnaire was filled and anthropometric measurements were taken. 2-D guided M-mode echocardiography, standard 12-1ead electrocardiogram, fasting insulin and the oral glucose tolerance test were performed. Main Outcome Measures The Penn formula was used to determine the left ventricular mass index, 125 g/m2 in males and 110 g/m2 in females as the cut-off for left ventricular hypertrophy. Using the fasting insulin and fasting glucose levels, the insulin resistance was estimated by the homeostatic model assessment formula. Logistic regression analysis was used to determine the association between left ventricular hypertrophy and insulin resistance. Results The mean Penn left ventricular mass index was 119.5 (±54.3) and the prevalence of Penn left ventricular mass index left ventricular hypertrophy was 41%. The mean fasting glucose was 5.6 (±2.5) mmol/l, fasting insulin was 6.39 (±5.49) ?U/ml and insulin resistance was 1.58 (±1.45). There was no association between Penn left ventricular mass index left ventricular hypertrophy and log of insulin resistance in univariate (OR?=?0.98, 95% CI?=?0.80 – 1.19, p?=?0.819) and multivariate logistic regression (OR?=?0.93, 95% CI?=?0.76–1.15, p?=?0.516) analysis. Conclusion No association was found in this study between left ventricular hypertrophy and insulin resistance in Gambians and this does not support the suggestion that insulin is an independent determinant of left ventricular hypertrophy in hypertensives.

Nkum, Bernard Cudjoe; Micah, Frank Botsi; Ankrah, Theophilus C.; Nyan, Ousman

2014-01-01

148

Association Between Diabetes Mellitus and Left Ventricular Hypertrophy in a Multi-Ethnic Population  

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It is still controversial whether type 2 diabetes mellitus (T2DM) is associated with increased left ventricular (LV) mass independent of body size. We tested the hypothesis that T2DM is independently associated with LV mass in a multi-ethnic cohort. In the Northern Manhattan Study (NOMAS) cohort sample, a total of 1932 subjects (67.9±9.6 years; 769 men and 1163 women; 443 DM and 1489 non-DM) were studied by transthoracic echocardiography, and LV mass was calculated. LV hypertrophy was define...

Eguchi, Kazuo; Boden-albala, Bernadette; Jin, Zhezhen; Rundek, Tatjana; Sacco, Ralph L.; Homma, Shunichi; Di Tullio, Marco R.

2008-01-01

149

Non-Dipper Status and Left Ventricular Hypertrophy as Predictors of Incident Chronic Kidney Disease  

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We have hypothesized that non-dipper status and left ventricular hypertrophy (LVH) are associated with the development of chronic kidney disease (CKD) in non-diabetic hypertensive patients. This study included 102 patients with an estimated glomerular filtration rate (eGFR) ? 60 mL/min/1.73 m2. Ambulatory blood pressure monitoring and echocardiography were performed at the beginning of the study, and the serum creatinine levels were followed. During the average follow-up period of 51 months...

2011-01-01

150

The role of ECG in the diagnosis of left ventricular hypertrophy.  

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The traditional approach to the ECG diagnosis of left ventricular hypertrophy (LVH) is focused on the best estimation of left ventricular mass (LVM) i.e. finding ECG criteria that agree with LVM as detected by imaging. However, it has been consistently reported that the magnitude of agreement is rather low as reflected in the low sensitivity of ECG criteria. As a result, the majority of cases with true anatomical LVH could be misclassified by using ECG criteria of LVH. Despite this limitation, it has been reported that the ECG criteria for LVH provide independent information on the cardiovascular risk even after adjusting for LVM. Understanding possible reasons for the frequent discrepancy between common ECG LVH criteria and LVH by echo or MRI would help understanding the genesis of ECG changes that occur as a consequence of increased LV mass. PMID:24827796

Bacharova, Ljuba; Schocken, Douglas; Estes, Edward H; Strauss, David

2014-08-01

151

Loss of T-tubules and other changes to surface topography in ventricular myocytes from failing human and rat heart.  

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T-tubular invaginations of the sarcolemma of ventricular cardiomyocytes contain junctional structures functionally coupling L-type calcium channels to the sarcoplasmic reticulum calcium-release channels (the ryanodine receptors), and therefore their configuration controls the gain of calcium-induced calcium release (CICR). Studies primarily in rodent myocardium have shown the importance of T-tubular structures for calcium transient kinetics and have linked T-tubule disruption to delayed CICR. However, there is disagreement as to the nature of T-tubule changes in human heart failure. We studied isolated ventricular myocytes from patients with ischemic heart disease, idiopathic dilated cardiomyopathy, and hypertrophic obstructive cardiomyopathy and determined T-tubule structure with either the fluorescent membrane dye di-8-ANNEPs or the scanning ion conductance microscope (SICM). The SICM uses a scanning pipette to produce a topographic representation of the surface of the live cell by a non-optical method. We have also compared ventricular myocytes from a rat model of chronic heart failure after myocardial infarction. T-tubule loss, shown by both ANNEPs staining and SICM imaging, was pronounced in human myocytes from all etiologies of disease. SICM imaging showed additional changes in surface structure, with flattening and loss of Z-groove definition common to all etiologies. Rat myocytes from the chronic heart failure model also showed both T-tubule and Z-groove loss, as well as increased spark frequency and greater spark amplitude. This study confirms the loss of T-tubules as part of the phenotypic change in the failing human myocyte, but it also shows that this is part of a wider spectrum of alterations in surface morphology. PMID:19342485

Lyon, Alexander R; MacLeod, Ken T; Zhang, Yanjun; Garcia, Edwin; Kanda, Gaelle Kikonda; Lab, Max J; Korchev, Yuri E; Harding, Sian E; Gorelik, Julia

2009-04-21

152

Phorbol ester and endothelin-1 alter functional expression of Na+/Ca2+ exchange, K+, and Ca2+ currents in cultured neonatal rat myocytes  

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Endothelin-1 (ET-1) and activation of protein kinase C (PKC) have been implicated in alterations of myocyte function in cardiac hypertrophy and heart failure. Changes in cellular Ca2+ handling and electrophysiological properties also occur in these states and may contribute to mechanical dysfunction and arrhythmias. While ET-1 or PKC stimulation induces cellular hypertrophy in cultured neonatal rat ventricular myocytes (NRVMs), a system widely used in studies of hypertrophic signaling, there ...

Puglisi, Jose? L.; Yuan, Weilong; Timofeyev, Valeriy; Myers, Richard E.; Chiamvimonvat, Nipavan; Samarel, Allen M.; Bers, Donald M.

2011-01-01

153

Reduction of Left Ventricular Hypertrophy by Sirolimus in Kidney Transplant Recipients: A Nonrandomized Clinical Trial  

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Full Text Available Background: Persistence of left ventricular hypertrophy (LVH in renal transplant recipients is associated with unfavorable outcomes. Calcineurin-inhibitor (CNI nephrotoxicity is a major cause of morbidity and mortality after kidney transplantation. In this study we compared sirolimus (SRL with calcineurin-inhibitor as primary immunosuppressants for the attenuation of left ventricular hypertrophy in renal transplantation recipients. Methods: In this prospective cohort study done in Shariati Hospital in 2010, we evaluated the effects of sirolimus and CNI on LVH of 55 renal transplant recipients. The cases (19 received sirolimus while the controls (36 received CNI while being matched for age and duration of transplantation. Data regarding blood pressure (BP, hemoglobin, serum creatinine, uric acid and lipid concentrations were assessed and changes in left ventricular (LV mass were evaluated by echocardiography over a one-year follow-up. Results: Left ventricular mass significantly decreased (P=0.0001 in the SRL group but blood pressure did not differ between the two groups. LV mass and LV mass index both decreased significantly (P?0.05 but the difference was not associated with changes in BP. The difference in interventricular septal thickness at end diastole (IVSD and posterior wall diameter (PWD were significant (P?0.05 in the SRL group but the difference in end diastolic diameter (EDD was not significant. Conclusion: Conversion from CNI to SRL-based immunosuppressive therapy in RTRs is safe and SRL may decrease LVH. SRL seems to be safe and improve renal function without cardiac compromise in kidney transplant recipients.

Ghorbani Yekta B

2012-02-01

154

TVP1022 protects neonatal rat ventricular myocytes against doxorubicin-induced functional derangements.  

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Our recent studies demonstrated that propargylamine derivatives such as rasagiline (Azilect, Food and Drug Administration-approved anti-Parkinson drug) and its S-isomer TVP1022 protect cardiac and neuronal cell cultures against apoptotic-inducing stimuli. Studies on structure-activity relationship revealed that their neuroprotective effect is associated with the propargylamine moiety, which protects mitochondrial viability and prevents apoptosis by activating Bcl-2 and protein kinase C-epsilon and by down-regulating the proapoptotic protein Bax. Based on the established cytoprotective and neuroprotective efficacies of propargylamine derivatives, as well as on our recent study showing that TVP1022 attenuates serum starvation-induced and doxorubicin-induced apoptosis in neonatal rat ventricular myocytes (NRVMs), we tested the hypothesis that TVP1022 will also provide protection against doxorubicin-induced NRVM functional derangements. The present study demonstrates that pretreatment of NRVMs with TVP1022 (1 microM, 24 h) prevented doxorubicin (0.5 microM, 24 h)-induced elevation of diastolic [Ca(2+)](i), the slowing of [Ca(2+)](i) relaxation kinetics, and the decrease in the rates of myocyte contraction and relaxation. Furthermore, pretreatment with TVP1022 attenuated the doxorubicin-induced reduction in the protein expression of sarco/endoplasmic reticulum calcium (Ca(2+)) ATPase, Na(+)/Ca(2+) exchanger 1, and total connexin 43. Finally, TVP1022 diminished the inhibitory effect of doxorubicin on gap junctional intercellular coupling (measured by means of Lucifer yellow transfer) and on conduction velocity, the amplitude of the activation phase, and the maximal rate of activation (dv/dt(max)) measured by the Micro-Electrode-Array system. In summary, our results indicate that TVP1022 acts as a novel cardioprotective agent against anthracycline cardiotoxicity, and therefore potentially can be coadmhence, theinistered with doxorubicin in the treatment of malignancies in humans. PMID:19915070

Berdichevski, Alexandra; Meiry, Gideon; Milman, Felix; Reiter, Irena; Sedan, Oshra; Eliyahu, Sivan; Duffy, Heather S; Youdim, Moussa B; Binah, Ofer

2010-02-01

155

Fenofibrate inhibits aldosterone-induced apoptosis in adult rat ventricular myocytes via stress-activated kinase-dependent mechanisms  

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Aldosterone induces extracellular signal-regulated kinase (ERK)-dependent cardiac remodeling. Fenofibrate improves cardiac remodeling in adult rat ventricular myocytes (ARVM) partly via inhibition of aldosterone-induced ERK1/2 phosphorylation and inhibition of matrix metalloproteinases. We sought to determine whether aldosterone caused apoptosis in cultured ARVM and whether fenofibrate ameliorated the apoptosis. Aldosterone (1 ?M) induced apoptosis by increasing terminal deoxynucleotidyltran...

2009-01-01

156

Aldosterone Upregulates Connective Tissue Growth Factor Gene Expression via p38 MAPK Pathway and Mineralocorticoid Receptor in Ventricular Myocytes  

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The effect of aldosterone on connective tissue growth factor (CTGF) was examined in rat embryonic ventricular myocytes. Upon aldosterone treatment, CTGF expression was significantly increased in a dose and time-dependent manner. To explore the molecular mechanism for this upregulation, we examined the role of mineralocorticoid receptor. Pre-treatment of an antagonist (spironolactone) at 5-fold excess of aldosterone blocked the CTGF induction by aldosterone, suggesting that the upregulation wa...

2004-01-01

157

Ca Sparks Do Not Explain all Ryanodine Receptor-Mediated SR Ca Leak in Mouse Ventricular Myocytes  

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Diastolic Ca leak from the sarcoplasmic reticulum (SR) of ventricular myocytes reduces the SR Ca content, stabilizing the activity of the SR Ca release channel ryanodine receptor for the next beat. SR Ca leak has been visualized globally using whole-cell fluorescence, or locally using confocal microscopy, but never both ways. When using confocal microscopy, leak is imaged as “Ca sparks,” which are fluorescent objects generated by the local reaction-diffusion of released Ca and cytosolic i...

Santiago, Demetrio J.; Curran, Jerald W.; Bers, Donald M.; Lederer, W. J.; Stern, Michael D.; Ri?os, Eduardo; Shannon, Thomas R.

2010-01-01

158

Effects of propafenone on electrical and mechanical activities of single ventricular myocytes isolated from guinea-pig hearts.  

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1. The effects of propafenone on the transmembrane action potential and sarcomere shortening during twitch contraction were investigated in single ventricular myocytes isolated from guinea-pig hearts. 2. Propafenone at low concentrations (3-5 x 10(-7) M) slightly lengthened action potential duration (APD), but shortened it at higher concentrations. The shortening of APD was accompanied by an attenuation of sarcomere shortening during twitch contraction. 3. Propafenone (greater than 10(-6) M) ...

1989-01-01

159

Right ventricular hypertrophy with heart failure in Holstein heifers at elevation of 1,600 meters.  

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A syndrome of progressive right-sided heart failure occurred among yearling Holsteins at a heifer-raising facility and 2 dairies on the Colorado Front Range between 2007 and 2011. Most cases were seen at the heifer-raising facility, where the disease ranked second only to pneumonia as a major cause of death in animals aged <1.5 years. The disease resulted in the death or premature sale of 55 animals over the 5-year period. Affected heifers were 4-15 months old when they developed dyspnea, tachycardia, distention and pulsation of jugular veins, lethargy, and weight loss. Clinical progression in most was rapid (2 days to 2 weeks). Ten cattle with typical clinical signs were examined postmortem between 2008 and 2010. Seven developed clinical signs after transportation 57-238 days earlier from Wisconsin (elevation: < 275 m); the remaining 3 animals were born and raised at an altitude of 1,600 m. At necropsy, the 10 cattle had marked hypertrophy of right ventricular myocardium, dilated right atria, right ventricles, and pulmonary trunks, as well as hepatomegaly, ascites, and serous atrophy of fat. The principal histological change in lungs was hypertrophied tunicae adventitia and media of muscular arteries. Hepatic changes were typical of chronic passive congestion. Ultrastructural changes in heart were consistent with uncomplicated hypertrophy of cardiocytes with no evidence of primary cardiomyopathy. The syndrome most likely represents brisket disease due to pulmonary hypertension at the modest elevation of 1,600 m. PMID:22914818

Malherbe, Christopher R; Marquard, Jana; Legg, David E; Cammack, Kristi M; O'Toole, Donal

2012-09-01

160

Development of left ventricular hypertrophy in a novel porcine model of mitral regurgitation.  

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Abstract Objectives. We aimed to develop a porcine model for chronic nonischemic mitral regurgitation (MR) to investigate left ventricular (LV) enlargement and eccentric hypertrophy. Design. Nonischemic MR was induced in 30 pigs by open-chest immobilization of the posterior mitral leaflet by transannular traction sutures that where applied in transmyocardial fashion. A sham operated control group (n = 13) was included. Echocardiographic LV size and heart weight assessed at euthanasia were used to evaluate the development of LV enlargement and eccentric hypertrophy after 8 weeks follow-up. Results. Eight pigs died and seven were excluded due to mediastinal infection (n = 2) or failure to produce MR (n = 5). Thus, 28 pigs were included and were divided into three groups: controls (n = 12), mild MR (mMR; n = 10), and moderate to severe MR (sMR; n = 6). The change in LV internal diameter in diastole (LVIDd) from baseline to follow-up was significantly higher in the sMR group compared to that of the control group (P = 0.0017). Furthermore, LV weight was significantly increased in the mMR (P = 0.047) and the sMR (P = 0.0087) groups compared to that of the control group. Conclusions. A new model for chronic moderate to severe nonischemic MR with development of LV enlargement and eccentric hypertrophy within 8 weeks has been established in pigs. PMID:24548173

Ravn, Nathja; Zois, Nora E; Moesgaard, Sophia G; Honge, Jesper L; Smerup, Morten H; Hasenkam, J Michael; Sloth, Erik; Cremer, Signe E; Olsen, Lisbeth H

2014-06-01

 
 
 
 
161

Degradation of [125I]-atrial natriuretic peptide by a soluble metallopeptidase isolated from rat ventricular myocytes  

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Atrial natriuretic peptide is rapidly degraded by a soluble, heat labile peptidase isolated from ventricular myocytes. Degradation of [125I]-ANP is antagonized by unlabelled ANP, bradykinin, glucagon, 1,10-phenanthroline, PCMB, EDTA and the bacterial antibiotic bacitracin, but not by phenylmethylsulphonyl fluoride, aprotinin, phosphoramidon, E-64, amastatin or the ACE inhibitor SQ 20881 and bradykinin potentiator C. In addition neither bovine serum albumin nor caesin afforded any protection against degradation. Peptidase activity was optimal at pH values above 8.5. The peptidase is likely to be of intracellular origin and may contribute to the extensive ANP degradative activity found in various ventricular muscle preparations

1988-04-15

162

Left ventricular hypertrophy are associated with increased ostial pulmonary vein diameter  

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Full Text Available Atrial fibrillation (AF, which is called as a global epidemic disease, frequently found in hypertensive patients with left ventricular hypertrophy (LVH. Pulmonary vein (PV, which is known to have an important role in AF initiation and maintenance, increases in its diameter during AF. We sought to investigate PVs diameter changes in LVH with sinus rhythm. Of 70 hypertensive patients with sinus rhythm, 42 subjects demonstrated LVH. The mean ostial diameter of patient with and without LVH, assessed by doing spiral multisliced CT scan in the axial plane, were as follow: right superior (RSPV of 19.6±2.78 vs 17.8±1.93 (p = 0.003, right inferior (RIPV of 18.4±3.12 vs 16.0±2.19 (p < 0.001, left superior (LSPV of 18.1±2.62 vs 16.0±2.16 (p < 0.001, and left inferior (LIPV of 15.9±1.93 vs 15.4±1.85 mm (p = 0.284, respectively. Even during sinus rhythm, LVH causes PV dilation. This result might give an explanation of frequent AF prevalence in hypertensive patients. (Med J Indones 2006; 15:173-6 Keywords: Pulmonary veins, Left ventricular hypertrophy

Yoga Yuniadi

2006-08-01

163

Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.  

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Alterations in the ubiquitin-proteasome system (UPS) have been described in left ventricular hypertrophy and failure, although results have been inconsistent. The role of the UPS in right ventricular (RV) hypertrophy (RVH) and RV failure (RVF) is unknown. Given the greater percent increase in RV mass associated with RV afterload stress, as present in many congenital heart lesions, we hypothesized that alterations in the UPS could play an important role in RVH/RVF. UPS expression and activity were measured in the RV from mice with RVH/RVF secondary to pulmonary artery constriction (PAC). Epoxomicin and MG132 were used to inhibit the proteasome, and overexpression of the 11S PA28? subunit was used to activate the proteasome. PAC mice developed RVH (109.3% increase in RV weight to body weight), RV dilation with septal shift, RV dysfunction, and clinical RVF. Proteasomal function (26S ?? chymotrypsin-like activity) was decreased 26% (P RVF. However, proteasome enhancement by cardiac-specific proteasome overexpression partially improved survival. Proteasome activity is decreased in RVH/RVF, associated with upregulation of key UPS regulators and pro-apoptotic signaling. Enhancement of proteasome function partially attenuates RVF, suggesting that UPS dysfunction contributes to RVF. PMID:23729213

Rajagopalan, Viswanathan; Zhao, Mingming; Reddy, Sushma; Fajardo, Giovanni; Wang, Xuejun; Dewey, Shannamar; Gomes, Aldrin V; Bernstein, Daniel

2013-08-15

164

The effects of implanted valve sizes on ventricular hypertrophy in aortic stenosis  

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Full Text Available Objective: We aimed to study the effects of the valve sizes according to body surface area on aortic gradient and ventricular hypertrophy in the cases of aortic valve replacement due to isolated aortic stenosis.Methods: Between January 2006 and April 2007, patients (12 men, 15 women; totally 27 followed up prospectively with echocardiography fourth and sixth month postoperatively. The patients were divided into two groups according to the prosthetic aortic valve diameters (19-21 mm vs 23-25 mm. The primary endpoints between the two groups (aortic regurgitation, left ventricular mass index and transvalvular gradient measured by color and continuous wave Doppler were compared. Fischer exact test and Mann-Whitney U test were used for intergroup comparison whereas intragroup analysis was done with Freidman test.Results: Mean systolic gradient and left ventricular mass index were significantly reduced in 23 mm and 25 mm valves (p<0.01 in the postoperative follow-up. In addition, especially, decline in the values of left ventricular mass, left ventricular mass index, peak systolic gradient and the mean systolic gradient were found to be significant. These values associated with regression were detectable at the postoperative 4th month, but actual significant regression was observed at the postoperative 6th month (p<0.01. On the other hand, the values obtained for 19 mm and 21 mm valves also showed significant progress (p<0.05.Conclusion: Factors such as age, gender and activity are important in the selection of appropriate valve sizes in aortic valve replacement. However, the patient's body surface is the most important prognostic factor compared to others.

Hikmet Selçuk Gedik

2012-02-01

165

Direct observation of the "oxygen paradox" in single rat ventricular myocytes.  

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By phase contrast microscopy with video length tracking, we followed the sequence of morphological changes in individual isolated rat ventricular myocytes during anoxia followed by reoxygenation. Cells appeared normal during early anoxia. After a duration of anoxia T1, which varied from 17-47 minutes in different cells, each cell abruptly contracted an average of 33% in length to an inert rectangular form presumed to be a rigor state. Cells which were reoxygenated before the onset of rigor showed normal morphology and an unchanged extent of shortening on field stimulation, compared to control. Cells that were reoxygenated after a time in the rigor state, T2, either partially recovered to a shortened rectangular form capable of stimulated twitches or rounded up rapidly to a disordered hypercontracture form. The distribution of T1 was the same for cells which recovered and which hypercontracted. In contrast, the outcome of reoxygenation depended markedly on T2: all cells that were reoxygenated after less than 10 minutes of rigor recovered function, whereas all cells that spent more than 20 minutes in rigor hypercontracted when reoxygenated. The hypercontracture appears to be the cellular analog of the "oxygen paradox" in whole hearts. Its occurrence is reliably related to duration of rigor state but not to duration of hypoxia, because of marked cellular variability in the time of onset of rigor. PMID:4006097

Stern, M D; Chien, A M; Capogrossi, M C; Pelto, D J; Lakatta, E G

1985-06-01

166

Differential effects of stretch and compression on membrane currents and [Na+]c in ventricular myocytes.  

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Mechano-electrical feedback was studied in the single ventricular myocytes. A small fraction (approximately 10%) of the cell surface could be stretched or compressed by a glass stylus. Stretch depolarised, shortened the action potential and induced extra systoles. Stretch activated non-selective cation currents (I(ns)) showed a linear voltage dependence, a reversal potential of 0 mV, a pure cation selectivity, and were blocked by 8 microM Gd(3+) or 30 microM streptomycin. Stretch reduced Ca(2+) and K(+) (I(K)) currents. Local compression of broadwise attached cells activated I(K) but not I(ns). Cytochalasin D or colchicin, thought to disrupt the cytoskeleton, suppressed the mechanosensitivity of I(ns) and I(K). During stretch, the cytosolic sodium concentration increased with spatial heterogeneities, local hotspots with [Na(+)](c)>24 mM appeared close to surface membrane and t-tubules (pseudoratiometric imaging using Sodium Green fluorescence). Electronprobe microanalysis confirmed this result and indicated that stretch increased total sodium [Na] in cell compartments such as mitochondria, nuclear envelope and nucleus. Our results obtained by local stretch differ from those obtained by end-to-end stretch (literature). We speculate that channels may be activated not only by axial but also by shear stress, and, that stretch can activate channels outside the deformed sarcomeres via second messenger. PMID:12732267

Isenberg, Gerrit; Kazanski, Victor; Kondratev, Denis; Gallitelli, Maria Fiora; Kiseleva, Irina; Kamkin, Andre

2003-01-01

167

Fibroblast-mediated pathways in cardiac hypertrophy.  

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Under normal physiological conditions, cardiac fibroblasts are the primary producers of extracellular matrix and supply a mechanical scaffold for efficacious heart contractions induced by cardiomyocytes. In the hypertrophic heart, cardiac fibroblasts provide a pivotal contribution to cardiac remodeling. Many growth factors and extracellular matrix components secreted by cardiac fibroblasts induce and modify cardiomyocyte hypertrophy. Recent evidence revealed that cardiomyocyte-cardiac fibroblast communications are complex and multifactorial. Many growth factors and molecules contribute to cardiac hypertrophy via different roles that include induction of hypertrophy and the feedback hypertrophic response, fine-tuning of adaptive hypertrophy, limitation of left ventricular dilation, and modification of interstitial changes. This review focuses on recent work and topics and provides a mechanistic insight into cardiomyocyte-cardiac fibroblast communication in cardiac hypertrophy. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium ". PMID:24492068

Fujiu, Katsuhito; Nagai, Ryozo

2014-05-01

168

Serum cystatin C concentration as an independent marker for hypertensive left ventricular hypertrophy  

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Full Text Available Background Serum cystatin C levels can be used to predict morbidity and mortality in patients with cardiovascular disease. However, the clinical relevance of serum cystatin C levels in patients with hypertensive left ventricular hypertrophy (LVH has rarely been investigated. We designed the present study to investigate whether serum cystatin C levels are associated with cardiac structural and functional alterations in hypertensive patients. Methods We enrolled 823 hypertensive patients and classified them into two groups: those with LVH (n = 287 and those without LVH (n = 536. All patients underwent echocardiography and serum cystatin C testing. We analyzed the relationship between serum cystatin C levels and LVH. Results Serum cystatin C levels were higher in hypertensive patients with LVH than in those without LVH (P < 0.05. Using linear correlation analysis, we found a positive correlation between serum cystatin C levels and interventricular septal thickness (r = 0.247, P < 0.01, posterior wall thickness (r = 0.216, P < 0.01, and left ventricular weight index (r = 0.347, P < 0.01. When analyzed by multiple linear regression, the positive correlations remained between serum cystatin C and interventricular septal thickness (? = 0.167, P < 0.05, posterior wall thickness (? = 0.187, P < 0.05, and left ventricular weight index (? = 0.245, P < 0.01. Conclusion Serum cystatin C concentration is an independent marker for hypertensive LVH.

Xin Li

2013-06-01

169

Subclinical nephrosclerosis is linked to left ventricular hypertrophy independent of classical atherogenic factors.  

Science.gov (United States)

Recently, cardio-renal interactions have been considered to be important and it has been demonstrated that mild renal dysfunction is associated with left ventricular hypertrophy (LVH). However, the correlation between LVH and subclinical renal damage is unclear. We investigated this association by assessing pretransplant biopsies from living kidney donors with normal renal function. We retrospectively categorized 238 living kidney donors into tertiles according to the percentage of global glomerulosclerosis (%GGS) observed in pretransplant biopsies (low, 0-3.45% (n=80); moderate, 3.46-11.76% (n=78); high, ?11.77% (n=80)) to analyze trends in their left ventricular mass index (LVMI) measured by echocardiography and baseline factors. LVH was defined as LVMI >110?g?m(-2) in female and >125?g?m(-2) in male subjects. We used a logistic regression model to evaluate any correlations between %GGS and LVH. LVMI increased significantly with increasing tertiles of %GGS, as did the prevalence of left ventricular remodeling and LVH. According to multivariate logistic regression analysis, subjects with high %GGS tertiles had a sevenfold greater risk of LVH than did those with low tertiles, even after adjusting for age, sex, systolic blood pressure, history of diabetes mellitus, total serum cholesterol and glomerular filtration rate (GFR) measured by a radioisotopic technique. There is an association between GGS and LVH in subjects with normal renal function. This association is significant after adjustment for age, sex, blood pressure, GFR and other atherogenic factors. PMID:24305517

Haruyama, Naoki; Tsuchimoto, Akihiro; Masutani, Kosuke; Nagata, Masaharu; Kitada, Hidehisa; Tanaka, Masao; Tsuruya, Kazuhiko; Kitazono, Takanari

2014-05-01

170

Serum uric acid is associated with new-onset diabetes in hypertensive patients with left ventricular hypertrophy: The LIFE Study  

DEFF Research Database (Denmark)

It is unclear whether serum uric acid (SUA) is associated with development of new-onset diabetes (NOD) in patients with hypertension and left ventricular hypertrophy (LVH). The aim of the present investigation was to test the hypothesis that SUA predicts development of NOD in these patients.

Wiik, Benedicte P; Larstorp, Anne C K

2010-01-01

171

Coronary artery calcification and ECG pattern of left ventricular hypertrophy or strain identify different healthy individuals at risk  

DEFF Research Database (Denmark)

To improve risk stratification for development of ischaemic heart disease, several markers have been proposed. Both the presence of coronary artery calcification (CAC) and ECG pattern of left ventricular hypertrophy/strain have been shown to provide independent prognostic information. In this study, we investigated the association between established risk factors, ECG measurements and the presence of coronary artery calcification.

Diederichsen, Søren Zöga; Gerke, Oke

2013-01-01

172

Functional and morphological preservation of adult ventricular myocytes in culture by sub-micromolar cytochalasin D supplement.  

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In cardiac myocytes, cytochalasin D (CytoD) was reported to act as an actin disruptor and mechanical uncoupler. Using confocal and super-resolution STED microscopy, we show that CytoD preserves the actin filament architecture of adult rat ventricular myocytes in culture. Five hundred nanomolar CytoD was the optimal concentration to achieve both preservation of the T-tubular structure during culture periods of 3 days and conservation of major functional characteristics such as action potentials, calcium transients and, importantly, the contractile properties of single myocytes. Therefore, we conclude that the addition of CytoD to the culture of adult cardiac myocytes can indeed be used to generate a solid single-cell model that preserves both morphology and function of freshly isolated cells. Moreover, we reveal a putative link between cytoskeletal and T-tubular remodeling. In the absence of CytoD, we observed a loss of T-tubules that led to significant dyssynchronous Ca(2+)-induced Ca(2+) release (CICR), while in the presence of 0.5 ?M CytoD, T-tubules and homogeneous CICR were majorly preserved. Such data suggested a possible link between the actin cytoskeleton, T-tubules and synchronous, reliable excitation-contraction-coupling. Thus, T-tubular re-organization in cell culture sheds some additional light onto similar processes found during many cardiac diseases and might link cytoskeletal alterations to changes in subcellular Ca(2+) signaling revealed under such pathophysiological conditions. PMID:21930133

Tian, Qinghai; Pahlavan, Sara; Oleinikow, Katharina; Jung, Jennifer; Ruppenthal, Sandra; Scholz, Anke; Schumann, Christian; Kraegeloh, Annette; Oberhofer, Martin; Lipp, Peter; Kaestner, Lars

2012-01-01

173

Frequent left ventricular hypertrophy independent of blood pressure in 1851 pre-western Inuit  

DEFF Research Database (Denmark)

BACKGROUND: Elevated blood pressure is a risk factor for cardiovascular disease and may be detected by left ventricular hypertrophy (LVH) in electrocardiogram (ECG). Pre-western Inuit had frequent signs of LVH in ECG predominantly in the 3rd decade while a low occurrence of ischemic heart disease. METHODS: We evaluated the association between blood pressures and ECG signs of LVH, cardiac auscultation, and symptoms related to heart disease in the recently recovered data from the survey of 1851 Inuit conducted in 1962-1964 in East Greenland. RESULTS: The participation rate was 97%. Among the 812 Inuit aged 18years or above blood pressure was unaltered until the age of 39years (systolic, p=76; diastolic, p=0.36) and increased subsequently (both, p140mmHg was more frequent when aged >40years (p90mmHg was more common in men (p40years (p

Andersen, Stig; Kjærgaard, Marie

2011-01-01

174

Association of glomerular filtration rate and inflammation with left ventricular hypertrophy in chronic kidney disease patients.  

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Background: Although left ventricular hypertrophy (LVH) is an independent predictor of mortality in patients with end stage renal disease, few have examined its prevalence before the initiation of dialysis. The aim of this study was to investigate the relationship between LVH, estimated glomerular filtration rate (GFR), and inflammatory markers in patients with chronic kidney disease (CKD). Methods: Forty-one CKD patients (18 women, 23 men, mean age 53±17 years) with an estimated GFR between 15 and 59 mL/min (mean 34.2 mL/min) were enrolled and the following tests performed: routine serum biochemical analyses, high sensitivity C-reactive protein (hs-CRP), fibrinogen, ferritin, and homocysteine, and left ventricular mass index (LVMI), left ventricular ejection fraction (LVEF), and left ventricular fractional shortening (LVFS). Results: LVH was diagnosed in 32/41 patients (78%). CKD patients with LVH (n=32) had significantly higher hs-CRP (p=0.012), fibrinogen (p=0.031), and lower serum albumin (p=0.028) levels than those without LVH (n=9). In all patients, LVMI correlated positively with hs-CRP (r=0.483, p=0.002) and serum fibrinogen (r=0.426, p=0.015). Estimated GFR correlated positively with LVEF (r=0.414, p=0.007) and LVFS (r=0.376, p=0.018). Conclusions: Important positive associations exist between markers of inflammation and LVMI in patients with CKD. In addition to hs-CRP, elevated fibrinogen may portend the development of LVH in patients with CKD who are not yet on dialysis. PMID:23935269

Dervisoglu, E; Kozdag, G; Etiler, N; Kalender, B

2012-04-01

175

Effect of nebivolol on QT dispersion in hypertensive patients with left ventricular hypertrophy.  

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Hypertensive patients with left ventricular hypertrophy (LVH) have increased QT dispersion, which is considered an early indicator of end-organ damage and a non-invasive marker of risk for clinically important ventricular arrhythmias and cardiac mortality. The purpose of this study was to examine the effect of nebivolol antihypertensive therapy on QT dispersion in hypertensive subjects. Twenty-five subjects (15 men and 10 women, mean age 53.6 +/- 4.5 years) with essential arterial hypertension and mild-to-moderate LVH (blood pressure: 147.2 +/- 6.2/90.6 +/- 3.8 mmHg; left ventricular mass indexed: 149.1 +/- 10.7 g/m(2)) were compared with 25 age-matched healthy control subjects. All the participants underwent a complete clinical examination, including electrocardiogram for QT interval measurements. The QT dispersion was defined as the difference between the longest and the shortest QT interval occurring in the 12-lead electrocardiogram. The QT dispersion was corrected (QTc) with Bazett's formula. Hypertensive subjects were treated with 5 mg daily of nebivolol. The ECG and echocardiogram were repeated after four weeks of treatment. At baseline, hypertensive patients showed QT dispersion (56.9 +/- 6.4 vs. 31.7 +/- 8.4 ms, P left ventricular mass (LVMi: 149.1 +/- 10.7 vs. 151.4 +/- 9.8 g/m(2), ns). Nebivolol-based treatment improved QT dispersion (56.9 +/- 6.4 vs. 40.5 +/- 5.8 ms, P QT dispersion did not correlate with arterial BP reduction. In conclusion, nebivolol reduced increased QT dispersion in hypertensive subjects after four weeks. This effect, occurred without any change in LVM, did not seem to be related to the blood pressure lowering and could contribute to reduce arrhythmias as well as sudden cardiac death in at-risk hypertensive patients. PMID:15740930

Galetta, F; Franzoni, F; Magagna, A; Femia, F R; Pentimone, F; Santoro, G; Carpi, A

2005-01-01

176

Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english OBJECTIVE: To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses. METHODS: Patients of both sexes with moderate hypertension confirmed by ambulatory monitoring of arte-rial bl [...] ood pressure and with left ventricular hypertrophy on echocardiogram were assigned to three groups: enalapril (35 mg/day, n=15), losartan (175 mg/day, n=15) and enalapril+losartan (15 mg+100 mg/day, n=16). The patients received the drugs for 10 months. RESULTS: The three therapeutic regimens were equally effective in reducing blood pressure and left ventricular mass index (LVMI, g/m²): 141±3.9 to 123±3.6 in the enalapril group (p

Avanza Jr, Antônio Carlos; El Aouar, Lilian Mameri; Mill, José Geraldo.

177

Renal Transplantation Is Not Associated with Regression of Left Ventricular Hypertrophy: A Magnetic Resonance Study  

Science.gov (United States)

Background and objectives: Patients with end-stage renal failure (ESRD) have an increased risk of premature cardiovascular (CV) disease. Left ventricular hypertrophy is an independent risk factor for CV events and death in ESRD. Renal transplantation has been associated with reduction in CV risk and echocardiographic regression of left ventricular hypertrophy. However, echocardiography overestimates LV mass in ESRD patients. Cardiac magnetic resonance (CMR) provides more detailed, volume-independent, measures of cardiac structure. Changes in LV mass measured by CMR after renal transplantation were studied. Design, setting, participants, & measurements: Fifty patients underwent CMR on two occasions. Twenty-five were transplanted before the second scan. CMR was performed to measure LV mass index (LVMI), ejection fraction, end-diastolic and end-systolic volumes. Changes were expressed as percentage change over time. Patients with CV events between scans (e.g., acute coronary syndrome, myocardial infarction) were excluded. All transplant patients had serum creatinine <150 ?mol/L. Results: There was no significant change in LVMI between patients who underwent renal transplantation and those who remained on dialysis (transplanted mean, 2.75%/yr, ± 9.1 versus dialysis, ?3.6%/yr ± 16.7). In addition, there were no significant changes in end-diastolic volume (transplant, 0.1%/yr ± 19.5 versus not transplanted, ?3.4%/yr ± 31.5), end-systolic volume (transplanted mean, 15.2%/yr ± 65.2 versus not transplanted, 3.0%/yr ± 55.5), or ejection fraction (transplant, 2.1%/yr ± 11.9 versus not transplanted, ?0.4%/yr ± 5.3). Conclusions: Renal transplantation is not associated with significant regression of LVMI on CMR compared with patients who remain on the transplant waiting list.

Patel, Rajan K.; Mark, Patrick B.; Johnston, Nicola; McGregor, Ellon; Dargie, Henry J.; Jardine, Alan G.

2008-01-01

178

Cardiac morphology in left ventricular hypertrophy using thallium-201 myocardial scintigraphy  

International Nuclear Information System (INIS)

To evaluate cardiac morphology in the patients with various cases of hypertrophy, we measured left ventricular (LV) size using thallium-201 myocardial scintigraphy in 29 normal subjects and in 90 patients. Cardiac shape and dimension were assessed by measuring the wall thickness and external length in the short and long axis of LV image in LAO projection. In aortic stenosis and hypertensive heart disease the shape was spherical and the wall was thickened. In both mitral (MR) and aortic (AR) regurgitations, LV dilatation were shown; spherical shape in chronic MR but ellipsoid shape in acute MR and AR. Decreased LV size but normal shape was observed in mitral stenosis and cor pulmonale. In hypertrophic cardiomyopathy the LV wall was asymmetrically hypertrophied, while in congestive cardiomyopathy the wall is thin with marked LV dilatation and the shape was spherical. We concluded that the heart had characteristic configuration which might reflect cardiac performance or compensate for the load to the heart, and that thallium-201 myocardial scintigraphy is useful in the evaluation of cardiac morphology as well as in diagnosis of myocardial ischemia. (author)

1985-01-01

179

A compartmentalized mathematical model of the ?1-adrenergic signaling system in mouse ventricular myocytes.  

Science.gov (United States)

The ?1-adrenergic signaling system plays an important role in the functioning of cardiac cells. Experimental data shows that the activation of this system produces inotropy, lusitropy, and chronotropy in the heart, such as increased magnitude and relaxation rates of [Ca(2+)]i transients and contraction force, and increased heart rhythm. However, excessive stimulation of ?1-adrenergic receptors leads to heart dysfunction and heart failure. In this paper, a comprehensive, experimentally based mathematical model of the ?1-adrenergic signaling system for mouse ventricular myocytes is developed, which includes major subcellular functional compartments (caveolae, extracaveolae, and cytosol). The model describes biochemical reactions that occur during stimulation of ?1-adrenoceptors, changes in ionic currents, and modifications of Ca(2+) handling system. Simulations describe the dynamics of major signaling molecules, such as cyclic AMP and protein kinase A, in different subcellular compartments; the effects of inhibition of phosphodiesterases on cAMP production; kinetics and magnitudes of phosphorylation of ion channels, transporters, and Ca(2+) handling proteins; modifications of action potential shape and duration; magnitudes and relaxation rates of [Ca(2+)]i transients; changes in intracellular and transmembrane Ca(2+) fluxes; and [Na(+)]i fluxes and dynamics. The model elucidates complex interactions of ionic currents upon activation of ?1-adrenoceptors at different stimulation frequencies, which ultimately lead to a relatively modest increase in action potential duration and significant increase in [Ca(2+)]i transients. In particular, the model includes two subpopulations of the L-type Ca(2+) channels, in caveolae and extracaveolae compartments, and their effects on the action potential and [Ca(2+)]i transients are investigated. The presented model can be used by researchers for the interpretation of experimental data and for the developments of mathematical models for other species or for pathological conditions. PMID:24586529

Bondarenko, Vladimir E

2014-01-01

180

A Compartmentalized Mathematical Model of the ?1-Adrenergic Signaling System in Mouse Ventricular Myocytes  

Science.gov (United States)

The ?1-adrenergic signaling system plays an important role in the functioning of cardiac cells. Experimental data shows that the activation of this system produces inotropy, lusitropy, and chronotropy in the heart, such as increased magnitude and relaxation rates of [Ca2+]i transients and contraction force, and increased heart rhythm. However, excessive stimulation of ?1-adrenergic receptors leads to heart dysfunction and heart failure. In this paper, a comprehensive, experimentally based mathematical model of the ?1-adrenergic signaling system for mouse ventricular myocytes is developed, which includes major subcellular functional compartments (caveolae, extracaveolae, and cytosol). The model describes biochemical reactions that occur during stimulation of ?1-adrenoceptors, changes in ionic currents, and modifications of Ca2+ handling system. Simulations describe the dynamics of major signaling molecules, such as cyclic AMP and protein kinase A, in different subcellular compartments; the effects of inhibition of phosphodiesterases on cAMP production; kinetics and magnitudes of phosphorylation of ion channels, transporters, and Ca2+ handling proteins; modifications of action potential shape and duration; magnitudes and relaxation rates of [Ca2+]i transients; changes in intracellular and transmembrane Ca2+ fluxes; and [Na+]i fluxes and dynamics. The model elucidates complex interactions of ionic currents upon activation of ?1-adrenoceptors at different stimulation frequencies, which ultimately lead to a relatively modest increase in action potential duration and significant increase in [Ca2+]i transients. In particular, the model includes two subpopulations of the L-type Ca2+ channels, in caveolae and extracaveolae compartments, and their effects on the action potential and [Ca2+]i transients are investigated. The presented model can be used by researchers for the interpretation of experimental data and for the developments of mathematical models for other species or for pathological conditions.

Bondarenko, Vladimir E.

2014-01-01

 
 
 
 
181

Distinct Transient Outward Potassium Current (Ito) Phenotypes and Distribution of Fast-inactivating Potassium Channel Alpha Subunits in Ferret Left Ventricular Myocytes  

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The biophysical characteristics and ? subunits underlying calcium-independent transient outward potassium current (Ito) phenotypes expressed in ferret left ventricular epicardial (LV epi) and endocardial (LV endo) myocytes were analyzed using patch clamp, fluorescent in situ hybridization (FISH), and immunofluorescent (IF) techniques. Two distinct Ito phenotypes were measured (21–22°C) in the majority of LV epi and LV endo myocytes studied. The two Ito phenotypes displayed marked diffe...

Brahmajothi, Mulugu V.; Campbell, Donald L.; Rasmusson, Randall L.; Morales, Michael J.; Trimmer, James S.; Nerbonne, Jeanne M.; Strauss, Harold C.

1999-01-01

182

Evaluation of myocardial disorders in patients with dilated cardiomyopathy and left ventricular eccentric hypertrophy  

International Nuclear Information System (INIS)

201Tl myocardial SPECT was performed in cases of dilated cardiomyopathy and valvular heart disease with left ventricular eccentric hypertrophy, and the two groups were compared from the standpoint of the mechanism of onset of myocardial disorders. Significant coefficients of correlation were seen between the Tl score and LVDd (r=0.792, r=0.785) and Tl score and LVEF (r=-0.634, r=-0.555) in both dilated cardiomyopathy and valvular heart disease. In cases of valvular heart disease, significant correlation coefficients (r=-0.756, r=-0.720) between LVDd and r-WR (relative-washout rate), and Tl score and r-WR were observed, but no such correlation was seen in dilated cardiomyopathy. In valvular heart disease, a decrease in myocardial perfusion associated with enlargement of the left ventricle appeared, while in dilated cardiomyopathy, there was a marked decrease in LVEF in proportion to the thallium defect. Therefore, it was assumed that left ventricular wall disorders occur due to myocardial metabolic disorders and coronary microcirculation disorders. (author)

1992-01-01

183

Organic Nitrates Favor Regression of Left Ventricular Hypertrophy in Hypertensive Patients on Chronic Peritoneal Dialysis  

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Full Text Available The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH in hypertensive patients on chronic peritoneal dialysis (PD. Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group took other antihypertensive drugs. Blood pressure (BP, left ventricular mass index (LVMI and plasma asymmetric dimethylarginine (ADMA were monitored. Subjects with normal renal function were included as the control group (n = 30. At baseline, plasma ADMA levels in PD patients were significantly higher than the control group, but there was no significant difference in plasma ADMA levels between the two groups. At the end of the 24-week period, BP, LVMI, LVH prevalence and plasma ADMA levels in the nitrate group were significantly lower than those in the non-nitrate group. BP did not show a significant difference between 12 and 24 weeks in the nitrate group with a reduced need for other medication. Logistic regression analysis showed that nitrate supplementation and SBP reduction were independent risk factors of LVMI change in PD patients after adjusting for age, gender, diabetes history and CCB supplementation. It was concluded that organic nitrates favor regression of LVH in hypertensive patients on chronic peritoneal dialysis, and nitrates may be considered for use before employing the five other antihypertensive agents other than nitrates.

Han Li

2013-01-01

184

Prevalence of cardiomegaly and left ventricular hypertrophy in scuba diving and traffic accident victims.  

Science.gov (United States)

Although frequently asymptomatic, left ventricular hypertrophy (LVH) is an independent predictor of sudden cardiac death (SCD). We hypothesized that diving may increase the propensity for pre-existent LVH to cause a lethal arrhythmia (and SCD) and therefore the prevalence of LVH may be greater among scuba fatalities than among traffic fatalities. We compared autopsy data for 100 scuba fatalities with 178 traffic fatalities. Extracted data contained information on age, sex, height, body mass, heart mass (HM), left ventricular wall thickness (LVWT), interventricular wall thickness (IVWT), and degree of coronary artery stenosis. A case was classified as LVH if the LVWT was > 15 mm. Log risk models were used to compare HM and LVWT in two groups while controlling for body mass, body length, age and sex. The prevalence of LVH was compared using Pearson's test. The mean HM was 428.3 +/- 100 for divers and 387 +/- 87 for controls. The crude HM ratio for scuba fatalities vs. controls was 1.11 (1.05, 1.17), and when controlled for sex, age and body mass the ratio was 1.06 (1.01, 1.09). The mean LVWT was 15 +/- 3.5 for divers and 14 +/- 2.7 for controls (p = 0.0017). HM and LVWT measured at autopsy were greater in scuba than in traffic fatalities. PMID:24851550

Denoble, Petar J; Nelson, Craig L; Ranapurwala, Shabbar I; Caruso, James L

2014-01-01

185

Adenylyl Cyclase Subtype-Specific Compartmentalization: Differential Regulation of L-type Ca2+ Current in Ventricular Myocytes  

Science.gov (United States)

Rationale Adenylyl cyclase (AC) represents one of the principal molecules in the ?-adrenergic receptor (?AR) signaling pathway, responsible for the conversion of ATP to the second messenger, cAMP. AC type 5 (ACV) and 6 (ACVI) are the two main isoforms in the heart. While highly homologous in sequence, these two proteins nevertheless play different roles during the development of heart failure. Caveolin-3 is a scaffolding protein, integrating many intracellular signaling molecules in specialized areas called caveolae. In cardiomyocytes, caveolin is predominantly located along invaginations of the cell membrane known as t-tubules. Objective We take advantage of ACV and ACVI knockout mouse models to test the hypothesis that there is distinct compartmentalization of these two isoforms in ventricular myocytes. Methods and Results We demonstrate that ACV and ACVI isoforms exhibit distinct subcellular localization. ACVI isoform is localized in the plasma membrane outside of the t-tubular region, and is responsible for ?1AR signaling-mediated enhancement of the L-type Ca2+ current (ICa,L) in ventricular myocytes. In contrast, ACV isoform is localized mainly in the t-tubular region where its influence on ICa,L is restricted by phosphodiesterase (PDE). We further demonstrate that the interaction between caveolin-3 with ACV and PDE is responsible for the compartmentalization of ACV signaling. Conclusions Our results provide new insights into the compartmentalization of the two AC isoforms in the regulation of ICa,L in ventricular myocytes. Since caveolae are found in most mammalian cells, the mechanism of ?AR and AC compartmentalization may also be important for ?AR signaling in other cell types.

Timofeyev, Valeriy; Myers, Richard E.; Kim, Hyo Jeong; Woltz, Ryan L.; Sirish, Padmini; Heiserman, James P.; Li, Ning; Singapuri, Anil; Tang, Tong; Yarov-Yarovoy, Vladimir; Yamoah, Ebenezer N.; Hammond, H. Kirk; Chiamvimonvat, Nipavan

2013-01-01

186

Alteration of the L-type calcium current in guinea-pig single ventricular myocytes by heptaminol hydrochloride.  

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1. The effects of heptaminol on calcium current amplitude and characteristics were studied in single ventricular myocytes of guinea-pig by use of the whole cell configuration of the patch clamp technique. 2. A concentration-dependent decrease in ICa amplitude was observed. At heptaminol concentration as low as 10(-6) M, this effect was observed in only two cells (n = 6). At 10(-5) M the reduction of ICa was of 30 +/- 15% (n = 11). 3. The current recovery from inactivation at -40 mV holding po...

Peineau, N.; Mongo, K. G.; Le Guennec, J. Y.; Garnier, D.; Argibay, J. A.

1992-01-01

187

Cross-signaling between L-type Ca2+ channels and ryanodine receptors in rat ventricular myocytes  

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Calcium-mediated cross-signaling between the dihydropyridine (DHP) receptor, ryanodine receptor, and Na(+)-Ca2+ exchanger was examined in single rat ventricular myocytes where the diffusion distance of Ca2+ was limited to < 50 nm by dialysis with high concentrations of Ca2+ buffers. Dialysis of the cell with 2 mM Ca(2+)- indicator dye, Fura-2, or 2 mM Fura-2 plus 14 mM EGTA decreased the magnitude of ICa-triggered intracellular Ca2+ transients (Cai-transients) from 500 to 20-100 nM and comple...

1996-01-01

188

Hypertension, fluid overload and micro inflammation are associated with left ventricular hypertrophy in maintenance hemodialysis patients.  

Science.gov (United States)

This cross-sectional study aims to identify the potential risk factors of left ventricular hypertrophy (LVH) in hemodialysis (HD) patients. Echocardiography, anthropometric measurements and biochemical analyses were performed for 112 HD patients. In univariate analysis, body mass index, systolic blood pressure, diastolic blood pressure, glycosylated hemoglobin, glycated albumin, high sensitivity C-reactive protein (hs-CRP), cardiac troponin T (cTnT), amino-terminal pro-B-natriuretic peptide (NT-proBNP) and carotid artery intima-media thickness were positively correlated with left ventricular mass index (LVMI); pre-albumin, serum creatinine, left ventricular ejection fraction (LVEF) and fractional shortening were negatively correlated with LVMI. Linear regression analysis showed systolic blood pressure, NT-proBNP and LVEF were independently associated with LVMI. According to a binary logistic regression model, higher systolic blood pressure, NT-proBNP and hs-CRP levels showed independent correlation with LVH. Receiver operator characteristic curves analysis showed the associations between NT-proBNP and LVH more closely than hs-CRP and cTnT. The area under the curve for NT-proBNP, hs-CRP and cTnT was 0.762 (95% CI: 0.660-0.864, p?0.844, p?

Xu, Yan; Chen, Yue; Li, Daming; Li, Jiangtao; Liu, Xi; Cui, Chunli; Yu, Chen

2013-10-01

189

Lithium ion alters Ins(1,4,5)P3 production and mobilisation of intracellular free calcium in k-agonist stimulated rat ventricular myocytes  

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The effect of lithium ion on the generation of inositol phosphates and the mobilisation of intracellular free calcium in isolated adult rat ventricular myocytes stimulated with k-agonist was studied. Dynorphin1-13 stimulated an increase in the levels of Inositol 1,4,5-trisphosphate (InsP3) and intracellular free calcium ([Ca2+ ]i). Preincubation of the ventricular myocytes with lOmM Li+ for 20 minutes prior to stimulation by dynorphin1-13 reduce the increase of both InsP3 and [Ca2+]i. This ef...

1995-01-01

190

Effect of spirapril on left ventricular hypertrophy due to volume overload in rats.  

Science.gov (United States)

The effect of the angiotensin-converting enzyme (ACE) inhibitor spirapril on structural and functional parameters of volume-overloaded rat hearts was evaluated in a time-course study. Left ventricular hypertrophy (LVH) was induced by graded disruption of the aortic valve in male Wistar rats. Four weeks later, structural (LV mass and LV wall thickness) as well as functional parameters [LV end-systolic and end-diastolic volumes, stroke volume (SV), ejection fraction (EF)] were determined in anesthetized animals by magnetic resonance imaging (MRI). The rats were then divided into two groups, one of them receiving spirapril (10 mg/kg/day) in food. LV parameters were evaluated by MRI at 4, 18, 25, and 32 days after treatment was started. MRI analysis before the start of treatment showed that both groups had developed a similar degree of eccentric LV hypertrophy. Similarly, LV wall thickness, end-systolic and end-diastolic volumes, SV, and EF did not differ between the groups. Treatment with spirapril resulted in stable LV weight during the follow-up period of 32 days, whereas the untreated group showed a significant steady increase in heart weight. LV end-diastolic volume, LV end-systolic volume, and SV were smaller in the spirapril group when measured after 25 and 32 days, but only the difference in end-diastolic volume reached statistical significance. LV wall thickness and EF were not affected by spirapril. After the last MRI determinations, blood pressure (BP) and the response to angiotensin I (ANGI) were measured in conscious animals. Systolic BP (SBP) and mean arterial pressure (MAP) were significantly lower in spirapril-treated rats, and the dose-response curve to ANGI was shifted to the right.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:1378117

Umemura, K; Zierhut, W; Rudin, M; Novosel, D; Robertson, E; Pedersen, B; Hof, R P

1992-03-01

191

Obesity is associated with left atrial enlargement, E/A reversal and left ventricular hypertrophy  

Science.gov (United States)

BACKGROUND AND OBJECTIVE Previous studies have found that obesity is associated with congestive heart failure. The goal of the present study was to evaluate the association between obesity and parameters of left ventricular (LV) diastolic dysfunction using a large echocardiographic database. METHOD Data from 13,382 echocardiograms were analyzed for associations between obesity and abnormal LV diastolic parameters. Body mass index (BMI) was categorized into two groups for univariate analysis (nonobese group: BMI less than 30 kg/m2; obese group: BMI 30 kg/m2 or greater). Obesity was correlated with left atrial (LA) enlargement (LA diameter greater than 40 mm), LV hypertrophy (posterior or anterior wall thickness greater than 11 mm), early versus late diastolic mitral flow reversal, abnormal LV mass (greater than 215 g) and abnormal relative wall thickness (greater than 0.43). Multivariate analysis was used to adjust for age and sex. RESULTS All diastolic parameters of heart failure were associated with obesity using univariate and multivariate analyses. The ORs for patients with a BMI of 30 kg/m2 or greater were 2.53 (95% CI 2.30 to 2.75; P<0.0001) for LA diameter greater than 40 mm, 1.61 (95% CI 1.45 to 1.80; P<0.0001) for LV hypertrophy, 1.14 (95% CI 1.02 to 1.25; P<0.0001) for early versus late diastolic mitral flow reversal, 2.33 (95% CI 2.10 to 2.58; P<0.0001) for LV mass greater than 215 g, and 1.14 (95% CI 1.02 to 1.26; P=0.01) for relative wall thickness greater than 0.43. CONCLUSION The present study suggests that obesity is associated with abnormal parameters of diastolic function.

Movahed, Mohammad Reza; Saito, Yuji

2008-01-01

192

Serum Uric Acid Is Associated with Left Ventricular Hypertrophy Independent of Serum Parathyroid Hormone in Male Cardiac Patients  

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Background Several studies have shown that serum uric acid (UA) is associated with left ventricular (LV) hypertrophy. Serum levels of parathyroid hormone (PTH), which has bbe shown to be correlated with UA, is also known to be associated with cardiac hypertrophy; however, whether the association between UA and cardiac hypertrophy is independent of PTH remains unknown. Purpose We investigated whether the relationship between serum uric acid (UA) and LV hypertrophy is independent of intact PTH and other calcium-phosphate metabolism-related factors in cardiac patients. Methods and Results In a retrospective study, the association between UA and left ventricular mass index was assessed among 116 male cardiac patients (mean age 65±12 years) who were not taking UA lowering drugs. The median UA value was 5.9 mg/dL. Neither age nor body mass index differed significantly among the UA quartile groups. Patients with higher UA levels were more likely to be taking loop diuretics. UA showed a significant correlation with intact PTH (R?=?0.34, Pventricular mass index, and this relationship was found to be significant exclusively in patients who were not taking loop and/or thiazide diuretics. Multivariate logistic regression analysis showed that log-transformed UA was independently associated with LV hypertrophy with an odds ratio of 2.79 (95% confidence interval 1.48–5.28, P?=?0.002 per one standard deviation increase). Conclusions Among cardiac patients, serum UA was associated with LV hypertrophy, and this relationship was, at least in part, independent of intact PTH levels, which showed a significant correlation with UA in the same population.

Fujita, Shu-ichi; Okamoto, Yusuke; Shibata, Kensaku; Morita, Hideaki; Ito, Takahide; Sohmiya, Koichi; Hoshiga, Masaaki; Ishizaka, Nobukazu

2013-01-01

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Effect of ajmaline on action potential and ionic currents in rat ventricular myocytes.  

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The effect of ajmaline on action potential (AP) and ionic current components has been investigated in right ventricular myocytes of rat at room temperature using the whole cell patch clamp technique. Ajmaline decreased the upstroke velocity ((dV/dt)max) of AP and the AP amplitude, increased the AP duration measured at 50 and 90% repolarization, and reversibly inhibited most components of membrane ionic current in a concentration-dependent manner. The following values of IC50 and of the Hill coefficient (nH) resulted from approximation of the measured data by the Hill formula: for fast sodium current (INa) IC50=27.8+/-1.14 micromol/l and nH=1.27+/-0.25 at holding potential -75 mV, IC50=47.2+/-1.16 micromol/l and nH=1.16+/-0.21 at holding potential -120 mV; for L-type calcium current (ICa-L) IC50=70.8+/-0.09 micromol/l and n(H)=0.99+/-0.09; for transient outward potassium current (Ito) IC50=25.9+/-2.91 micromol/l and nH=1.07+/-0.15; for ATP-sensitive potassium current (IK(ATP)) IC50=13.3+/-1.1 micromol/l and nH=1.16+/-0.15. The current measured at the end of 300 ms depolarizing impulse was composed of an ajmaline-insensitive component and a component inhibited with IC50=61.0+/-1.1 micromol/l and nH=0.91+/-0.08. At hyperpolarizing voltages, ajmaline at high concentration of 300 micromol/l reduced the inward moiety of time-independent potassium current (IK1) by 36%. The results indicate that the inhibition of INa causes both the decreased rate of rise of depolarizing phase and the lowered amplitude of AP. The inhibition of Ito is responsible for the ajmaline-induced AP prolongation. PMID:16308426

Bébarová, M; Matejovic, P; Pásek, M; Simurdová, M; Simurda, J

2005-09-01

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The occurrence of left ventricular hypertrophy in normotensive individuals in a community setting in North-East Trinidad  

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Romel Bacchus, Kristianna Singh, Ijaz Ogeer, Kameel MungrueDepartment Paraclinical Sciences, Public Health and Primary Care Unit, Faculty of Medical Sciences, University of the West Indies, EWMSC, Mt Hope TrinidadObjective: The purpose of this study is to determine primarily the occurrence of left ventricular hypertrophy (LVH) in normotensive Trinidadians.Design and methods: Enrolment into the study required participants to have normal blood pressure (?140/90) using the JNC 7 (The Seventh ...

Bacchus R; Singh K; Ogeer I; Mungrue K

2011-01-01

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Genetic variation in angiotensin-converting enzyme 2 gene is associated with extent of left ventricular hypertrophy in hypertrophic cardiomyopathy  

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Hypertrophic cardiomyopathy, a common, inherited cardiac muscle disease, is primarily caused by mutations in sarcomeric protein-encoding genes and is characterized by overgrowth of ventricular muscle that is highly variable in extent and location. This variability has been partially attributed to locus and allelic heterogeneity of the disease-causing gene, but other factors, including unknown genetic factors, also modulate the extent of hypertrophy that develops in response to the defective s...

Merwe, Lize; Cloete, Ruben; Revera, Miriam; Heradien, Marshall; Goosen, Althea; Corfield, Valerie A.; Brink, Paul A.; Moolman-smook, Johanna C.

2008-01-01

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Mid-Septal Hypertrophy and Apical Ballooning; Potential Mechanism of Ventricular Tachycardia Storm in Patients with Hypertrophic Cardiomyopathy  

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Medically refractory ventricular tachycardia (VT) storm can be controlled with radiofrequency catheter ablation (RFCA), however, it may be difficult to control in some patients with hemodynamic overload. We experienced a patient with intractable VT storm controlled by hemodynamic unloading. The patient had mid-septal hypertrophic cardiomyopathy with an implantable cardioverter defibrillator (ICD) back-up. Because of the severe mid-septal hypertrophy, his left ventricle (LV) had an hourglass-l...

Hwang, Eui-seock; Pak, Hui-nam

2012-01-01

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Phenotyping of Left and Right Ventricular Function in Mouse Models of Compensated Hypertrophy and Heart Failure with Cardiac MRI  

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Background Left ventricular (LV) and right ventricular (RV) function have an important impact on symptom occurrence, disease progression and exercise tolerance in pressure overload-induced heart failure, but particularly RV functional changes are not well described in the relevant aortic banding mouse model. Therefore, we quantified time-dependent alterations in the ventricular morphology and function in two models of hypertrophy and heart failure and we studied the relationship between RV and LV function during the transition from hypertrophy to heart failure. Methods MRI was used to quantify RV and LV function and morphology in healthy (n?=?4) and sham operated (n?=?3) C57BL/6 mice, and animals with a mild (n?=?5) and a severe aortic constriction (n?=?10). Results Mice subjected to a mild constriction showed increased LV mass (PRVEF (P>0.05). Animals with a severe constriction progressively developed LV hypertrophy (PRVEF (P<0.001) and the development of pulmonary remodeling, as compared to controls during a 10-week follow-up. Myocardial strain, as a measure for local cardiac function, decreased in mice with a severe constriction compared to controls (P<0.05). Conclusions Relevant changes in mouse RV and LV function following an aortic constriction could be quantified using MRI. The well-controlled models described here open opportunities to assess the added value of new MRI techniques for the diagnosis of heart failure and to study the impact of new therapeutic strategies on disease progression and symptom occurrence.

van Nierop, Bastiaan J.; van Assen, Hans C.; van Deel, Elza D.; Niesen, Leonie B. P.; Duncker, Dirk J.; Strijkers, Gustav J.; Nicolay, Klaas

2013-01-01

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QRS Voltage-Duration Product in the Identification of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats  

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Full Text Available OBJECTIVE - Evaluation of the performance of the QRS voltage-duration product (VDP for detection of left ventricular hypertrophy (LVH in spontaneously hypertensive rats (SHR. METHODS - Orthogonal electrocardiograms (ECG were recorded in male SHR at the age of 12 and 20 weeks, when systolic blood pressure (sBP reached the average values of 165±3 mmHg and 195±12 mmHg, respectively. Age- and sex- matched normotensive Wistar Kyoto (WKY rats were used as controls. VDP was calculated as a product of maximum QRS spatial vector magnitude and QRS duration. Left ventricular mass (LVM was weighed after rats were sacrificed. RESULTS - LVM in SHR at 12 and 20 weeks of age (0.86±0.05 g and 1.05±0.07 g, respectively was significantly higher as compared with that in WKY (0.65±0.07 g and 0.70±0.02 g. The increase in LVM closely correlated with the sBP increase. VDP did not reflect the increase in LVM in SHR. VDP was lower in SHR as compared with that in WKY, and the difference was significant at the age of 20 weeks (18.2mVms compared with 10.7mVms, p<0.01. On the contrary, a significant increase in the VDP was observed in the control WKY at the age of 20 weeks without changes in LVM. The changes in VDP were influenced mainly by the changes in QRSmax. CONCLUSION - LVM was not the major determinant of QRS voltage changes and consequently of the VDP. These data point to the importance of the nonspatial determinants of the recorded QRS voltage in terms of the solid angle theory.

Bacharova Ljuba

2002-01-01

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Biological, electrical and echocardiographic indices versus cardiac magnetic resonance imaging in diagnosing left ventricular hypertrophy.  

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The aim of this study was to compare the diagnostic performance of N-terminal pro-brain natriuretic peptide (NT-proBNP), electrocardiographic (ECG) criteria and transthoracic echocardiography (TTE) versus cardiac magnetic resonance imaging in detecting left ventricular hypertrophy (LVH). The study included 42 hypertensive subjects with mean±s.d. age 48.1±12.3 years, 57.1% men, 24-h ambulatory blood pressure 144/89?mm?Hg, left ventricular ejection fraction >50%, without symptoms of heart failure, and not taking any drugs that interfere with hormonal regulation. The accuracies of the methods in detecting LVH were compared at two diagnostic LVH cutoffs: low, 83?g?m(-2) in men and 67?g?m(-2) in women; and high, 96?g?m(-2) in men and 81?g?m(-2) in women. With the low and high LVH cutoffs, the areas under the receiver-operating characteristic curves and the optimal values for NT-proBNP were 0.761, 0.849, 200 and 421?pg?ml(-1), respectively. An NT-proBNP level under 30?pg?ml(-1) ruled out LVH with 100% sensitivity. The optimal values and literature-based values of NT-proBNP allowed a correct classification of 73-81% of the subjects. In 80-90% of the cases, the diagnostic accuracy of NT-proBNP was close to that of ECG criteria but lower than that of TTE criteria. Interestingly, combining ECG criteria and NT-proBNP level improved the diagnostic performance to be at least comparable to that of TTE: the percentages of correctly classified subjects were 73-95% vs. 67-86%, respectively. Of note, the range considers both diagnostic LVH cutoffs. The simultaneous use of ECG criteria and NT-proBNP plasma levels seemed to be powerful enough to detect LVH in most hypertensive subjects. PMID:24132010

Courand, Pierre-Yves; Gaudebout, Nathalie; Mouly-Bertin, Carine; Thomson, Vivien; Fauvel, Jean-Pierre; Bricca, Giampiero; Lantelme, Pierre

2014-05-01

200

Economic benefits of left ventricular hypertrophy regression in patients with arterial hypertension  

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Full Text Available Aim. To evaluate by modelling the economic benefits of left ventricular hypertrophy (LVH regression in patients with arterial hypertension (HT due to therapy with fixed combination of valsartan/amlodipine.Material and methods. 20 patients (15 females and 5 males, aged 18 to 70 years with essential HT accompanied by metabolic syndrome with a history of previous ineffective antihypertensive therapy were included into the study. All patients were treated with fixed combination of amlodipine/valsartan in doses of 5/160 and 10/160 mg depending on blood pressure (BP level. Treatment duration was 24 weeks. Changes in BP level, LVH regression were assessed. Economic evaluation was performed on the basis of modelling with the specialized software Decision Tree 4.xla.Results. Effect of fixed amlodipine/valsartan combination therapy on LVH was used to estimate treatment effectiveness and to build the model. Patients were distributed according to left ventricular (LV mass (at baseline and after 24 weeks of therapy. Significant decrease in LV mass from 205.8±50.4 to 181.9±45.1 g (p<0.05 was revealed. The model took into account economic and frequency factors for 10 year prognosis: this therapy prevents 36 deaths, 6 strokes, 24 myocardial infarction per 1000 patients. Absence of need in treatment of these prevented events can save 2 516 772.42 RUR for every 1 000 patients. It would reduce the total costs per patient during 10 years.Conclusion. Treatment with amlodipine/valsartan single pill combination has not only clinical advantages, but also pharmacoeconomic benefits. This combination reduces risk of acute myocardial infarction and death more effectively. Treatment with fixed valsartan/amlodipine combination saves maximum years of life with less cost during 10 years. Despite of higher pharmacotherapy costs, fixed valsartan/amlodipine combination reduces total costs due to prevention of fatal and nonfatal cardiovascular events.

E.I. Tarlovskaya

2011-01-01

 
 
 
 
201

Left ventricular hypertrophy and blood pressure control in automated and continuous ambulatory peritoneal dialysis patients.  

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Hypertension, non-dipper blood pressure (BP) pattern and decrease in daily urine output have been associated with left ventricular hypertrophy (LVH) in peritoneal dialysis (PD) patients. However, there is lack of data regarding the impact of different PD regimens on these factors. We aimed to investigate the impact of circadian rhythm of BP on LVH in end-stage renal disease patients using automated peritoneal dialysis (APD) or continuous ambulatory peritoneal dialysis (CAPD) modalities. Twenty APD (7 men, 13 women) and 28 CAPD (16 men, 12 women) patients were included into the study. 24-h ambulatory blood pressure monitoring (ABPM) and transthoracic echocardiography besides routine blood examinations were performed. Two groups were compared with each other for ABPM measurements, BP loads, dipping patterns, left ventricular mass index (LVMI) and daily urine output. Mean systolic and diastolic BP measurements, BP loads, LVMI, residual renal function (RRF) and percentage of non-dippers were found to be similar for the two groups. There were positive correlations of LVMI with BP measurements and BP loads. LVMI was found to be significantly higher in diastolic non-dippers compared to dippers (140.4?±?35.3 vs 114.5?±?29.7, respectively, P?=?0.02). RRF and BP were found to be independent predictors of LVMI. Non-dipping BP pattern was a frequent finding among all PD patients without an inter-group difference. Additionally, higher BP measurements, decrease in daily urine output and non-dipper diastolic BP pattern were associated with LVMI. In order to avoid LVH, besides correction of anemia and volume control, circadian BP variability and diastolic dipping should also be taken into consideration in PD patients. PMID:24965296

Ata?, Nuh; Erten, Yasemin; Okyay, Gülay Ulusal; Inal, Salih; Topal, Salih; Oneç, Kür?ad; Akyel, Ahmet; Celik, Bülent; Tavil, Yusuf; Bali, Musa; Ar?nsoy, Turgay

2014-06-01

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Cardiac myocyte nuclear size and ploidy status decrease after mechanical support.  

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Two patients with end-stage dilated cardiomyopathy of ischemic and idiopathic origin were treated with a left ventricular assist device (LVAD) as a bridge for heart transplantation. Myocardial tissue was collected during LVAD insertion and from the left ventricular apex of the explanted hearts. The myocyte diameter, nuclear area and DNA content of myocyte nuclei were measured by static cytomorphometry in tissue sections and in isolated myocytes with a digital analysis system. The presence of apoptotic nuclei was investigated by the TdT mediated X-dUTP nick end labeling technique (TUNEL). The prolonged use of a LVAD was associated with a reduction in myocyte diameter, indicating that the LVAD may induce a reversion of myocyte hypertrophy, a process described as "reverse remodeling." In addition, unloading of the heart induced a reduction in the size and DNA content of myocyte nuclei. These results suggest that the cardiomyocyte nuclei are in a dynamic state and, as it occurs with cell hypertrophy, nuclear hypertrophy and polyploidization may be a reversible phenomenon. PMID:11425598

Rivello, H G; Meckert, P C; Vigliano, C; Favaloro, R; Laguens, R P

2001-01-01

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Vitamin D Receptor Gene Polymorphism and Left Ventricular Hypertrophy in Chronic Kidney Disease  

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Full Text Available FokI and BsmI polymorphisms of vitamin D receptor (VDR gene are regarded as reliable markers of disturbed vitamin D signaling pathway. Left ventricular hypertrophy (LVH is a strong cardiovascular risk marker in end stage renal disease (ESRD patients. Since BsmI polymorphism has been associated with LVH in ESRD patients, we addressed this study in patients with chronic kidney disease (CKD not yet on dialysis. One hundred and forty five patients with CKD stage 3 were genotyped for FokI and BsmI VDR polymorphisms, in order to assess the relationships between these VDR polymorphisms, some markers of mineral bone disorders, and LVH measured by echocardiography. Patients bearing either the Ff heterozygous or FF homozygous genotype had significantly higher PTH values than those bearing the ff genotype. The relationships between VDR genotypes and LVH revealed a highly significant association of the BsmI Bb heterozygous genotype with LVH. In patients with CKD stage 3 BsmI B allele was independently related to LVH. Since LVH is a frequent finding in dialysis population due to several mechanisms, the presence of the same relationship in patients with CKD strengthens the hypothesis that alterations of vitamin D signaling are implicated in LVH development in patients with renal diseases.

Domenico Santoro

2014-03-01

204

Vitamin D Receptor Gene Polymorphism and Left Ventricular Hypertrophy in Chronic Kidney Disease  

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FokI and BsmI polymorphisms of vitamin D receptor (VDR) gene are regarded as reliable markers of disturbed vitamin D signaling pathway. Left ventricular hypertrophy (LVH) is a strong cardiovascular risk marker in end stage renal disease (ESRD) patients. Since BsmI polymorphism has been associated with LVH in ESRD patients, we addressed this study in patients with chronic kidney disease (CKD) not yet on dialysis. One hundred and forty five patients with CKD stage 3 were genotyped for FokI and BsmI VDR polymorphisms, in order to assess the relationships between these VDR polymorphisms, some markers of mineral bone disorders, and LVH measured by echocardiography. Patients bearing either the Ff heterozygous or FF homozygous genotype had significantly higher PTH values than those bearing the ff genotype. The relationships between VDR genotypes and LVH revealed a highly significant association of the BsmI Bb heterozygous genotype with LVH. In patients with CKD stage 3 BsmI B allele was independently related to LVH. Since LVH is a frequent finding in dialysis population due to several mechanisms, the presence of the same relationship in patients with CKD strengthens the hypothesis that alterations of vitamin D signaling are implicated in LVH development in patients with renal diseases.

Santoro, Domenico; Gagliostro, Giorgia; Alibrandi, Angela; Ientile, Riccardo; Bellinghieri, Guido; Savica, Vincenzo; Buemi, Michele; Caccamo, Daniela

2014-01-01

205

The impact of left ventricular hypertrophy on survival in candidates for liver transplantation.  

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Left ventricular hypertrophy (LVH) occurs in 12% to 30% of patients with cirrhosis; however, its prognostic significance is not well studied. We assessed the association of LVH with survival in patients undergoing a liver transplantation (LT) evaluation. We performed a multicenter cohort study of patients undergoing an evaluation for LT. LVH was defined with transthoracic echocardiography. The outcome of interest was all-cause mortality. LVH was present in 138 of 485 patients (28%). Patients with LVH were older, more likely to be male and African American, and were more likely to have hypertension. Three hundred forty-five patients did not undergo transplantation (212 declined, and 133 were waiting): 36 of 110 patients with LVH (33%) died, whereas 57 of 235 patients without LVH (24%) died (P?=?0.23). After LT, 8 of 28 patients with LVH (29%) died over the course of 3 years, whereas 9 of 112 patients without LVH (8%) died (P?=?0.007). This finding was independent of conventional risk factors for LVH, and all deaths for patients with LVH occurred within 9 months of LT. No clinical or demographic characteristics were associated with mortality among LVH patients. In conclusion, the presence of LVH is associated with an early increase in mortality after LT, and this is independent of conventional risk factors for LVH. Further studies are needed to confirm these findings and identify factors associated with mortality after transplantation to improve outcomes. Liver Transpl 20:705-712, 2014. © 2014 AASLD. PMID:24659368

Batra, Sachin; Machicao, Victor I; Bynon, John S; Mehta, Shivang; Tanikella, Rajasekhar; Krowka, Michael J; Zacks, Steven; Trotter, James; Roberts, Kari E; Brown, Robert S; Kawut, Steven M; Fallon, Michael B

2014-06-01

206

Obesity in adolescence is associated with left ventricular hypertrophy and hypertension.  

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Background: Obesity is a risk factor for hypertension (HTN) and left ventricular hypertrophy (LVH). However, the association between obesity, HTN or LVH in adolescents has not been studied in a large population. Method: Utilizing a database of screening echocardiograms, we assessed for the presence of LVH and HTN (defined as systolic blood pressure (SBP) > 140 mmHg or diastolic blood pressure (DBP) > 90 mmHg) in obese adolescents (BMI > 30) using univariate and multivariate analysis. Results: A total of 2072 subjects were identified between the ages of 13-19 years. LVH was significantly more prevalent in obese subjects (47/166 [28.3%] vs. nonobese subjects (99/1612 [6.1%]) with a P-value of 140 was present in 38% of obese subjects (54/142) versus 12.7% of nonobese subjects (172/1, 353). DBP > 90 was present in 10.6% of obese subjects (15/141) of versus 3.1% of nonobese subjects (42/1352). After adjustment for age, gender and LVH, obesity remained independently associated with HTN (for SBP > 140, OR 2.24, CI: 1.46-3.45, P 90, OR 2.10, CI: 1.063-4.17, P = 0.03). Conclusion: Obese adolescents have a significantly higher prevalence of HTN and LVH. Our analysis suggests a direct negative effect of obesity on cardiovascular function starting early in teenage years. (Echocardiography 2011;28:150-153). PMID:21276070

Movahed, Mohammad-Reza; Bates, Sharon; Strootman, Deborah; Sattur, Sudhakar

2011-02-01

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Improvement of diastolic function after regression of left ventricular hypertrophy / Mejora de la función diastólica tras regresión de la hipertrofia ventricular izquierda  

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Full Text Available SciELO Mexico | Language: English Abstract in spanish Objetivo: Evaluar la función diastólica después de revertir la hipertrofia ventricular izquierda, en hipertensión leve a moderada tratada con inhibidores de la enzima convertidora angiotensina (ECA) y, si era necesario, con un diurético. Métodos: Noventa y ocho pacientes hipertensos con hipertrofia [...] ventricular izquierda e índices de función diastólica anormal del ventrículo izquierdo recibieron captopril 50 a 200 mg/día (Capotena®) más clortalidona durante 12 meses para lograr el control de la presión arterial, definido como presión diastólica Abstract in english Objective: To evaluate the diastolic function after regression of left ventricular hypertrophy, in mild to moderate hypertension treated with angiotensin converting enzyme(ACE) inhibitor and, if necessary, with a diuretic. Methods: Ninety-eight hypertensive patients with left ventricular hypertrophy [...] (LVH) and abnormal left ventricle diastolic function indexes received captopril (Capotena® ) 50 to 200 mg/day plus chlortalidone during 12 months to reach blood pressure control, defined as a diastolic blood pressure

Raúl, Teniente-Valente; Sergio, Solorio; Enrique, Vargas-Salado; Carlos, Aguirre-Vázquez; Martha A, Hernández-González; José Antonio, Olvera-Lopez; Leticia, Rodríguez-Mariscal; Miguel Angel, Luna-Ruiz; José Manuel, Guillén Contreras; Blanca Olivia, Murillo Ortiz.

208

Matrix elasticity regulates the optimal cardiac myocyte shape for contractility.  

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Concentric hypertrophy is characterized by ventricular wall thickening, fibrosis, and decreased myocyte length-to-width aspect ratio. Ventricular thickening is considered compensatory because it reduces wall stress, but the functional consequences of cell shape remodeling in this pathological setting are unknown. We hypothesized that decreases in myocyte aspect ratio allow myocytes to maximize contractility when the extracellular matrix becomes stiffer due to conditions such as fibrosis. To test this, we engineered neonatal rat ventricular myocytes into rectangles mimicking the 2-D profiles of healthy and hypertrophied myocytes on hydrogels with moderate (13 kPa) and high (90 kPa) elastic moduli. Actin alignment was unaffected by matrix elasticity, but sarcomere content was typically higher on stiff gels. Microtubule polymerization was higher on stiff gels, implying increased intracellular elastic modulus. On moderate gels, myocytes with moderate aspect ratios (?7:1) generated the most peak systolic work compared with other cell shapes. However, on stiffer gels, low aspect ratios (?2:1) generated the most peak systolic work. To compare the relative contributions of intracellular vs. extracellular elasticity to contractility, we developed an analytical model and used our experimental data to fit unknown parameters. Our model predicted that matrix elasticity dominates over intracellular elasticity, suggesting that the extracellular matrix may potentially be a more effective therapeutic target than microtubules. Our data and model suggest that myocytes with lower aspect ratios have a functional advantage when the elasticity of the extracellular matrix decreases due to conditions such as fibrosis, highlighting the role of the extracellular matrix in cardiac disease. PMID:24682394

McCain, Megan L; Yuan, Hongyan; Pasqualini, Francesco S; Campbell, Patrick H; Parker, Kevin Kit

2014-06-01

209

Cardiotrofina-1 circulante puede diferenciar la hipertrofia ventricular fisiológica del atleta de la hipertrofia patológica del paciente hipertenso / Circulating cardiotrophyn-1 may help differenciate left ventricular hypertrophy seen in athletes from pathologic left ventricular hypertrophy associated to hypertension  

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Full Text Available SciELO Chile | Language: Spanish Abstract in spanish Introducción: Cardiotrofina-1 (CT-1), una citoquina perteneciente a la superfamilia de la interleukina-6, se encuentra elevada en pacientes con hipertensión arterial (HTA) e hipertrofia ventricular izquierda (HVI). Sus niveles se correlacionan con el tamaño auricular izquierdo y con las presiones de [...] llenado del ventrículo izquierdo. Los niveles de CT-1 en atletas con HVI fisiológica no han sido investigados. Métodos: Estudio transversal. Se incluyeron pacientes con HTA esencial con y sin evidencia ecográfica de cardiopatía hipertensiva (CH)(HVI y relación E/E'>10), recientemente diagnosticada y sin tratamiento. Un grupo de atletas normotensos con diagnóstico ecográfico de HVI y un grupo control de sujetos normotensos pareados por edad y sexo. En todos los sujetos se midieron los niveles plasmáticos de CT-1 (ELISA). Se definió HVI mediante diagnóstico ecocargiográfico, utilizando el índice de masa ventricular izquierda usando la fórmula de Devereux (hombres ³115 gramos/m², mujer ³95 gramos/m²). Las presiones de llenado del VI se estimaron con la relación E/E' (doppler tisular en el anillo mitral medial). Resultados: Se incluyeron 10 pacientes por grupo. Los atletas con HVI presentaron una relación E/E' Abstract in english Background: Cardiotrophyn-1 (CT-1), is a cytokine which is increased in patients with hypertension (HT) and left ventricular hypertrophy (LVH). This increase occurs in proportion to left atrial size and left ventricular filling pressures. CT-1 levels in athletes with LVH have not been investigated M [...] ethods: Crossectional study. We evaluated: a) hypertensive patients with LVH and E/E' > 10 by echocardiography, recently diagnosed and receiving no medications; b) normotensive athletes with LVH as shown by echocardiography, and c) normotensive subjects, paired by age and sex. Plasma levels of CT-1 (ELISA) were measured in all. LVH was defined as left ventricular mass index > 115 G/m² (males) or > 95 G/m² (females). Results: E/E' was lower in athletes than hypertensive patients with LVH (6.5 ± 1 vs 12.9 ± 1.1, p

Gabrielli, Luigi; Yañez, Fernando; Ocaranza, María Paz; Godoy, Iván; Castro, Pablo; Greig, Douglas; Hernández, Claudia; Llevaneras, Silvana; Jalil, Jorge.

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Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan  

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Full Text Available OBJECTIVE: To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses. METHODS: Patients of both sexes with moderate hypertension confirmed by ambulatory monitoring of arte-rial blood pressure and with left ventricular hypertrophy on echocardiogram were assigned to three groups: enalapril (35 mg/day, n=15, losartan (175 mg/day, n=15 and enalapril+losartan (15 mg+100 mg/day, n=16. The patients received the drugs for 10 months. RESULTS: The three therapeutic regimens were equally effective in reducing blood pressure and left ventricular mass index (LVMI, g/m²: 141±3.9 to 123±3.6 in the enalapril group (p<0.05, from 147±3.8 to 133±2.8 in the losartan group (p<0.05, and from 146±3.0 to 116±4.0 in the enalapril+losartan group (p<0.05. However, the percent reduction of LVMI was significantly greater (p<0.01 in the enalapril+losartan group (20.5±5.0% than in enalapril (12.4±3.2% and the losartan (9.1±2.1% groups. Normalization of LVMI was obtained in 10 out of the 16 patients who received enalapril+ losartan, in 6 out of the 15 patients who received only enalapril and in 4 out of the 15 patients treated with losartan. CONCLUSION: The combination of an angiotensin-converting enzyme inhibitor and an angiotensin II receptor antagonist (AT1 receptor antagonist in patients produced an additional effect on the reduction of left ventricular hypertrophy. This finding may depend on a more complete inhibition of the cardiac renin-angiotensin.

Avanza Jr Antônio Carlos

2000-01-01

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Changing pattern of gene expression is associated with ventricular myocyte dysfunction and altered mechanisms of Ca2+ signalling in young type 2 Zucker diabetic fatty rat heart.  

Science.gov (United States)

The association between type 2 diabetes and obesity is very strong, and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The aim of this study was to investigate early changes in the pattern of genes encoding cardiac muscle regulatory proteins and associated changes in ventricular myocyte contraction and Ca(2+) transport in young (9- to 13-week-old) type 2 Zucker diabetic fatty (ZDF) rats. The amplitude of myocyte shortening was unaltered; however, time-to-peak shortening and time to half-relaxation of shortening were prolonged in ZDF myocytes (163 ± 5 and 127 ± 7 ms, respectively) compared with age-matched control rats (136 ± 5 and 103 ± 4 ms, respectively). The amplitude of the Ca(2+) transient was unaltered; however, time-to-peak Ca(2+) transient was prolonged in ZDF myocytes (66.9 ± 2.6 ms) compared with control myocytes (57.6 ± 2.3 ms). The L-type Ca(2+) current was reduced, and inactivation was prolonged over a range of test potentials in ZDF myocytes. At 0 mV, the density of L-type Ca(2+) current was 1.19 ± 0.28 pA pF(-1) in ZDF myocytes compared with 2.42 ± 0.40 pA pF(-1) in control myocytes. Sarcoplasmic reticulum Ca(2+) content, release and uptake and myofilament sensitivity to Ca(2+) were unaltered in ZDF myocytes compared with control myocytes. Expression of genes encoding various L-type Ca(2+) channel proteins (Cacna1c, Cacna1g, Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca(2+) transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart. A change in the expression of genes encoding myosin heavy chain and L-type Ca(2+) channel proteins might partly underlie alterations in the time course of contraction and Ca(2+) transients in ventricular myocytes from ZDF rats. PMID:21216827

Howarth, F C; Qureshi, M A; Hassan, Z; Al Kury, L T; Isaev, D; Parekh, K; Yammahi, S R K D; Oz, M; Adrian, T E; Adeghate, E

2011-03-01

212

-Adrenergic receptors on rat ventricular myocytes: characteristics and linkage to cAMP metabolism  

Energy Technology Data Exchange (ETDEWEB)

When incubated with purified cardiomyocytes from adult rat ventricle, the 1-antagonist (TH)prazosin binds to a single class of sites with high affinity. Competition for (TH)prazosin binding by the 2-selective antagonist yohimbine and the nonselective -antagonist phentolamine demonstrates that these receptors are of the 1-subtype. In addition, incubation of myocyte membranes with (TH)yohimbine results in no measurable specific binding. Agonist competition for (TH)prazosin binding to membranes prepared from purified myocytes demonstrates the presence of two components of binding: 28% of 1-receptors interact with norepinephrine with high affinity (K/sub D/ = 36 nM), whereas the majority of receptors (72%) have a low affinity for agonist (K/sub D/ = 2.2 M). After addition of 10 M GTP, norepinephrine competes for (TH)prazosin binding to a single class of sites with lower affinity (K/sub D/ = 2.2 M). Incubation of intact myocytes for 2 min with 1 M norepinephrine leads to significantly less cyclic AMP (cAMP) accumulation than stimulation with either norepinephrine plus prazosin or isoproterenol. Likewise, incubation of intact myocytes with 10 W M norepinephrine leads to significantly less activation of cAMP-dependent protein kinase than when myocytes are stimulated by both norepinephrine and the 1-adrenergic antagonist, prazosin or the US -adrenergic agonist, isoproterenol. They conclude that the cardiomyocyte 1 receptor is coupled to a guanine nucleotide-binding protein, that 1-receptors are functionally linked to decreased intracellular cAMP content, and that this change in cellular cAMP is expressed as described activation of cAMP-dependent protein kinase.

Buxton, I.L.O.; Brunton, L.L.

1986-08-01

213

?-Adrenergic receptors on rat ventricular myocytes: characteristics and linkage to cAMP metabolism  

International Nuclear Information System (INIS)

When incubated with purified cardiomyocytes from adult rat ventricle, the ?_1-antagonist ["3H]prazosin binds to a single class of sites with high affinity. Competition for ["3H]prazosin binding by the ?_2-selective antagonist yohimbine and the nonselective ?-antagonist phentolamine demonstrates that these receptors are of the ?_1-subtype. In addition, incubation of myocyte membranes with ["3H]yohimbine results in no measurable specific binding. Agonist competition for ["3H]prazosin binding to membranes prepared from purified myocytes demonstrates the presence of two components of binding: 28% of ?_1-receptors interact with norepinephrine with high affinity (K/sub D/ = 36 nM), whereas the majority of receptors (72%) have a low affinity for agonist (K/sub D/ = 2.2 ?M). After addition of 10 ?M GTP, norepinephrine competes for ["3H]prazosin binding to a single class of sites with lower affinity (K/sub D/ = 2.2 ?M). Incubation of intact myocytes for 2 min with 1 ?M norepinephrine leads to significantly less cyclic AMP (cAMP) accumulation than stimulation with either norepinephrine plus prazosin or isoproterenol. Likewise, incubation of intact myocytes with 10"-"6 M norepinephrine leads to significantly less activation of cAMP-dependent protein kinase than when myocytes are stimulated by both norepinephrine and the ?_1-adrenergic antagonist, prazosin or the ?-adrenergic agonist, isoproterenol. They conclude that the cardiomyocyte ?_1 receptor is coupled to a guanine nucleotide-binding protein, that ?_1-receptors are functionally linked to decreased intracellular cAMP content, and that this change in cellular cAMP is expressed as described activation of cAMP-dependent protein kinase

1986-01-01

214

The relation between peripheral vascular structure, left ventricular hypertrophy, and ambulatory blood pressure in essential hypertension  

DEFF Research Database (Denmark)

The relations between left ventricular mass (LVM), peripheral resistance artery structure, and ambulatory BP were studied in 83 patients with previously untreated or poorly regulated essential hypertension and 20 healthy controls of similar age and sex. LVM was assessed by echocardiography. Signs of left ventricular hypertrophy (LVH) were present in 67 (81%) of the patients and in none of the controls. Peripheral resistance arteries were isolated from surgical gluteal skin biopsies and mounted in a Mulvany-Halpern isometric small vessel myograph, and their media:lumen ratio, media thickness, and media cross-sectional area were determined under standardized conditions. Mean (+/- SD) ambulatory BP was 122 +/- 9 mm Hg among patients and 96 +/- 8 mm Hg among controls (P <.001). LVM was 327 +/- 99 g among patients and 197 +/- 37 g among controls (P <.001). Media thickness of resistance arteries was 21.0 +/- 4.2 microns among hypertensives and 16.2 +/- 2.6 microns among controls (P <.001). The media:lumen ratio of arteries from patients was 10.2 +/- 2.6% v 7.9 +/- 2.0% in arteries of similar internal diameter from controls (P <.01). Both LVM index (LVMI) and media/lumen ratio correlated significantly with BP. There was significant correlation between media:lumen ratio and LVMI among hypertensive patients (r = 0.45, P <.001), but if patients were subdivided according to the presence of LVH this correlation was found only among patients with LVH (r = 0.60 P<.001) and not among patient without LVH nor controls. Multiple regression analyses of age, body surface area, media/lumen ratio, and BP on LVM or LVMI revealed independent contributions of media/lumen ratio and BP. Age had no influence in the models. Similar results were obtained when casual BP was replaced with ambulatory BP in these analyses. No correlation was found between LVMI and media cross-sectional area. A minor subset of patients with complete absence of nocturnal BP drop had particularly great LVM and media:lumen ratio. The study suggests that cardiac and arteriolar tissue undergo parallel structural remodeling in essential hypertension.

Sihm, I; Schroeder, A P

1995-01-01

215

Nanoscale distribution of ryanodine receptors and caveolin-3 in mouse ventricular myocytes: dilation of t-tubules near junctions.  

Science.gov (United States)

We conducted super-resolution light microscopy (LM) imaging of the distribution of ryanodine receptors (RyRs) and caveolin-3 (CAV3) in mouse ventricular myocytes. Quantitative analysis of data at the surface sarcolemma showed that 4.8% of RyR labeling colocalized with CAV3 whereas 3.5% of CAV3 was in areas with RyR labeling. These values increased to 9.2 and 9.0%, respectively, in the interior of myocytes where CAV3 was widely expressed in the t-system but reduced in regions associated with junctional couplings. Electron microscopic (EM) tomography independently showed only few couplings with caveolae and little evidence for caveolar shapes on the t-system. Unexpectedly, both super-resolution LM and three-dimensional EM data (including serial block-face scanning EM) revealed significant increases in local t-system diameters in many regions associated with junctions. We suggest that this regional specialization helps reduce ionic accumulation and depletion in t-system lumen during excitation-contraction coupling to ensure effective local Ca²? release. Our data demonstrate that super-resolution LM and volume EM techniques complementarily enhance information on subcellular structure at the nanoscale. PMID:23746531

Wong, Joseph; Baddeley, David; Bushong, Eric A; Yu, Zeyun; Ellisman, Mark H; Hoshijima, Masahiko; Soeller, Christian

2013-06-01

216

Refinement of total 12-lead QRS voltage criteria for diagnosing left ventricular hypertrophy  

Directory of Open Access Journals (Sweden)

Full Text Available Objective: We sought to test the hypothesis that the total QRS voltage without either set of the limb leads (I, II, III or (R, L, F may be a better indicator of LVH as compared to the total QRS voltage. Background: The total 12 lead QRS voltage has been a validated electrocardiographic criterion for left ventricular hypertrophy (LVH, with an upper limit of175 mm. However, there is some redundancy in this measurement as the output of the limb leads is repeated because leads I, II, III, and R, L, F use the same three electrodes. Methods: 43 unselected, consecutive echocardiograms were examined for evidence of LVH by wall thickness. Electrocardiogram (ECG of these patients within a week of the echocardiogram were then examined for the total 12 leads QRS voltage, minus I, II, III and total minus R, L, F voltages. ECG findings were then compared with corresponding echocardiographic dimensions. Results: A total QRS voltage of123 mmon ECG yielded a sensitivity of 73% and specificity of 67% for diagnosing LVH with 95% CI = 0.59 - 0.89, p = 0.007. Total minus (R, L and F value of110 mmon ECG appears to give the best sensitivity (73%, specificity (72%, and accuracy (64% negative predictive value and 82% positive predictive value for LVH. Conclusion: It appears that total QRS voltage minus either set of the limb leads, especially the total minus R, L and F is a better criterion, with110 mmbeing the best specific, sensitive and accurate index for diagnosing LVH.

Deepti Kumar

2013-04-01

217

Effects of the venom of the spider Ornithoctonus hainana on neonatal rat ventricular myocytes cellular and ionic electrophysiology.  

Science.gov (United States)

Cardiac ion channels are membrane-spanning proteins that allow the passive movement of ions across the cell membrane along its electrochemical gradient, which regulates the resting membrane potential as well as the shape and duration of the cardiac action potential. Additionally, they have been recognized as potential targets for the actions of neurotransmitters, hormones and drugs of cardiac diseases. Spider venoms contain high abundant of toxins that target diverse ion channels and have been considered as a potential resource of new constituents with speci?c pharmacological properties. However, few peptides from spider venoms were detected as cardiac channel antagonists. In order to explore the effects of the venom of Ornithoctonus hainana on the action potential and ionic currents of neonatal rat ventricular myocytes (NRVMs), whole cell patch clamp technique was used to record action potential duration (APD), sodium current (INa), L calcium current (ICaL), rapidly activating and inactivating transient outward currents (Ito1), rapid (IKr) and slow (IKs) components of the delayed rectifier currents and the inward rectifier currents (IK1). Our results showed that 100 ?g/mL venom obviously prolonged APDs. Signi?cantly, the venom could inhibit INa and ICaL effectively, while no evident inhibitory effects on cardiac K(+) channels (Ito1, Iks, Ikr and Ik1) were observed, suggesting that the venom represented a multifaceted pharmacological profile. The effect of venom on Na(+) and Ca(2+) currents of ventricular myocytes revealed that the hainan venom as a rich resource of cardiac channel antagonists might be valuable tools for the investigation of both channels and drug development. PMID:24930961

Zhang, Yiya; Liu, Jinyan; Liu, Zhonghua; Wang, Meichi; Wang, Jing; Lu, Shanshan; Zhu, Li; Zeng, Xiongzhi; Liang, Songping

2014-09-01

218

The role of dyadic organization in regulation of sarcoplasmic reticulum Ca(2+) handling during rest in rabbit ventricular myocytes.  

Science.gov (United States)

The dyadic organization of ventricular myocytes ensures synchronized activation of sarcoplasmic reticulum (SR) Ca(2+) release during systole. However, it remains obscure how the dyadic organization affects SR Ca(2+) handling during diastole. By measuring intraluminal SR Ca(2+) ([Ca(2+)]SR) decline during rest in rabbit ventricular myocytes, we found that ?76% of leaked SR Ca(2+) is extruded from the cytosol and only ?24% is pumped back into the SR. Thus, the majority of Ca(2+) that leaks from the SR is removed from the cytosol before it can be sequestered back into the SR by the SR Ca(2+)-ATPase (SERCA). Detubulation decreased [Ca(2+)]SR decline during rest, thus making the leaked SR Ca(2+) more accessible for SERCA. These results suggest that Ca(2+) extrusion systems are localized in T-tubules. Inhibition of Na(+)-Ca(2+) exchanger (NCX) slowed [Ca(2+)]SR decline during rest by threefold, however did not prevent it. Depolarization of mitochondrial membrane potential during NCX inhibition completely prevented the rest-dependent [Ca(2+)]SR decline. Despite a significant SR Ca(2+) leak, Ca(2+) sparks were very rare events in control conditions. NCX inhibition or detubulation increased Ca(2+) spark activity independent of SR Ca(2+) load. Overall, these results indicate that during rest NCX effectively competes with SERCA for cytosolic Ca(2+) that leaks from the SR. This can be explained if the majority of SR Ca(2+) leak occurs through ryanodine receptors in the junctional SR that are located closely to NCX in the dyadic cleft. Such control of the dyadic [Ca(2+)] by NCX play a critical role in suppressing Ca(2+) sparks during rest. PMID:24806922

Bovo, Elisa; de Tombe, Pieter P; Zima, Aleksey V

2014-05-01

219

Regresión de la hipertrofia ventricular izquierda con el uso del captopril / Regression of left ventricular hypertrophy with the use of captopril  

Scientific Electronic Library Online (English)

Full Text Available SciELO Cuba | Language: Spanish Abstract in spanish Fundamento: la hipertensión arterial está asociada a cambios estructurales del aparato cardiovascular que le sirve para adaptarse al funcionamiento de un entorno de tensión alta. Objetivo: determinar la efectividad del captropil en la regresión de la hipertrofia ventricular izquierda en pacientes hi [...] pertensos, atendidos en consulta especializada en hipertensión arterial del Hospital universitario Manuel Ascunce Domenech desde Enero hasta Diciembre de 2008. Método: se realizó un estudio cuasi-experimental en ciento cuarenta y nueve pacientes. La muestra quedó constituida por cien pacientes. Resultados: se encontró un predominio de la hipertrofia ventricular izquierda en pacientes hipertensos entre treinta y seis y cuarenta y cinco años, después del uso del Captopril se produjo una disminución del 12,0% de pacientes con patrón geométrico anormal del ventrículo izquierdo con cuatro años de evolución de hipertensión arterial, y los pacientes con patrón geométrico anormal del ventrículo izquierdo con hipertensión arterial en estadio uno fueron veintiséis. Luego del uso de dicho fármaco veintiséis pacientes presentaron patrón geométrico normal del ventrículo izquierdo. Conclusiones: el captropil es efectivo en el tratamiento de la hipertrofia ventricular izquierda principalmente en pacientes con hipertensión en estadio uno, con menos de cuatros años de evolución. Abstract in english Background: arterial hypertension is associate to structural changes of the cardiovascular apparatus that are used for adapting to the function in a high tension environment. Objective: to determine the effectiveness of captopril in the regression of left ventricular hypertrophy in hypertensive pati [...] ents, attended in a specialized consultation of arterial hypertension at the Manuel Ascunce Domenech University Hospital from January to December 2008. Method: a quasi-experimental study in one hundred forty-nine patients was carried out. The sample was constituted by a hundred patients. Results: a prevalence of left ventricular hypertrophy in hypertensive patients between thirty-six and forty-five years was found, after the use of captopril brought about a decrease of 12,0% of patients with abnormal geometric pattern of left ventricle with four years of evolution of arterial hypertension, and patients with abnormal geometric pattern of left ventricle with arterial hypertension in stage one was twenty-six. After the use of this drug, twenty-six patients presented normal geometric pattern of left ventricle. Conclusions: captopril is effective in the treatment of left ventricular hypertrophy mainly in patients with hypertension in stage one, with less than four years of evolution.

Tomás Noel, Santana Téllez; Alina, Monteagudo Canto; Leandro, Segura Pujal; Angie Yohana, del Águila Grandez.

220

Telomerase expression and activity are coupled with myocyte proliferation and preservation of telomeric length in the failing heart.  

Science.gov (United States)

The role and even the existence of myocyte proliferation in the adult heart remain controversial. Documentation of cell cycle regulators, DNA synthesis, and mitotic images has not modified the view that myocardial growth can only occur from hypertrophy of an irreplaceable population of differentiated myocytes. To improve understanding the biology of the heart and obtain supportive evidence of myocyte replication, three indices of cell proliferation were analyzed in dogs affected by a progressive deterioration of cardiac performance and dilated cardiomyopathy. The magnitude of cycling myocytes was evaluated by the expression of Ki67 in nuclei. Ki67 labeling of left ventricular myocytes increased 5-fold, 12-fold, and 17-fold with the onset of moderate and severe ventricular dysfunction and overt failure, respectively. Telomerase activity in vivo is present only in multiplying cells; this enzyme increased 2.4-fold and 3.1-fold in the decompensated heart, preserving telomeric length in myocytes. The contribution of cycling myocytes to telomerase activity was determined by the colocalization of Ki67 and telomerase in myocyte nuclei. More than 50% of Ki67-positive cells expressed telomerase in the overloaded myocardium, suggesting that these myocytes were the morphological counterpart of the biochemical assay of enzyme activity. Moreover, we report that 20--30% of canine myocytes were telomerase competent, and this value was not changed by cardiac failure. In conclusion, the enhanced expression of Ki67 and telomerase activity, in combination with Ki67-telomerase labeling of myocyte nuclei, support the notion that myocyte proliferation contributes to cardiac hypertrophy of the diseased heart. PMID:11447262

Leri, A; Barlucchi, L; Limana, F; Deptala, A; Darzynkiewicz, Z; Hintze, T H; Kajstura, J; Nadal-Ginard, B; Anversa, P

2001-07-17

 
 
 
 
221

Telomerase expression and activity are coupled with myocyte proliferation and preservation of telomeric length in the failing heart  

Science.gov (United States)

The role and even the existence of myocyte proliferation in the adult heart remain controversial. Documentation of cell cycle regulators, DNA synthesis, and mitotic images has not modified the view that myocardial growth can only occur from hypertrophy of an irreplaceable population of differentiated myocytes. To improve understanding the biology of the heart and obtain supportive evidence of myocyte replication, three indices of cell proliferation were analyzed in dogs affected by a progressive deterioration of cardiac performance and dilated cardiomyopathy. The magnitude of cycling myocytes was evaluated by the expression of Ki67 in nuclei. Ki67 labeling of left ventricular myocytes increased 5-fold, 12-fold, and 17-fold with the onset of moderate and severe ventricular dysfunction and overt failure, respectively. Telomerase activity in vivo is present only in multiplying cells; this enzyme increased 2.4-fold and 3.1-fold in the decompensated heart, preserving telomeric length in myocytes. The contribution of cycling myocytes to telomerase activity was determined by the colocalization of Ki67 and telomerase in myocyte nuclei. More than 50% of Ki67-positive cells expressed telomerase in the overloaded myocardium, suggesting that these myocytes were the morphological counterpart of the biochemical assay of enzyme activity. Moreover, we report that 20–30% of canine myocytes were telomerase competent, and this value was not changed by cardiac failure. In conclusion, the enhanced expression of Ki67 and telomerase activity, in combination with Ki67-telomerase labeling of myocyte nuclei, support the notion that myocyte proliferation contributes to cardiac hypertrophy of the diseased heart.

Leri, Annarosa; Barlucchi, Laura; Limana, Federica; Deptala, Andrzej; Darzynkiewicz, Zbigniew; Hintze, Thomas H.; Kajstura, Jan; Nadal-Ginard, Bernardo; Anversa, Piero

2001-01-01

222

Sustained subthreshold-for-twitch depolarization in rat single ventricular myocytes causes sustained calcium channel activation and sarcoplasmic reticulum calcium release  

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Single rat ventricular myocytes, voltage-clamped at -50 to -40 mV, were depolarized in small steps in order to define the mechanisms that govern the increase in cytosolic [Ca2+] (Cai) and contraction, measured as a reduction in myocyte length. Small (3-5 mV), sustained (seconds) depolarizations that caused a small inward or no detectable change in current were followed after a delay by small (less than 2% of the resting length), steady reductions in cell length measured via a photodiode array...

1990-01-01

223

Stretch-Induced Regulation of Angiotensinogen Gene Expression in Cardiac Myocytes and Fibroblasts: Opposing Roles of JNK1/2 and p38? MAP Kinases  

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The cardiac renin-angiotensin system (RAS) has been implicated in mediating myocyte hypertrophy, remodeling, and fibroblast proliferation in the hemodynamically overloaded heart. However, the intracellular signaling mechanisms responsible for regulation of angiotensinogen (Ao), a substrate of the RAS system, are largely unknown. Here we report the identification of JNK1/2 as a negative, and p38? as a major positive regulator of Ao gene expression. Isolated neonatal rat ventricular myocytes (...

Lal, Hind; Verma, Suresh K.; Golden, Honey B.; Foster, Donald M.; Smith, Manuela; Dostal, David E.

2008-01-01

224

Cardiotrofina-1 circulante puede diferenciar la hipertrofia ventricular fisiológica del atleta de la hipertrofia patológica del paciente hipertenso Circulating cardiotrophyn-1 may help differenciate left ventricular hypertrophy seen in athletes from pathologic left ventricular hypertrophy associated to hypertension  

Directory of Open Access Journals (Sweden)

Full Text Available Introducción: Cardiotrofina-1 (CT-1, una citoquina perteneciente a la superfamilia de la interleukina-6, se encuentra elevada en pacientes con hipertensión arterial (HTA e hipertrofia ventricular izquierda (HVI. Sus niveles se correlacionan con el tamaño auricular izquierdo y con las presiones de llenado del ventrículo izquierdo. Los niveles de CT-1 en atletas con HVI fisiológica no han sido investigados. Métodos: Estudio transversal. Se incluyeron pacientes con HTA esencial con y sin evidencia ecográfica de cardiopatía hipertensiva (CH(HVI y relación E/E'>10, recientemente diagnosticada y sin tratamiento. Un grupo de atletas normotensos con diagnóstico ecográfico de HVI y un grupo control de sujetos normotensos pareados por edad y sexo. En todos los sujetos se midieron los niveles plasmáticos de CT-1 (ELISA. Se definió HVI mediante diagnóstico ecocargiográfico, utilizando el índice de masa ventricular izquierda usando la fórmula de Devereux (hombres ³115 gramos/m², mujer ³95 gramos/m². Las presiones de llenado del VI se estimaron con la relación E/E' (doppler tisular en el anillo mitral medial. Resultados: Se incluyeron 10 pacientes por grupo. Los atletas con HVI presentaron una relación E/E' Background: Cardiotrophyn-1 (CT-1, is a cytokine which is increased in patients with hypertension (HT and left ventricular hypertrophy (LVH. This increase occurs in proportion to left atrial size and left ventricular filling pressures. CT-1 levels in athletes with LVH have not been investigated Methods: Crossectional study. We evaluated: a hypertensive patients with LVH and E/E' > 10 by echocardiography, recently diagnosed and receiving no medications; b normotensive athletes with LVH as shown by echocardiography, and c normotensive subjects, paired by age and sex. Plasma levels of CT-1 (ELISA were measured in all. LVH was defined as left ventricular mass index > 115 G/m² (males or > 95 G/m² (females. Results: E/E' was lower in athletes than hypertensive patients with LVH (6.5 ± 1 vs 12.9 ± 1.1, p<0.01. E/E' in both control subjects and patients with HTA but no LVH did not differ from E/E' in athletes. CT-1 was lower in athletes than patients with HTA and LVH (6.6 ± 0.4 vs 18.2 ± 5.6 fmol/ml, respectively, p<0.001. CT-1 levels in control subjects and hypertensive patients without LVH did not differ from that found in athletes. Conclusion: CT-1 levels are similar in athletes compared to normal subjects and patients with HTA and no LVH. Hypertensive patients with similar grades of LVH and left ventricular diastolic dysfunction had significantly greater leves of CT-1. Thus, CT-1 levels could help differentiate pathological HVI from physiologic LVH in athletes.

Luigi Gabrielli

2009-04-01

225

A Simplified Local Control Model of Calcium-Induced Calcium Release in Cardiac Ventricular Myocytes  

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Calcium (Ca2+)-induced Ca2+ release (CICR) in cardiac myocytes exhibits high gain and is graded. These properties result from local control of Ca2+ release. Existing local control models of Ca2+ release in which interactions between L-Type Ca2+ channels (LCCs) and ryanodine-sensitive Ca2+ release channels (RyRs) are simulated stochastically are able to reconstruct these properties, but only at high computational cost. Here we present a general analytical approach for deriving simplified model...

2004-01-01

226

A Dynamic Model of Excitation-Contraction Coupling during Acidosis in Cardiac Ventricular Myocytes  

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Acidosis in cardiac myocytes is a major factor in the reduced inotropy that occurs in the ischemic heart. During acidosis, diastolic calcium concentration and the amplitude of the calcium transient increase, while the strength of contraction decreases. This has been attributed to the inhibition by protons of calcium uptake and release by the sarcoplasmic reticulum, to a rise of intracellular sodium caused by activation of sodium-hydrogen exchange, decreased calcium binding affinity to Troponi...

Crampin, Edmund J.; Smith, Nicolas P.

2006-01-01

227

Nongenomic steroid action: Inhibiting effects on cell-to-cell communication between rat ventricular myocytes  

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Numerous steroids are now believed to possess rapid membrane effects independent of the classical gene activation pathways and are potent modulators of membrane proteins, including voltage-and ligand-operated channels. The effects of steroids on the functional state of the intercellular channels clustered in gap junctions were compared by estimation of either the permeability for a fluorescent dye or the electrical conductance in cardiac myocytes of newborn rat. At 25 ?M, the esters of 17?-...

Verrecchia, Franck; Sarrouilhe, Denis; Herve?, Jean-claude

2001-01-01

228

Genetic variation in angiotensin II type 2 receptor gene influences extent of left ventricular hypertrophy in hypertrophic cardiomyopathy independent of blood pressure  

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Introduction. Hypertrophic cardiomyopathy (HCM), an inherited primary cardiac disorder mostly caused by defective sarcomeric proteins, serves as a model to investigate left ventricular hypertrophy (LVH). HCM manifests extreme variability in the degree and distribution of LVH, even in patients with the same causal mutation. Genes coding for renin-angiotensin-aldosterone system components have been studied as hypertrophy modifiers in HCM, with emphasis on the angiotensin (Ang) II type 1 recepto...

Carstens, Nadia; Merwe, Lize; Revera, Miriam; Heradien, Marshall; Goosen, Althea; Brink, Paul A.; Moolman-smook, Johanna C.

2011-01-01

229

Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study.  

Science.gov (United States)

We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) index ?49 g/h(2.7) in men and ?45 g/h(2.7) in women; B) LVM index ?125 g/m(2) in men and ?110 g/m(2) in women. Prevalence of LVH was calculated by indexing LVM to both self-reported and measured anthropometric values. In the whole population, LVH tended to be underestimated by self-reported values by 5.4% according to criterion A (48.5% vs. 53.9%, p < 0.001) and by 1.2% according to criterion B (29.6% vs. 30.8%, p < 0.01); similar findings were observed in the hypertensive subgroup encompassing one-half of the sample. Underestimation of LVH was more pronounced in older patients than in younger patients: 8.6% vs. 3.2% (p < 0.001) by criterion A, 3.1% vs. 0.1% (p < 0.001) by criterion B, in women than in men (8.6% vs. 3.3% (p < 0.001) by criterion A and 1.8% vs. 0.5% (p < 0.01) by criterion B. In a sample of outpatients attending echocardiographic laboratories, LVH is misclassified when left ventricular mass is normalized to self-reported weight and height. The error is related to the clinical characteristics of patients and is more pronounced when LVM is normalized to height(2.7). PMID:21446894

Cuspidi, Cesare; Negri, Francesca; Giudici, Valentina; Muiesan, Maria Lorenza; Grandi, Anna Maria; Ganau, Antonello; Lonati, Laura; Degli Esposti, Daniela; Capra, Anna; Milan, Alberto; Sala, Carla; Longo, Marcella; Morganti, Alberto

2011-01-01

230

Pleiotropic Effects of Neutrophils on Myocyte Apoptosis and Left Ventricular Remodeling During Early Volume Overload  

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Most of the available evidence on the role of neutrophils on pathological cardiac remodeling has been pertained after acute myocardial infarction. However, whether neutrophils directly contribute to the pathogenesis of cardiac remodeling after events other than acute myocardial infarction remains unknown. Here we show that acute eccentric hypertrophy induced by aorto-caval fistula (ACF) in the rats induced an increase in the inflammatory response characterized by activation of the STAT pathwa...

2009-01-01

231

The H1–H2 domain of the ?1 isoform of Na+–K+–ATPase is involved in ouabain toxicity in rat ventricular myocytes  

International Nuclear Information System (INIS)

The composition of different isoforms of Na+-K+-ATPase (NKA, Na/K pump) in ventricular myocytes is an important factor in determining the therapeutic effect and toxicity of cardiac glycosides (CGs) on heart failure. The mechanism whereby CGs cause these effects is still not completely clear. In the present study, we prepared two site-specific antibodies (SSA78 and WJS) against the H1–H2 domain of ?1 and ?2 isoforms of NKA in rat heart, respectively, and compared their influences on the effect of ouabain (OUA) in isolated rat ventricular myocytes. SSA78 or WJS, which can specifically bind with the ?1 or ?2 isoform, were assessed with enzyme linked immunosorbent assay (ELISA), Western blot and immunofluorescent staining methods. Preincubation of myocytes with SSA78 inhibited low OUA affinity pump current but not high OUA affinity pump current, reduced the rise in cytosolic calcium concentration ([Ca2+]i), attenuated mitochondrial Ca2+ overload, restored mitochondrial membrane potential reduction, and delayed the decrease of the myocardial contractile force as well as the occurrence of arrhythmic contraction induced by high concentrations (1 mM) but not low concentrations (1 ?M) of OUA. Similarly, preincubation of myocytes with WJS inhibited high OUA affinity pump current, reduced the increase of [Ca2+]i and the contractility induced by 1 ?M but not that induced by 1 mM OUA. These results indicate that the H1–H2 domain of the NKA ?1 isoform mediates OUA-induced cardiac toxicity in rat ventricular myocytes, and inhibitors for this binding site may be used as an adjunct to CGs treatment for cardiovascular disease. -- Highlights: ? We prepared two antibodies against the H1-H2 domain of ?1 and ?2 isoforms of NKA. ? The H1-H2 domain of the NKA ?1 isoform mediates OUA-induced cardiac toxicity. ? The H1-H2 domain of the NKA ?2 isoform mediates OUA-induced positive inotropic.

2012-07-01

232

Rescue of cardiomyocyte dysfunction by phospholamban ablation does not prevent ventricular failure in genetic hypertrophy  

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Cardiac hypertrophy, either compensated or decompensated, is associated with cardiomyocyte contractile dysfunction from depressed sarcoplasmic reticulum (SR) Ca2+ cycling. Normalization of Ca2+ cycling by ablation or inhibition of the SR inhibitor phospholamban (PLN) has prevented cardiac failure in experimental dilated cardiomyopathy and is a promising therapeutic approach for human heart failure. However, the potential benefits of restoring SR function on primary cardiac hypertrophy, a comm...

Song, Qiujing; Schmidt, Albrecht G.; Hahn, Harvey S.; Carr, Andrew N.; Frank, Beate; Pater, Luke; Gerst, Mike; Young, Karen; Hoit, Brian D.; Mcconnell, Bradley K.; Haghighi, Kobra; Seidman, Christine E.; Seidman, Jonathan G.; Dorn, Gerald W.; Kranias, Evangelia G.

2003-01-01

233

Intracellular Ca2+ modulation during short exposure to ischemia-mimetic factors in isolated rat ventricular myocytes  

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We investigated the effects of different ischemia-mimetic factors on intracellular Ca2+ concentration ([Ca2+]i). Ventricular myocytes were isolated from adult Wistar rats, and [Ca2+]i was measured using fluorescent indicator fluo-4 AM by confocal microscopy. Intracellular pH was measured using c5-(and-6)-carboxy SNARF-1 AM, a dual emission pH-sensitive ionophore. Myocytes were exposed to hypoxia, extracellular acidosis (pH 6.8), Na-lactate (10 mM), or to combination of those factors for 25 min. Monitoring of [Ca2+]i using fluo-4 AM fluorescent indicator revealed that [Ca2+]i accumulation increased immediately after exposing the cells to Na-lactate and extracellular acidosis, but not during cell exposure to moderate ischemia. Increase in [Ca2+]i during Na-lactate exposure decreased to control levels at the end of exposure period at extracellular pH 7.4, but not at pH 6.8. When combined, Na-lactate and acidosis had an additive effect on [Ca2+]i increase. After removal of solutions, [Ca2+]i continued to rise only when acidosis, hypoxia, and Na-lactate were applied together. Analysis of intracellular pH revealed that treatment of cells by Na-lactate and acidosis caused intracellular acidification, while short ischemia did not significantly change intracellular pH. Our experiments suggest that increase in [Ca2+]i during short hypoxia does not happen if pHi does not fall, while extracellular acidosis is required for sustained rise in [Ca2+]i induced by Na-lactate. Comparing to the effect of Na-lactate, extracellular acidosis induced slower [Ca2+]i elevation, accompanied with slower decrease in intracellular pH. These multiple effects of hypoxia, extracellular acidosis, and Na-lactate are likely to cause [Ca2+]i accumulation after the hypoxic stress.

Danijel, Pravdic; Nikolina, Vladic; Zeljko, Bosnjak J.

2013-01-01

234

Computational modeling and numerical methods for spatiotemporal calcium cycling in ventricular myocytes  

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Full Text Available Intracellular calcium (Ca cycling dynamics in cardiac myocytes is regulated by a complex network of spatially distributed organelles, such as sarcoplasmic reticulum (SR, mitochondria, and myofibrils. In this study, we present a mathematical model of intracellular Ca cycling and numerical and computational methods for computer simulations. The model consists of a coupled Ca release unit (CRU network, which includes a SR domain and a myoplasm domain. Each CRU contains 10 L-type Ca channels and 100 ryanodine receptor channels, with individual channels simulated stochastically using a varient of Gillespie’s method, modified here to handle time-dependent transition rates. Both the SR domain and the myoplasm domain in each CRU are modeled by 5x5x5 voxels to maintain proper Ca diffusion. Advanced numerical algorithms implemented on graphical processing units were used for fast computational simulations. For a myocyte containing 100x20x10 CRUs, a one-second heart time simulation takes about 10 minutes of machine time on a single NVIDIA Tesla C2050. Examples of simulated Ca cycling dynamics, such as Ca sparks, Ca waves, and Ca alternans, are shown.

MichaelNivala

2012-05-01

235

Tribulosin suppresses apoptosis via PKC epsilon and ERK1/2 signaling pathway during hypoxia/reoxygenation in neonatal rat ventricular cardiac myocytes.  

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Tribulosin (tigogenin 3-O-?-D-xylopyranosyl(1-2)-[?-D-xylopyranosyl (1-3)]-?-D-glucopyranosyl (1-4)-[a-L-rhamnopyranosyl(1-2)]-?-D-galactopyranoside), a component of gross saponins of Tribulus terrestris, has been shown to produce cytoprotective effects in heart. Yet, the precise mechanisms are not fully understood. We examined the mechanisms of tribulosin on myocardial protection. Ventricular myocytes were isolated from the heart of neonatal rats and were exposed to 3 h of hypoxia followed by 2 h reoxygenation. Apoptosis was induced by hypoxia/reoxygenation (H/R), and the expression of protein kinase C epsilon (PKC?) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) in cultured neonatal rat cardiac myocytes was detected. The results indicated that treatment with tribulosin in the culture medium protected cardiac myocytes against apoptosis induced by H/R. PKC? and ERK1/2 expression increased after pretreated with tribulosin. In the presence of PKC? inhibitor co-treated with tribulosin, the expression of ERK1/2 was decreased in H/R cardiac myocytes. While preconditioned with PD98059, ERK1/2 inhibitor, no effects on the expression of PKC? were detected. Tribulosin has protective effects on cardiac myocytes against apoptosis induced by H/R injury via PKC? and ERK1/2 signaling pathway. PMID:22115037

Zhang, Shuang; Li, Hong; Yang, Shi-Jie

2011-12-01

236

P128Ellagic acid reduces L-type Ca2+ current and induces negative inotropy through NO-GC-cGMP pathway in rat ventricular myocytes.  

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Recent evidences have shown that phenolic structures can exert many biological functions. Ellagic acid (EA), a phenolic compound, has been suggested to have cardioprotective effects. In this study we aimed to investigate the effect of EA on cardiac Ca2+ currents and contractility in rat ventricular myocytes and to elucidate the underlying mechanisms of these changes. All records measured from the freshly isolated ventricular myocytes of rat heart at 36±1 °C by using whole-cell configuration of voltage clamp. Cell shortening was measured by detecting the length of edges with video-based system at 1 Hz frequency of field stimulation. We found that EA dose dependently reduced Ca2+ currents with EC50= 23 nM. EA decreased voltage dependent L-type Ca2+ current density (ICaL) but it didn't affect the inactivation and reactivation parameters. Inhibition of adenylate cyclase (AC) with SQ-22536 (10 ?M) and using probucol (antioxidant, 5 ?M) had no effect on EA modulation of ICaL. Interestingly, blockage of nitric oxide synthase (NOS) with L-NAME (500 ?M) and guanylate cyclase (GC) with ODQ (1 ?M) abolished inhibitory effect of EA on ICaL. Moreover, EA dose dependently blunted fractional shorthening of ventricular myocytes. In conclusion, EA affects ionic and mechanical properties of ventricular myocytes starting at nanomolar concentrations. Our findings indicated that EA suppresses ICaL and exerts negative inotropic effects through activation of NOS-GC-cGMP pathway. Accordingly, EA may be useful in pathophysiological conditions whereby these effects might be favorable such as hypertension and ischemic heart diseases. PMID:25020549

Ozdemir, S; Olgar, Y; Ozturk, N; Usta, C; Puddu, Pe

2014-07-15

237

Endothelin downregulates SERCA2 gene and protein expression in adult rat ventricular myocytes: regulation by pertussis toxin-sensitive Gi protein and cAMP  

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Downregulation of the sarcoplasmic reticulum calcium ATPase (SERCA2) is associated with diastolic dysfunction in the failing heart. Elevated plasma endothelin-1 (ET) levels are correlated with congestive heart failure suggesting that ET may play a pathophysiological role. We have investigated the ability of ET to regulate SERCA2 gene expression in isolated adult rat ventricular myocytes. We find that ET enhances net protein synthesis by ?40% but significantly downregulates SERCA2 mRNA expre...

Hilal-dandan, Randa; He, Huaping; Martin, Jody L.; Brunton, Laurence L.; Dillmann, Wolfgang H.

2009-01-01

238

Electrophysiological effects of OPC-88117, a new antiarrhythmic agent on papillary muscles and single ventricular myocytes isolated from guinea-pig hearts.  

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1. The effects of OPC-88117, a new antiarrhythmic agent, on transmembrane action potentials were examined in right ventricular papillary muscles and in single ventricular myocytes isolated from guinea-pig hearts. 2. In papillary muscles, OPC-88117 above 3 x 10(-6) M caused a dose-dependent prolongation of action potential duration (APD). 3. OPC-88117 above 3 x 10(-5) M caused a significant decrease in the maximum upstroke velocity (Vmax) of the action potential without affecting the resting m...

Toyama, J.; Kodama, I.; Honjo, H.; Kamiya, K.

1989-01-01

239

Tissue Doppler Imaging can be useful to distinguish pathological from physiological left ventricular hypertrophy: a study in master athletes and mild hypertensive subjects  

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Abstract Background Transthoracic echocardiography left ventricular wall thickness is often increased in master athletes and it results by intense physical training. Left Ventricular Hypertrophy can also be due to a constant pressure overload. Conventional Pulsed Wave (PW) Doppler analysis of diastolic function sometimes fails to distinguish physiological from pathological LVH. The aim of this study is to evaluate the role of Pulsed Wave Tissue Doppler Imaging in diffe...

Galanti Giorgio; Toncelli Loira; Del Furia Francesca; Stefani Laura; Cappelli Brunello; De Luca Alessio; Vono Maria

2009-01-01

240

BET acetyl-lysine binding proteins control pathological cardiac hypertrophy.  

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Cardiac hypertrophy is an independent predictor of adverse outcomes in patients with heart failure, and thus represents an attractive target for novel therapeutic intervention. JQ1, a small molecule inhibitor of bromodomain and extraterminal (BET) acetyl-lysine reader proteins, was identified in a high throughput screen designed to discover novel small molecule regulators of cardiomyocyte hypertrophy. JQ1 dose-dependently blocked agonist-dependent hypertrophy of cultured neonatal rat ventricular myocytes (NRVMs) and reversed the prototypical gene program associated with pathological cardiac hypertrophy. JQ1 also blocked left ventricular hypertrophy (LVH) and improved cardiac function in adult mice subjected to transverse aortic constriction (TAC). The BET family consists of BRD2, BRD3, BRD4 and BRDT. BRD4 protein expression was increased during cardiac hypertrophy, and hypertrophic stimuli promoted recruitment of BRD4 to the transcriptional start site (TSS) of the gene encoding atrial natriuretic factor (ANF). Binding of BRD4 to the ANF TSS was associated with increased phosphorylation of local RNA polymerase II. These findings define a novel function for BET proteins as signal-responsive regulators of cardiac hypertrophy, and suggest that small molecule inhibitors of these epigenetic reader proteins have potential as therapeutics for heart failure. PMID:23939492

Spiltoir, Jessica I; Stratton, Matthew S; Cavasin, Maria A; Demos-Davies, Kim; Reid, Brian G; Qi, Jun; Bradner, James E; McKinsey, Timothy A

2013-10-01

 
 
 
 
241

Clinical impact of ' in-treatment' wall motion abnormalities in hypertensive patients with left ventricular hypertrophy: the LIFE study  

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Objectives Left ventricular systolic wall motion abnormalities have prognostic value. Whether wall motion detected by serial echocardiographic examinations predicts prognosis in hypertensive patients with left ventricular hypertrophy ( LVH) without clinically recognized atherosclerotic disease has, however, never been investigated. We examined whether 'in- treatment' wall motion abnormalities predicted outcome in the Losartan Intervention For Endpoint ( LIFE) reduction in hypertension echocardiographic substudy. Methods We studied 749 patients without coronary artery disease, myocardial infarction ( MI), or stroke history. Echocardiographic segmental wall motion abnormalities at baseline and annual re-evaluations (' as time- varying covariate') were examined in relation to endpoints ( cardiovascular mortality, MI, stroke, and hospitalized heart failure). Adjusted Cox regression was used to analyze the primary composite endpoint of cardiovascular death, MI, or stroke and, separately, for fatal and nonfatal MI and hospitalized heart failure. Results During a mean follow-up of 4.8 years, an event was recorded in 67 ( 9%) patients. In Cox models after adjusting for age, gender, treatment, blood pressure lowering, and serial change of left ventricular mass index, ' in-treatment' segmental wall motion abnormalities were associated with subsequent composite endpoint [ hazard ratio =2.1, 95% confidence interval ( CI) 1.1-3.8; P=0.019] and MI [ hazard ratio =3.7 ( 1.5 - 8.9); P=0.004]. Conclusion In hypertensive patients with LVH and no history of cardiovascular disease, ' in- treatment' left ventricular wall motion abnormalities are associated with increased likelihood of subsequent cardiovascular events independent of age, gender, blood pressure lowering, treatment modality, and in- treatment left ventricular mass index Udgivelsesdato: 2008/4

Cicala, S.; Simone, G. de

2008-01-01

242

Concordance of measures of left-ventricular hypertrophy in pediatric hypertension.  

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The American Academy of Pediatrics (AAP) recommends that any child diagnosed with hypertension have an echocardiogram to evaluate for the presence of left-ventricular (LV) hypertrophy (LVH) and advocates that LVH is an indication to initiate or intensify antihypertensive therapy. However, there is no consensus on the ideal method of defining LVH in the pediatric population. Many pediatric cardiologists rely on wall-thickness z-score of the LV posterior wall and/or interventricular septum to determine LVH. Yet, the AAP advocates using LV mass indexed to 2.7 (LVMI(2.7)) ? 51 g/m(2.7) to diagnose LVH. Recently, age-specific reference values for LVMI ? 95% were developed. The objective of the study was to determine the concordance between diagnosis of LVH by wall-thickness z-score and diagnosis by LVMI(2.7) criteria. A retrospective chart review was performed for subjects diagnosed with hypertension at a single tertiary care center (2009-2012). Echocardiogram reports were reviewed, and assessment of LVH was recorded. Diagnosis of LVH was assigned to each report reviewed according to three criteria: (1) LV wall-thickness z-score > 2.00; (2) age-specific reference values for LVMI(2.7) > 95th percentile; and (3) LVMI(2.7) > 51 g/m(2.7). Cohen's kappa statistic was used as a measurement of agreement between diagnosis by wall-thickness z-score and diagnosis using LVMI(2.7). A total of 159 echocardiograms in 109 subjects were reviewed. Subjects included 31 females and 77 males, age 13.2 ± 4.4 years, and 39 (42%) with a diagnosis of secondary hypertension. LVH was diagnosed in 31 cases (20%) based on increased wall-thickness z-score. Using LVMI(2.7) > 95%, LVH was found in 75 (47%) cases (mean LVMI(2.7)42.3 ± 17.2 g/m(2.7) [range 11.0-111 g/m(2.7)]). The wall-thickness z-score method agreed with LVMI(2.7) > 95% diagnosis 71% of the time (kappa 0.4). Using LVH criteria of LVMI(2.7) ? 51 g/m(2.7), 33 (21%) subjects were diagnosed with LVH. There was 79% agreement in the diagnosis of LVH between the wall-thickness z-score method and LVMI(2.7) > 51 g/m(2.7) (kappa 0.37). There is poor concordance between the diagnosis of LVH on echocardiogram reports using wall-thickness z-score and diagnosis of LVH using LVMI(2.7) criteria. It is important to establish a consensus method for diagnosing LVH because of the high frequency of cardiovascular complications in children with hypertension. PMID:24253610

Mirchandani, D; Bhatia, J; Leisman, D; Kwon, E N; Cooper, R; Chorny, N; Frank, R; Infante, L; Sethna, C

2014-04-01

243

Cardiac MRI assessed left ventricular hypertrophy in differentiating hypertensive heart disease from hypertrophic cardiomyopathy attributable to a sarcomeric gene mutation  

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To evaluate the value of cardiac magnetic resonance imaging (CMRI)-assessed left ventricular hypertrophy (LVH) in differentiating between hypertensive heart disease and hypertrophic cardiomyopathy (HCM). 95 unselected subjects with mild-to-moderate hypertension, 24 patients with HCM attributable to the D175N mutation of the {alpha}-tropomyosin gene and 17 control subjects were studied by cine CMRI. Left ventricular (LV) quantitative and qualitative characteristics were evaluated. LV maximal end-diastolic wall thickness, wall thickness-to-LV volume ratio, end-diastolic septum thickness and septum-to-lateral wall thickness ratio were useful measures for differentiating between LVH due to hypertension and HCM. The most accurate measure for identifying patients with HCM was the LV maximal wall thickness {>=}17 mm, with a sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of 90%, 93%, 86%, 95% and 91%, respectively. LV maximal wall thickness in the anterior wall, or regional bulging in left ventricular wall was found only in patients with HCM. LV mass index was not discriminant between patients with HCM and those with LVH due to hypertension. LV maximal thickness measured by CMRI is the best anatomical parameter in differentiating between LVH due to mild-to-moderate hypertension and HCM attributable to a sarcomeric mutation. CMRI assessment of location and quality of LVH is also of value in differential diagnosis. (orig.)

Sipola, Petri [Kuopio University Hospital, Department of Clinical Radiology, Kuopio (Finland); University of Eastern Finland, Institute of Clinical Medicine, Faculty of Health Sciences, Kuopio (Finland); Magga, Jarkko; Peuhkurinen, Keijo [Kuopio University Hospital, Department of Medicine, Kuopio (Finland); Husso, Minna [Kuopio University Hospital, Department of Clinical Radiology, Kuopio (Finland); Jaeaeskelaeinen, Pertti; Kuusisto, Johanna [Kuopio University Hospital, Department of Medicine, Kuopio (Finland); Kuopio University Hospital, Heart Center, P.O. Box 1777, Kuopio (Finland)

2011-07-15

244

QT dispersion measured by automatic computerized 12-lead electrocardiography contributes significantly to detection of left ventricular hypertrophy in Japanese patients.  

Science.gov (United States)

This study assessed the diagnostic value of QT dispersion for left ventricular hypertrophy (LVH) as determined by echocardiography. The QT and QRS interval parameters were determined automatically using computerized 12-lead electrocardiography in 153 Japanese out-patients. Corrected QT dispersion (QTcD) and maximal QRS duration (MaxQRS) were significantly correlated with left ventricular mass index. The sum of QTcD and MaxQRS showed the highest correlation with left ventricular mass index among QT and QRS interval parameters and their combinations. The cut-off points for LVH discrimination in this study were different to those reported in Western, mainly Caucasian, populations, suggesting the need for ethnicity-specific LVH detection criteria. A scoring system derived from multiple logistic regression analysis, employing a combination of QTcD, QRS time-voltage product and ST-T change, showed a specificity of 86.3%. It was concluded that QTcD, in addition to QRS time-voltage product and ST-T change, improved the detection of LVH. PMID:21672307

Izumi, R; Shinohata, R; Ohmaru, N; Kitawaki, T; Usui, S; Ikeda, S; Kusachi, S

2011-01-01

245

Myocyte necrosis underlies progressive myocardial dystrophy in mouse dsg2-related arrhythmogenic right ventricular cardiomyopathy  

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Mutations in the cardiac desmosomal protein desmoglein-2 (DSG2) are associated with arrhythmogenic right ventricular cardiomyopathy (ARVC). We studied the explanted heart of a proband carrying the DSG2-N266S mutation as well as transgenic mice (Tg-NS) with cardiac overexpression of the mouse equivalent of this mutation, N271S-dsg2, with the aim of investigating the pathophysiological mechanisms involved. Transgenic mice recapitulated the clinical features of ARVC, including sudden death at yo...

Pilichou, K.; Remme, C. A.; Basso, C.; Campian, M. E.; Rizzo, S.; Barnett, P.; Scicluna, B. P.; Bauce, B.; Hoff, M. J. B. Den; Bakker, J. M. T.; Tan, H. L.; Valente, M.; Nava, A.; Wilde, A. A. M.; Moorman, A. F. M.

2009-01-01

246

Relationship of left atrial enlargement to persistence or development of ECG left ventricular hypertrophy in hypertensive patients: implications for the development of new atrial fibrillation  

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Persistence and development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria are associated with an increased risk of atrial fibrillation compared with regression or continued absence of LVH. We postulated that this association might be in part mediated via greater left atrial enlargement (LAE) in patients with new and persistent ECG LVH.

Okin, Peter M; Gerdts, Eva

2010-01-01

247

Alteration of the L-type calcium current in guinea-pig single ventricular myocytes by heptaminol hydrochloride.  

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1. The effects of heptaminol on calcium current amplitude and characteristics were studied in single ventricular myocytes of guinea-pig by use of the whole cell configuration of the patch clamp technique. 2. A concentration-dependent decrease in ICa amplitude was observed. At heptaminol concentration as low as 10(-6) M, this effect was observed in only two cells (n = 6). At 10(-5) M the reduction of ICa was of 30 +/- 15% (n = 11). 3. The current recovery from inactivation at -40 mV holding potential (HP) seemed less sensitive to perfusion with heptaminol (greater than 10(-6) M). However, at -80 mV HP the overshoot of the recovery curve was decreased by heptaminol. 4. Both at -40 mV and -80 mV HP, heptaminol (10(-5) M) significantly increased the steady state inactivation of ICa. 5. As previously proposed by others to explain the effects of membrane active substances, the effects of heptaminol may result from alterations in cell membrane properties and possibly from an increase in intracellular free calcium ion concentration. PMID:1422567

Peineau, N; Mongo, K G; Le Guennec, J Y; Garnier, D; Argibay, J A

1992-09-01

248

Antagonism by adenosine and ATP of an isoprenaline-induced background current in guinea-pig ventricular myocytes.  

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A background current induced by isoprenaline, and its modulation by adenosine and ATP, have been studied using the whole cell patch clamp technique in guinea-pig ventricular myocytes. Isoprenaline (1-2000 nM) caused an inward shift of the holding current, in addition to increasing the inward calcium current (ICa). The effect on the background current was maximal earlier than the increase in ICa, but was of shorter duration. The magnitude of the background current was concentration dependent with a EC50 of 8 nM. This current was unaffected by tetrodotoxin 20 microM, Cd 200 microM or verapamil, 10 microM and potassium channel blockade (intracellular Cs, extracellular Cs 20 mM, Ba 2 mM or tetraethylammonium 10 mM). Lowering the chloride content of the electrode solution reduced the magnitude of the background current. The background current was also induced by histamine (1 or 10 microM). Adenosine (10-1000 microM) and and ATP (200 microM) antagonised the isoprenaline induced background current and the increase in ICa. The histamine effects on these currents were also reduced by adenosine. These results suggest that this background current may be carried by chloride ions and may be mediated via an increase in intracellular cyclic AMP concentration. Antagonism of this current may contribute to the antiarrhythmic actions of adenosine and ATP but their mechanisms of action are yet to be determined. PMID:2089155

Rankin, A C; Sitsapesan, R; Kane, K A

1990-12-01

249

Fragmented QRS and Left Ventricular Geometry in Hypertensive Patients  

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Full Text Available Introduction: Fragmented QRS is a depolarization abnormality detected with routin ECG recording. It is related with conduction defect which occurs after myocardial fibrosis. In the left ventricular hypertrophy, an excessive amount of collagen accumulates in the interstitium when the myocytes became hypertrophied, resulting in myocardial fibrosis. In this study, we aimed to investigate the relationship of fragmented QRS which was detected on ECG recordings of the hypertensive patients with the left ventricular geometry.Patients and Methods: Essential hypertension patients referred to our hospital on outpatient bases were included in the study. 12-lead resting ECG was taken in all the patients. Left ventricular geometry defined using left ventricular mass index and relative wall thickness with transthorasic echocardiography.Results: Sixy seven patients with fragmented QRS and 63 patients without fragmented QRS included the study. We found that patients in the group with fragmented QRS detected have a wider mean left atrium diameter, greater left ventricular mass and left ventricular mass index compared with the group without fragmented QRS. Concentric and eccentric hypertrophy were more common in fragmented QRS group, while normal geometry and concentric remodelling have greater rates in the normal group.Conclusion: Left ventricular hypertrophy is observed more frequently in the patients with fragmented QRS than without fragmented QRS. This may be associated with the increased myocardial fibrosis in the left ventricular hypertrophy. Existence of fragmented QRS can be used for risk stratification in the hypertensive patients.

Lütfü Bekar

2013-08-01

250

Sensibilidade do eletrocardiograma na hipertrofia ventricular de acordo com gênero e massa cardíaca / Electrocardiogram sensitivity in left ventricular hypertrophy according to gender and cardiac mass  

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Full Text Available SciELO Brazil | Language: Portuguese Abstract in portuguese FUNDAMENTO: Sabe-se que vários fatores interferem na sensibilidade do Eletrocardiograma (ECG) no diagnóstico da Hipertrofia Ventricular Esquerda (HVE), sendo o gênero e a massa cardíaca alguns dos principais. OBJETIVO: Avaliar a influência do sexo na sensibilidade de alguns dos critérios utilizados [...] para a detecção de HVE, de acordo com a progressão do grau de hipertrofia ventricular. MÉTODOS: De acordo com o gênero e com o grau de HVE ao ecocardiograma, os pacientes foram divididos em três grupos: HVE leve, moderada e severa. Avaliou-se a sensibilidade do ECG para detectar HVE entre homens e mulheres, conforme o grau de HVE. RESULTADOS: Dos 874 pacientes, 265 eram homens (30,3%) e 609, mulheres (69,7%). Os critérios [(S + R) X QRS], Sokolow-Lyon, Romhilt-Estes, Perúgia e padrão strain mostraram alto poder discriminatório no diagnóstico de HVE entre homens e mulheres nos três grupos de HVE, com desempenho superior na população masculina e destaque para os escores [(S + R) X QRS] e Perúgia. CONCLUSÃO: A sensibilidade diagnóstica do ECG é maior com o aumento da massa cardíaca. O exame é mais sensível entre homens, destacando-se os escores [(S + R) X QRS] e Perúgia. Abstract in english BACKGROUND: Several factors are known to interfere with electrocardiogram (ECG) sensitivity when diagnosing Left Ventricular Hypertrophy (LVH), with gender and cardiac mass being two of the most important ones OBJECTIVE: To evaluate the influence of gender on the sensitivity of some of the criteria [...] used to detect LVH, according to the progression of ventricular hypertrophy degree. METHODS: According to gender and the degree of LVH at the echocardiogram, the patients were divided in three groups: mild, moderate and severe LVH. ECG sensitivity to detect LVH was assessed between men and women, according to the LVH degree. RESULTS: Of the 874 patients, 265 were males (30.3%) and 609, females (69.7%). The [(S + R) X QRS], Sokolow-Lyon, Romhilt-Estes, Perugia and strain criteria showed high discriminatory power in the diagnosis of LVH between men and women in the three groups with LVH, with a superior performance in the male population and highlighting the importance of the [(S + R) X QRS] and Perugia scores. Conclusion: The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R) X QRS] and Perugia scores. CONCLUSION: The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R) X QRS] and Perugia scores.

Ana P., Colossimo; Francisco de Assis, Costa; Andrés R. P., Riera; Maria T. N., Bombig; Valter C., Lima; Francisco A. H., Fonseca; Maria C. O., Izar; Bráulio, L. Filho; Dilma, Souza; Rui M. S., Povoa.

251

Sensibilidade do eletrocardiograma na hipertrofia ventricular de acordo com gênero e massa cardíaca Electrocardiogram sensitivity in left ventricular hypertrophy according to gender and cardiac mass  

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Full Text Available FUNDAMENTO: Sabe-se que vários fatores interferem na sensibilidade do Eletrocardiograma (ECG no diagnóstico da Hipertrofia Ventricular Esquerda (HVE, sendo o gênero e a massa cardíaca alguns dos principais. OBJETIVO: Avaliar a influência do sexo na sensibilidade de alguns dos critérios utilizados para a detecção de HVE, de acordo com a progressão do grau de hipertrofia ventricular. MÉTODOS: De acordo com o gênero e com o grau de HVE ao ecocardiograma, os pacientes foram divididos em três grupos: HVE leve, moderada e severa. Avaliou-se a sensibilidade do ECG para detectar HVE entre homens e mulheres, conforme o grau de HVE. RESULTADOS: Dos 874 pacientes, 265 eram homens (30,3% e 609, mulheres (69,7%. Os critérios [(S + R X QRS], Sokolow-Lyon, Romhilt-Estes, Perúgia e padrão strain mostraram alto poder discriminatório no diagnóstico de HVE entre homens e mulheres nos três grupos de HVE, com desempenho superior na população masculina e destaque para os escores [(S + R X QRS] e Perúgia. CONCLUSÃO: A sensibilidade diagnóstica do ECG é maior com o aumento da massa cardíaca. O exame é mais sensível entre homens, destacando-se os escores [(S + R X QRS] e Perúgia.BACKGROUND: Several factors are known to interfere with electrocardiogram (ECG sensitivity when diagnosing Left Ventricular Hypertrophy (LVH, with gender and cardiac mass being two of the most important ones OBJECTIVE: To evaluate the influence of gender on the sensitivity of some of the criteria used to detect LVH, according to the progression of ventricular hypertrophy degree. METHODS: According to gender and the degree of LVH at the echocardiogram, the patients were divided in three groups: mild, moderate and severe LVH. ECG sensitivity to detect LVH was assessed between men and women, according to the LVH degree. RESULTS: Of the 874 patients, 265 were males (30.3% and 609, females (69.7%. The [(S + R X QRS], Sokolow-Lyon, Romhilt-Estes, Perugia and strain criteria showed high discriminatory power in the diagnosis of LVH between men and women in the three groups with LVH, with a superior performance in the male population and highlighting the importance of the [(S + R X QRS] and Perugia scores. Conclusion: The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R X QRS] and Perugia scores. CONCLUSION: The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R X QRS] and Perugia scores.

Ana P. Colossimo

2011-09-01

252

Novel approaches to determine contractile function of the isolated adult zebrafish ventricular cardiac myocyte.  

Science.gov (United States)

The zebrafish (Danio rerio) has been used extensively in cardiovascular biology, but mainly in the study of heart development. The relative ease of its genetic manipulation may indicate the suitability of this species as a cost-effective model system for the study of cardiac contractile biology. However, whether the zebrafish heart is an appropriate model system for investigations pertaining to mammalian cardiac contractile structure-function relationships remains to be resolved. Myocytes were isolated from adult zebrafish hearts by enzymatic digestion, attached to carbon rods, and twitch force and intracellular Ca(2+) were measured. We observed the modulation of twitch force, but not of intracellular Ca(2+), by both extracellular [Ca(2+)] and sarcomere length. In permeabilized cells/myofibrils, we found robust myofilament length-dependent activation. Moreover, modulation of myofilament activation-relaxation and force redevelopment kinetics by varied Ca(2+) activation levels resembled that found previously in mammalian myofilaments. We conclude that the zebrafish is a valid model system for the study of cardiac contractile structure-function relationships. PMID:24591576

Dvornikov, Alexey V; Dewan, Sukriti; Alekhina, Olga V; Pickett, F Bryan; de Tombe, Pieter P

2014-05-01

253

24-h Ambulatory blood pressure in patients with ECG-determined left ventricular hypertrophy: left ventricular geometry and urinary albumin excretion-a LIFE substudy.  

Science.gov (United States)

This study was undertaken to evaluate the relationships among left ventricular (LV) geometric patterns and urinary albumin excretion in patients with hypertension and electrocardiographic (ECG) LV hypertrophy. In 143 patients with stage II-III hypertension, 24-h ambulatory blood pressure (BP) monitoring, single urine albumin determination, and echocardiography were performed after 14 days of placebo treatment. Mean age was 68+/-7 years, 35% were women, body mass index was 28+/-5 kg/m(2), LV mass index (LVMI) was 125+/-26 g/m(2), and 24% had microalbuminuria. The mean office BP was 176+/-15/99+/-8 mmHg and the mean daytime ambulatory BP was 161+/-18/92+/-12 mmHg. Ambulatory BP, but not office BP, was higher among albuminuric compared to normoalbuminuric patients. In patients with established hypertension, daytime pulse pressure and office BP were different in the four patterns of LV geometry, with the highest pressure in those with abnormal geometry. Furthermore, microalbuminuria was more frequent in hypertensive patients with LV hypertrophy than in those with either normal geometry or concentric remodelling. White coat hypertensives (10%) showed lower LVMI and no microalbuminuria compared to patients with established hypertension. There were no differences in the prevalence of nondippers (26%) among the four LV geometric patterns or in microalbuminuria. In conclusion, increased daytime pulse pressure and office BP were associated with increased prevalence of abnormal LV geometry. Microalbuminuria was more frequent in groups with concentric and eccentric LV hypertrophy. Ambulatory BP, but not office BP, was higher in albuminuric than normoalbuminuric patients. With regard to the relationship among BP, LV geometric patterns, and urine albumin excretion in this population, 24-h ambulatory BP did not provide additional information beyond the office BP. PMID:15057254

Wiinberg, N; Bang, L E; Wachtell, K; Larsen, J; Olsen, M H; Tuxen, C; Hildebrandt, P R; Rokkedal, J; Ibsen, H; Devereux, R B

2004-06-01

254

AT1 blockade abolishes left ventricular hypertrophy in heterozygous cMyBP-C null mice: role of FHL1.  

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This research investigated the impact of angiotensin AT1 receptor (Agtr1) blockade on left ventricular (LV) hypertrophy in a mouse model of human hypertrophic cardiomyopathy (HCM), which carries one functional allele of Mybpc3 gene coding cardiac myosin-binding protein C (cMyBP-C). Five-month-old heterozygous cMyBP-C knockout (Het-KO) and wild-type mice were treated with irbesartan (50 mg/kg/day) or vehicle for 8 weeks. Arterial blood pressure was measured by tail cuff plethysmography. LV dimension and function were accessed by echocardiography. Myocardial gene expression was evaluated using RT-qPCR. Compared with wild-type littermates, Het-KO mice had greater LV/body weight ratio (4.0 ± 0.1 vs. 3.3 ± 0.1 mg/g, P < 0.001), thicker interventricular septal wall (0.70 ± 0.02 vs. 0.65 ± 0.01 mm, P < 0.02), lower Mybpc3 mRNA level (-43%, P < 0.02), higher four-and-a-half LIM domains 1 (Fhl1, +110%, P < 0.01), and angiotensin-converting enzyme 1 (Ace1, +67%, P < 0.05), but unchanged Agtr1 mRNA levels in the septum. Treatment with irbesartan had no effect in wild-type mice but abolished septum-predominant LV hypertrophy and Fhl1 upregulation without changes in Ace1 but with an increased Agtr1 (+42%) in Het-KO mice. Thus, septum-predominant LV hypertrophy in Het-KO mice is combined with higher Fhl1 expression, which can be abolished by AT1 receptor blockade, indicating a role of the renin-angiotensin system and Fhl1 in cMyBP-C-related HCM. PMID:23600722

Vignier, Nicolas; Le Corvoisier, Philippe; Blard, Charlotte; Sambin, Lucien; Azibani, Feriel; Schlossarek, Saskia; Delcayre, Claude; Carrier, Lucie; Hittinger, Luc; Su, Jin Bo

2014-06-01

255

Effect of genetic polymorphisms of vascular endothelial growth factor on left ventricular hypertrophy in patients with systemic hypertension.  

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Vascular endothelial growth factor (VEGF) is a cytokine involved in angiogenesis and upregulated during adaptive heart hypertrophy. Downregulation of VEGF seems to trigger the transition from adaptive to dilated cardiac hypertrophy. We investigated for the first time whether 3 clinically relevant polymorphisms in the VEGFA gene are associated with altered echocardiographic parameters in hypertensive patients. We determined genotypes for 3 polymorphisms in VEGFA promoter in 179 hypertensive patients and 169 healthy controls: g.-2578C>A (rs699947), g.-1154G>A (rs1570360), and g.-634G>C (rs2010963). Although the variant genotypes of the g.-634G>C (GC + CC) were associated with reduced left ventricular mass index (p = 0.030), the variant genotypes for the g.-1154G>A (GA + AA) were associated with reduced ejection fraction (p = 0.008). In addition, we found that VEGFA haplotypes were associated with altered ejection fraction (p = 0.024). The AAG haplotype was associated with reduced ejection fraction (p = 0.006), whereas the AGG haplotype was associated with increased ejection fraction (p = 0.010). Our results suggest that VEGF polymorphisms affect cardiac remodeling. Genotypes for VEGFA polymorphisms can be useful to help to identify hypertensive patients at greater intrinsic risk for heart failure. PMID:24321896

Lacchini, Riccardo; Luizon, Marcelo Rizzatti; Gasparini, Sandra; Ferreira-Sae, Maria C; Schreiber, Roberto; Nadruz, Wilson; Tanus-Santos, Jose E

2014-02-01

256

Obesidad central y regresión de hipertrofia ventricular izquierda / Central obesity and left ventricular hypertrophy regression / Obesidade central e regressão da hipertrofia esquerda  

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Full Text Available SciELO Argentina | Language: Spanish Abstract in portuguese Em sujeitos hipertensos, os níveis de pressão arterial per se seriam a principal determinante do desenvolvimento de hiperetrofia ventricular esquerda. Por outra parte, o índice de massa corporal e o perímetro de cintura se associaram em forma lineal, contínua e positiva com o índice de massa ventric [...] ular esquerdo ainda em não hipertensos. Um tratamento insuficiente seria a principal causa da falta de regressão do dano no órgão branco. O objetivo do presente trabalho é determinar o impacto da obesidade central sobre a regressão do índice de massa ventricular esquerdo. Material e métodos: incluíram-se 102 pacientes (p) HTA que concorreram por primeira vez a um consultório especializado em forma consecutiva, mediulhes o índice de massa ventricular esquerdo (IMVE) pelo método de Devereux ao início e logo de pelo menos 1 ano de tratamento. Foram divididos em dois grupos: GA: perímetro cintura (PC) Abstract in spanish En sujetos hipertensos, los niveles de presión arterial per se serían el principal determinante del desarrollo de hipertrofia ventricular izquierda. Por otra parte, el índice de masa corporal y el perímetro de cintura se han asociado en forma lineal, continua y positiva con elíndice de masa ventricu [...] lar izquierdo aún en no hipertensos. Un tratamiento insuficiente sería la principal causa de falta de regresión del daño en órgano blanco. El objetivo del presente trabajo es determinar el impacto de la obesidad central sobre la regresión del índice de masa ventricular izquierdo. Material y métodos: se incluyeron 102 pacientes (p) HTA que concurrieron por primera vez a un consultorio especializado en forma consecutiva, se les midió el índice de masa ventricular izquierdo (IMVI) por método de Devereux al inicio y luego de al menos 1 año de tratamiento. Fueron divididos en dos grupos: GA: perímetro cintura (PC) Abstract in english Blood pressure per se may be the main determinant of left ventricle hypertrophy development in hypertensive subjects. On the other side, body mass index and waist circumference are related to left ventricle mass index (LVMI) positively, continuously and linearly even in non hypertensive patients. An [...] insufficient treatment may be the main reason of not achieving regression of target organ damage. The objective of this trial is to establish the impact of central obesity on LVMI regression. Material and methods: 102 consecutive hypertensive patients (p) wich attended for the first time to a specialized consultory room were included. LVMI was measured with the Devereux method at the begining and after at least one year of treatment. The patients were divided into two groups: GA: waist circumference (WC)

Piskorz, Daniel; Citta, Luciano; Citta, Norberto; Lanzotti, Marcelo; Lanzotti, Roberto; Locatelli, Horacio; Tommasi, Alicia.

257

Left Ventricular Hypertrophy Is Associated with Diastolic Filling Alterations in Normotensive Offspring of Hypertensive Nigerians  

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Contribution of left ventricular diastolic dysfunction to adverse events in patients with cardiovascular diseases is increasingly being recognized and individuals with pedigree for hypertension are thought to exhibit anatomic and or functional changes in their left ventricle before they become hypertensive. This study aimed at characterizing left ventricular diastolic function in normotensive offspring of hypertensive Nigerians. Sixty-five offspring of hypertensive parents aged 15–25 years ...

Kolo, P. M.; Sanya, E. O.; Omotoso, A. B.; Soladoye, A.; Ogunmodede, J. A.

2012-01-01

258

Effect of hypertrophy on left ventricular diastolic function in patients with hypertrophic cardiomyopathy  

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Background. Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric LV hypertrophy (LVH) and impairment in diastolic function. We assess the relationship between LVH and invasive indexes of diastolic function. Methods. 21 HCM patients underwent cardiac catheterization to assess pulmonary capillary wedge pressure, LV end-diastolic pressure (measured by microtip catheters), and LV volumes (calculated by simultaneous radionuclide angiography). We calculated from LV pressure the time con...

Quirino Ciampi; Sandro Betocchi; Maria Angela Losi; Raffaella Lombardi; Bruno Villari; Massimo Chiariello

2010-01-01

259

Effect of hypertrophy on left ventricular diastolic function in patients with hypertrophic cardiomyopathy  

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Background. Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric LV hypertrophy (LVH) and impairment in diastolic function. We assess the relationship between LVH and invasive indexes of diastolic function. Methods. 21 HCM patients underwent cardiac catheterization to assess pulmonary capillary wedge pressure, LV end-diastolic pressure (measured by microtip catheters), and LV volumes (calculated by simultaneous radionuclide angiography). We calculated from LV pressure the time con...

Quirino Ciampi; Sandro Betocchi; Maria Angela Losi; Raffaella Lombardi; Bruno Villari; Massimo Chiariello

2006-01-01

260

Accuracy of advanced versus strictly conventional 12-lead ECG for detection and screening of coronary artery disease, left ventricular hypertrophy and left ventricular systolic dysfunction  

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Full Text Available Abstract Background Resting conventional 12-lead ECG has low sensitivity for detection of coronary artery disease (CAD and left ventricular hypertrophy (LVH and low positive predictive value (PPV for prediction of left ventricular systolic dysfunction (LVSD. We hypothesized that a ~5-min resting 12-lead advanced ECG test ("A-ECG" that combined results from both the advanced and conventional ECG could more accurately screen for these conditions than strictly conventional ECG. Methods Results from nearly every conventional and advanced resting ECG parameter known from the literature to have diagnostic or predictive value were first retrospectively evaluated in 418 healthy controls and 290 patients with imaging-proven CAD, LVH and/or LVSD. Each ECG parameter was examined for potential inclusion within multi-parameter A-ECG scores derived from multivariate regression models that were designed to optimally screen for disease in general or LVSD in particular. The performance of the best retrospectively-validated A-ECG scores was then compared against that of optimized pooled criteria from the strictly conventional ECG in a test set of 315 additional individuals. Results Compared to optimized pooled criteria from the strictly conventional ECG, a 7-parameter A-ECG score validated in the training set increased the sensitivity of resting ECG for identifying disease in the test set from 78% (72-84% to 92% (88-96% (P Conclusion Resting 12-lead A-ECG scoring is more accurate than strictly conventional ECG in screening for CAD, LVH and LVSD.

Warren Stafford G

2010-06-01

 
 
 
 
261

An Analysis of the Global Expression of MicroRNAs in an Experimental Model of Physiological Left Ventricular Hypertrophy  

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Background MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Studies of transgenic mouse models have indicated that deregulation of a single miR can induce pathological cardiac hypertrophy and cardiac failure. The roles of miRs in the genesis of physiological left ventricular hypertrophy (LVH), however, are not well understood. Objective To evaluate the global miR expression in an experimental model of exercise-induced LVH. Methods Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed on an odometer-monitored metal wheels for 35 days. Various tests were performed after 7 and 35 days of training, including a transthoracic echocardiography, a maximal exercise test, a miR microarray (miRBase v.16) and qRT-PCR analysis. Results The ratio between the left ventricular weight and body weight was increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at day 35 of training (p<0.001). After 7 days of training, the microarray identified 35 miRs that were differentially expressed between the two groups: 20 were up-regulated and 15 were down-regulated in the EXE group compared with the SED group (p?=?0.01). At day 35 of training, 25 miRs were differentially expressed: 15 were up-regulated and 10 were decreased in the EXE animals compared with the SED animals (p<0.01). The qRT-PCR analysis demonstrated an increase in miR-150 levels after 35 days and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. Conclusions We have identified new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, -27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not changed in physiological LVH.

Martinelli, Nidiane C.; Cohen, Carolina R.; Santos, Katia G.; Castro, Mauro A.; Biolo, Andreia; Frick, Luzia; Silvello, Daiane; Lopes, Amanda; Schneider, Stefanie; Andrades, Michael E.; Clausell, Nadine; Matte, Ursula; Rohde, Luis E.

2014-01-01

262

Diverse effects of renal denervation on ventricular hypertrophy and blood pressure in DOCA-salt hypertensive rats  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english Cardiac hypertrophy that accompanies hypertension seems to be a phenomenon of multifactorial origin whose development does not seem to depend on an increased pressure load alone, but also on local growth factors and cardioadrenergic activity. The aim of the present study was to determine if sympathe [...] tic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also delay the onset and attenuate the severity of deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt treatment was initiated in rats seven days after uninephrectomy and contralateral renal denervation or sham renal denervation. DOCA (15 mg/kg, sc) or vehicle (soybean oil, 0.25 ml per animal) was administered twice a week for two weeks. Rats treated with DOCA or vehicle (control) were provided drinking water containing 1% NaCl and 0.03% KCl. At the end of the treatment period, mean arterial pressure (MAP) and heart rate measurements were made in conscious animals. Under ether anesthesia, the heart was removed and the right and left ventricles (including the septum) were separated and weighed. DOCA-salt treatment produced a significant increase in left ventricular weight/body weight (LVW/BW) ratio (2.44 ± 0.09 mg/g) and right ventricular weight/body weight (RVW/BW) ratio (0.53 ± 0.01 mg/g) compared to control (1.92 ± 0.04 and 0.48 ± 0.01 mg/g, respectively) rats. MAP was significantly higher (39%) in DOCA-salt rats. Renal denervation prevented (P>0.05) the development of hypertension in DOCA-salt rats but did not prevent the increase in LVW/BW (2.27 ± 0.03 mg/g) and RVW/BW (0.52 ± 0.01 mg/g). We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, which may be more related to other events associated with DOCA-salt hypertension, such as an increase in cardiac sympathetic activity

Cabral, A.M.; Silva, I.F.; Gardioli, C.R.; Mauad, H.; Vasquez, E.C..

263

Diverse effects of renal denervation on ventricular hypertrophy and blood pressure in DOCA-salt hypertensive rats  

Directory of Open Access Journals (Sweden)

Full Text Available Cardiac hypertrophy that accompanies hypertension seems to be a phenomenon of multifactorial origin whose development does not seem to depend on an increased pressure load alone, but also on local growth factors and cardioadrenergic activity. The aim of the present study was to determine if sympathetic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also delay the onset and attenuate the severity of deoxycorticosterone acetate (DOCA-salt hypertension. DOCA-salt treatment was initiated in rats seven days after uninephrectomy and contralateral renal denervation or sham renal denervation. DOCA (15 mg/kg, sc or vehicle (soybean oil, 0.25 ml per animal was administered twice a week for two weeks. Rats treated with DOCA or vehicle (control were provided drinking water containing 1% NaCl and 0.03% KCl. At the end of the treatment period, mean arterial pressure (MAP and heart rate measurements were made in conscious animals. Under ether anesthesia, the heart was removed and the right and left ventricles (including the septum were separated and weighed. DOCA-salt treatment produced a significant increase in left ventricular weight/body weight (LVW/BW ratio (2.44 ± 0.09 mg/g and right ventricular weight/body weight (RVW/BW ratio (0.53 ± 0.01 mg/g compared to control (1.92 ± 0.04 and 0.48 ± 0.01 mg/g, respectively rats. MAP was significantly higher (39% in DOCA-salt rats. Renal denervation prevented (P>0.05 the development of hypertension in DOCA-salt rats but did not prevent the increase in LVW/BW (2.27 ± 0.03 mg/g and RVW/BW (0.52 ± 0.01 mg/g. We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, which may be more related to other events associated with DOCA-salt hypertension, such as an increase in cardiac sympathetic activity

Cabral A.M.

1998-01-01

264

Evaluation of myocardial disorders in patients with dilated cardiomyopathy and left ventricular eccentric hypertrophy; By sup 201 Tl myocardial SPECT  

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{sup 201}Tl myocardial SPECT was performed in cases of dilated cardiomyopathy and valvular heart disease with left ventricular eccentric hypertrophy, and the two groups were compared from the standpoint of the mechanism of onset of myocardial disorders. Significant coefficients of correlation were seen between the Tl score and LVDd (r=0.792, r=0.785) and Tl score and LVEF (r=-0.634, r=-0.555) in both dilated cardiomyopathy and valvular heart disease. In cases of valvular heart disease, significant correlation coefficients (r=-0.756, r=-0.720) between LVDd and r-WR (relative-washout rate), and Tl score and r-WR were observed, but no such correlation was seen in dilated cardiomyopathy. In valvular heart disease, a decrease in myocardial perfusion associated with enlargement of the left ventricle appeared, while in dilated cardiomyopathy, there was a marked decrease in LVEF in proportion to the thallium defect. Therefore, it was assumed that left ventricular wall disorders occur due to myocardial metabolic disorders and coronary microcirculation disorders. (author).

Yamazaki, Junichi; Ohsawa, Hidefumi; Uchi, Takashi (Toho Univ., Tokyo (Japan). School of Medicine) (and others)

1992-03-01

265

Dual effect of the local anaesthetic penticainide on the Na+ current of guinea-pig ventricular myocytes.  

Science.gov (United States)

1. The effect of the local anaesthetic penticainide (2-alkyl-(4-dialkylamino)-2-pyridyl-butyramide) on macroscopic and single-channel sodium current (INa) of guinea-pig ventricular myocytes was studied with the patch-clamp technique in the cell-attached and inside-out mode. 2. Penticainide (3-60 microM) affected the INa from the outside as well as from the cytoplasmic side. 3. Peak INa was reduced by penticainide at concentrations of 6, 30 and 60 microM, and this decrease of peak INa was more pronounced when the holding potential was more negative. Despite a reduction of peak INa, the time integral of the Na+ current was not changed (60 microM) or was even enhanced (6 microM), and this enhancement became more pronounced at less negative potentials. 4. At a concentration of 3 microM, penticainide increased both the time integral of the current and peak INa. 5. The shape of the steady-state current-voltage relationship and the steady-state inactivation curve were not influenced by penticainide. 6. In pronase-modified inside-out patches penticainide reduced INa at the beginning of a depolarizing pulse to the same extent as at the end (400 ms), indicating a very fast blockade of the bursting Na+ channel. The most prominent effects on pronase-modified single-channel INa were an increase of sweeps without activity, and a fast, repeatedly occurring block (flickering) of the bursting Na+ channel. 7. The amplitude of the unitary current was not altered. 8. It is concluded that penticainide blocks the open Na+ channel, and in addition shows the macroscopic inactivation. PMID:1663162

Gruber, R; Vereecke, J; Carmeliet, E

1991-04-01

266

A Major Role for hERG in Determining Frequency of Reentry in Neonatal Rat Ventricular Myocyte Monolayer  

Science.gov (United States)

Rationale The rapid delayed rectifier potassium current, IKr, which flows through the human ether-a-go-go-related (hERG) channel is a major determinant of the shape and duration of the human cardiac action potential (APD). However, it is unknown whether the time dependency of IKr enables it to control APD, conduction velocity (CV) and wavelength (WL) at the exceedingly high activation frequencies that are relevant to cardiac reentry and fibrillation. Objective To test the hypothesis that upregulation of hERG increases functional reentry frequency and contributes to its stability. Methods and Results Using optical mapping, we investigated the effects of IKr upregulation on reentry frequency, APD, CV and WL in neonatal rat ventricular myocyte (NRVM) monolayers infected with GFP (control), hERG (IKr), or dominant negative mutant hERG G628S. Reentry frequency was higher in the IKr-infected monolayers (21.12±0.8 Hz; n=43 vs. 9.21±0.58 Hz; n=16; p50%) than control during pacing at 1 to 5 Hz. CV was similar in both groups at low frequency pacing. In contrast, during high frequency reentry, the CV measured at varying distances from the center of rotation was significantly faster in IKr-infected monolayers than controls. Simulations using a modified NRVM model predicted that rotor acceleration was due in part to a transient hyperpolarization immediately following the AP. The transient hyperpolarization was confirmed experimentally. Conclusion hERG overexpression dramatically accelerates reentry frequency in NRVM monolayers. Both APD and WL shortening, together with transient hyperpolarization, underlies the increased rotor frequency and stability.

Hou, Luqia; Deo, Makarand; Furspan, Philip; Pandit, Sandeep V.; Mironov, Sergey; Auerbach, David S; Gong, Qiuming; Zhou, Zhengfeng; Berenfeld, Omer; Jalife, Jose

2010-01-01

267

Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation.  

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We compared the activity and physiologic effects of cardiac angiotensin converting enzyme (ACE) using isovolumic hearts from male Wistar rats with left ventricular hypertrophy due to chronic experimental aortic stenosis and from control rats. In response to the infusion of 3.5 X 10(-8) M angiotensin I in the isolated buffer perfused beating hearts, the intracardiac fractional conversion to angiotensin II was higher in the hypertrophied hearts compared with the controls (17.3 +/- 4.1% vs 6.8 +...

Schunkert, H.; Dzau, V. J.; Tang, S. S.; Hirsch, A. T.; Apstein, C. S.; Lorell, B. H.

1990-01-01

268

Characteristics of left ventricular hypertrophy estimated by MIBG and BMIPP cardiac scintigraphy in patients undergoing peritoneal dialysis  

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Left ventricular hypertrophy (LVH) has been reported as a major factor in morbidity and mortality in chronic dialysis patients. However, cardiovascular mortality in peritoneal dialysis (PD) patients with LVH is substantially similar to that in hemodialysis (HD) patients. The present study sought to study whether sympathetic nerve activity and fatty acid metabolism of the myocardium estimated by {sup 123}I metaiodobenzylguanidine (MIBG) and {sup 123}I {beta}-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) myocardial scintigraphy are impaired or not in PD patients with LVH. The underlying disease of 45 PD patients enrolled in this study was chronic glomerulonephritis in all cases. Serum levels of natriuretic peptides (arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP)) and free carnitine and MIBG, BMIPP myocardial scintigraphy and 2-dimensional echocardiography were measured in these 45 PD patients. The following results were obtained. The prevalence of increased left ventricular mass index (LVMI) was 84.4%. LVMI correlated with age, and serum levels of ANP and BNP, and inversely correlated with a heart-to-mediastinum ratio (H/M) estimated by MIBG and BMIPP myocardial scintigraphy. Percentages of the normal image of MIBG and BMIPP measured with a single photon emission computed tomography (SPECT) were 37.8% and 62.2%, respectively. The PD patients showing the diffuse defect of MIBG or BMIPP imaging had the decrease in left ventricular ejection fraction (LVEF). Especially, the serum level of free carnitine was reduced in the PD patients with diffuse defect of BMIPP SPECT. From these results, we concluded that PD patients with LVH showed impaired sympathetic nerve activity and fatty acid metabolism of the myocardium. Metabolic and functional disturbances of the myocardium may influence mortality in PD patients. (author)

Ohashi, Hiroshige; Oda, Hiroshi; Ohno, Michiya; Watanabe, Sachirow; Kotoo, Yasunori; Matsuno, Yukihiko [Gifu Prefectural Hospital (Japan)

2002-12-01

269

Characteristics of left ventricular hypertrophy estimated by MIBG and BMIPP cardiac scintigraphy in patients undergoing peritoneal dialysis  

International Nuclear Information System (INIS)

Left ventricular hypertrophy (LVH) has been reported as a major factor in morbidity and mortality in chronic dialysis patients. However, cardiovascular mortality in peritoneal dialysis (PD) patients with LVH is substantially similar to that in hemodialysis (HD) patients. The present study sought to study whether sympathetic nerve activity and fatty acid metabolism of the myocardium estimated by 123I metaiodobenzylguanidine (MIBG) and 123I ?-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) myocardial scintigraphy are impaired or not in PD patients with LVH. The underlying disease of 45 PD patients enrolled in this study was chronic glomerulonephritis in all cases. Serum levels of natriuretic peptides (arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP)) and free carnitine and MIBG, BMIPP myocardial scintigraphy and 2-dimensional echocardiography were measured in these 45 PD patients. The following results were obtained. The prevalence of increased left ventricular mass index (LVMI) was 84.4%. LVMI correlated with age, and serum levels of ANP and BNP, and inversely correlated with a heart-to-mediastinum ratio (H/M) estimated by MIBG and BMIPP myocardial scintigraphy. Percentages of the normal image of MIBG and BMIPP measured with a single photon emission computed tomography (SPECT) were 37.8% and 62.2%, respectively. The PD patients showing the diffuse defect of MIBG or BMIPP imaging had the decrease in left ventricular ejection fraction (LVEF). Especially, the serum level of free carnitine was reduced in the PD patients with diffuse defect of BMIPP SPECT. From these results, we concluded that PD patients with LVH showed impaired sympathetic nerve activity and fatty acid metabolism of the myocardium. Metabolic and functional disturbances of the myocardium may influence mortality in PD patients. (author)

2002-12-01

270

Effect of trimetazidine treatment on the transient outward potassium current of the left ventricular myocytes of rats with streptozotocin-induced type 1 diabetes mellitus  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: English Abstract in english Cardiovascular complications are a leading cause of mortality in patients with diabetes mellitus (DM). The present study was designed to investigate the effects of trimetazidine (TMZ), an anti-angina drug, on transient outward potassium current (Ito) remodeling in ventricular myocytes and the plasma [...] contents of free fatty acid (FFA) and glucose in DM. Sprague-Dawley rats, 8 weeks old and weighing 200-250 g, were randomly divided into three groups of 20 animals each. The control group was injected with vehicle (1 mM citrate buffer), the DM group was injected with 65 mg/kg streptozotocin (STZ) for induction of type 1 DM, and the DM + TMZ group was injected with the same dose of STZ followed by a 4-week treatment with TMZ (60 mg·kg-1·day-1). All animals were then euthanized and their hearts excised and subjected to electrophysiological measurements or gene expression analyses. TMZ exposure significantly reversed the increased plasma FFA level in diabetic rats, but failed to change the plasma glucose level. The amplitude of Ito was significantly decreased in left ventricular myocytes from diabetic rats relative to control animals (6.25 ± 1.45 vs 20.72 ± 2.93 pA/pF at +40 mV). The DM-associated Ito reduction was attenuated by TMZ. Moreover, TMZ treatment reversed the increased expression of the channel-forming alpha subunit Kv1.4 and the decreased expression of Kv4.2 and Kv4.3 in diabetic rat hearts. These data demonstrate that TMZ can normalize, or partially normalize, the increased plasma FFA content, the reduced Ito of ventricular myocytes, and the altered expression Kv1.4, Kv4.2, and Kv4.3 in type 1 DM.

Yu-luan, Xiang; Li, He; Jun, Xiao; Shuang, Xia; Song-bai, Deng; Yun, Xiu; Qiang, She.

271

Usefulness of QRS Voltage Correction by Body Mass Index to Improve Electrocardiographic Detection of Left Ventricular Hypertrophy in Patients With Systemic Hypertension.  

Science.gov (United States)

Obesity reduces the accuracy of voltage-based electrocardiographic (ECG) criteria for diagnosis of left ventricular (LV) hypertrophy. We developed a new ECG score for diagnosis of LV hypertrophy, defined either by a typical strain pattern or a product of the Cornell voltage (R wave height in lead aVL plus S wave depth in lead V3) by body mass index >604 mm?kg/m(2). We examined a population of 2,747 untreated hypertensive subjects (mean age 49 ± 11 years) with good quality ECG and echocardiographic tracings. Several traditional ECG criteria for LV hypertrophy were compared with the new score, with echocardiographic LV mass taken as reference. Among the tested criteria, the highest sensitivity combined with specificity was yielded by the new score (sensitivity 36.1%, 95% confidence interval [CI] 32.9 to 39.4; specificity 90.5%, 95% CI 89.1 to 91.8; and accuracy 73.1%, 95% CI 71.5 to 74.8). Prevalence of ECG LV hypertrophy with the new score was 18%. On the basis of comparisons between areas under the receiver operating characteristic curves, the best performance was achieved by the new score with respect to other ECG criteria for LV hypertrophy (all p <0.0001). In conclusion, correction of Cornell voltage by body mass index as a marker of obesity improves the performance of traditional electrocardiography for diagnosis of LV hypertrophy in patients with hypertension. PMID:24934758

Angeli, Fabio; Verdecchia, Paolo; Iacobellis, Gianluca; Reboldi, Gianpaolo

2014-08-01

272

Na/K Pump Current and [Na]i in Rabbit Ventricular Myocytes: Local [Na]i Depletion and Na Buffering  

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Na/K pump current (Ipump) and intracellular Na concentration ([Na]i) were measured simultaneously in voltage-clamped rabbit ventricular myocytes, under conditions where [Na]i is controlled mainly by membrane transport. Upon abrupt pump reactivation (after 10–12 min blockade), Ipump decays in two phases. Initially, Ipump declines with little [Na]i change, whereas the second phase is accompanied by [Na]i decline. Initial Ipump sag was still present at external [K] = 15 mM, but prevented by [N...

Despa, Sanda; Bers, Donald M.

2003-01-01

273

[Left ventricular efficiency of hypertensive without hypertrophy: Echographic study with modelisation of left ventricular-aortic coupling].  

Science.gov (United States)

Because the functional interaction between the LV and arterial systems, termed ventricular-arterial coupling, is recognized as a key determinant of LV performance, the objective of the present study was to assess the impact of uncomplicated HT without LVH on LV performance using simultaneously echocardiography and carotid tonometry. LV maximal power (PmaxVG), cardiac power output (CPO), LV efficiency (CPO/PmaxVG), input aortic and output LV elastance (Ea and Ees) were assessed in 20 normotensive control subjects (NT) and 10 patients with untreated HT. PmaxVG was calculated according to the integral of the product of LV wall stress with strain rate (as an index of gradient velocity). Cyclic variation of wall thickness and SR were measured by speckel-tracking. Ea and Ees were derived and modelized from the pressure-volume curve. No difference in age, BMI and sex ratio was observed between NT and HT. Systolic BP (160±18 vs. 119±10mmHg), LV mass (99±15 vs. 76±12g/m(2)), PWV (9.7±2 vs. 6.9±1m/s) were significantly higher (P<0.01) in HT when compared to NT. In HT increased of CPO and Ea was compensated by an increase of LV (15±4 vs. 12±3%, P<0.02) and Ees (5.5±2 vs. 4.5±1.5mmHg/mL), which are significantly elevated in HT (P<0.05). No difference was observed in Ea/Ees between NT and HT. In conclusion at the early phase of HT, in patients without LVH, LV performance and ventricular-arterial coupling were adapted to post-load elevation. This adaptation may be the result of an increased of LV contractility. PMID:24952676

Bonnet, B; Jourdan, F; du Cailar, G; Mimran, A; Fesler, P

2014-06-01

274

Usefulness of thallium-201 scintigraphy in predicting the development of angina pectoris in hypertensive patients with left ventricular hypertrophy  

International Nuclear Information System (INIS)

Hypertension and left ventricular (LV) hypertrophy are independent risk factors for the development of coronary artery disease. To determine whether patients at higher risk for coronary artery disease can be identified, 40 asymptomatic hypertensive men with LV hypertrophy were prospectively studied using exercise thallium-201 scintigraphy and exercise radionuclide angiography. Endpoints indicative of coronary artery disease were defined as the subsequent development of typical angina pectoris, which occurred in 8 patients during a median follow-up of 38 months, or myocardial infarction, which did not occur. The exercise electrocardiogram was interpreted by standard ST-segment criteria and by a computerized treadmill exercise score. Abnormal ST-segment responses were present in 16 of the 40 hypertensives (40%), whereas the treadmill score was positive in 8 of those same 40 patients (20%). Scintigraphic perfusion defects assessed both visually and semiquantitatively were observed in 8 of 40 (20%) patients. An abnormal ejection fraction response to exercise was present in 40% (16 of 40) of patients, and 3 of 40 (7.5%) developed new wall motion abnormalities during exercise. Six of 8 patients with either perfusion defects or abnormal treadmill score developed typical angina during follow-up. All 5 patients with concordant positive exercise scintigrams and treadmill score developed chest pain during follow-up and had coronary artery disease confirmed by coronary angiography. However, only 7 of 16 (44%) patients with positive ST changes or abnormal ejection fraction responses during exercise developed chest pain during follow-up. In contrast, of 32 patients with negative scintigrams only 2 developed atypical chest pain syndromes, and significant coronary artery disease was excluded by angiography in 1 patient

1989-07-01

275

Ecto-5'-nucleotidase deficiency exacerbates pressure-overload induced left ventricular hypertrophy and dysfunction  

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This study examined whether endogenous extracellular adenosine acts to facilitate the adaptive response of the heart to chronic systolic overload. To examine whether endogenous extracellular adenosine can protect the heart against pressure overload induced heart failure, transverse aortic constriction (TAC) was performed on mice deficient in extracellular adenosine production as the result of genetic deletion of CD73. While there was no difference in left ventricular (LV) size or function bet...

2008-01-01

276

Extracellular Superoxide Dismutase Deficiency Exacerbates Pressure Overload–Induced Left Ventricular Hypertrophy and Dysfunction  

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Extracellular superoxide dismutase (SOD) contributes only a small fraction to total SOD activity in the normal heart but is strategically located to scavenge free radicals in the extracellular compartment. To examine the physiological significance of extracellular SOD in the response of the heart to hemodynamic stress, we studied the effect of extracellular SOD deficiency on transverse aortic constriction (TAC)–induced left ventricular remodeling. Under unstressed conditions extracellular S...

2008-01-01

277

Extracellular superoxide dismutase deficiency exacerbates pressure overload-induced left ventricular hypertrophy and dysfunction  

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Extracellular superoxide dismutase (SOD) contributes only a small fraction to total SOD activity in the normal heart but is strategically located to scavenge free radicals in the extracellular compartment. To examine the physiological significance of extracellular SOD in the response of the heart to hemodynamic stress, we studied the effect of extracellular SOD deficiency on transverse aortic constriction (TAC)-induced left ventricular remodeling. Under unstressed conditions extracellular SOD...

2008-01-01

278

A genetic variant of the atrial natriuretic peptide gene is associated with left ventricular hypertrophy in a non-diabetic population - the Malmo preventive project study  

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Background: Epidemiological studies have shown considerable heritability of blood pressure, thus suggesting a role for genetic factors. Previous studies have shown an association of a single nucleotide polymorphism rs5068 in the NPPA locus gene with higher levels of circulating atrial natriuretic peptide as well as with lower intra individual blood pressure, but up to date, no association between rs5068 and cardiac organ damage, i.e. left ventricular hypertrophy, has been accounted for in hum...

Jujic, Amra; Leosdottir, Margre?t; O?stling, Gerd; Gudmundsson, Petri; Nilsson, Peter; Melander, Olle; Magnusson, Martin

2013-01-01

279

Comparison of Blood Pressure Control and Left Ventricular Hypertrophy in Patients on Continuous Ambulatory Peritoneal Dialysis (CAPD) and Automated Peritoneal Dialysis (APD)  

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This study aimed to investigate the influence of different peritoneal dialysis regimens on blood pressure control, the diurnal pattern of blood pressure and left ventricular hypertrophy in patients on peritoneal dialysis. Forty-four patients undergoing peritoneal dialysis were enrolled into the study. Patients were treated with different regimens of peritoneal dialysis: 26 patients on continuous ambulatory peritoneal dialysis (CAPD) and 18 patients on automated peritoneal dialysis (APD). All ...

Jang, Jong Soon; Kwon, Soon Kil; Kim, Hye-young

2011-01-01

280

Whole-exome Sequencing and an iPSC-Derived Cardiomyocyte Model Provides a Powerful Platform for Gene Discovery in Left Ventricular Hypertrophy  

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Rationale: Left ventricular hypertrophy (LVH) is a heritable predictor of cardiovascular disease, particularly in blacks. Objective: Determine the feasibility of combining evidence from two distinct but complementary experimental approaches to identify novel genetic predictors of increased LV mass. Methods: Whole-exome sequencing (WES) was conducted in seven African-American sibling trios ascertained on high average familial LV mass indexed to height (LVMHT) using Illumina HiSeq technology. I...

Zhi, D.; Irvin, M. R.; Gu, C. C.; Stoddard, A. J.; Lorier, R.; Matter, A; Rao, D. C.; Srinivasasainagendra, V.; Tiwari, H. K.; Turner, A.; Broeckel, U.; Arnett, D. K.

2012-01-01

 
 
 
 
281

Effect of microalbuminuria-lowering on regression of left ventricular hypertrophy in children and adolescents with essential hypertension  

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Full Text Available Background: Microalbuminuria (MA is associated with increased cardiovascular risk in hypertensive patients, but not many studies have specifically examined the effects of MA-lowering on regression of left ventricular hypertrophy (LVH among pediatric patients with hypertension. Methods: Fifty-five patients with essential hypertension, 11 to 19 years old were prospectively studied. All patients received concomitant therapy of hydrochlorothiazide and angiotensin-converting-enzyme inhibitor. Five patients also required angiotensin-receptor blocker to achieve the blood pressure goal. Baseline and 12-month follow-up measures of left ventricular mass index (LVMI determined by echocardiography and urine microalbumin/creatinine ratio (MA/Cr were collected. MA was defined as MA/Cr>30. LVH was defined as LVMI>38.6 g/m2. The primary end points were 25% or more reductions in MA and the LVMI. Results: Weight (r=0.83, body surface area (r=0.85, body mass index (BMI (r=0.86, systolic blood pressure (SBP (r=0.57, diastolic blood pressure (DBP (r=0.49, mean arterial pressure (r=0.53 and MA (r=0.87 were all univariate correlates of LVMI. In a multiple regression analysis, MA, BMI and SBP were significant correlates of LVMI. MA alone explained 76% of the variance of LVMI, whereas BMI and SBP explained only 1.6% and 0.4% of the variance, respectively. MA was the most significant correlate of follow-up LVMI after BMI and SBP were included in the overall multiple regression models. Conclusion: MA is a strong predictor of LVH in hypertensive children and adolescents. MA-lowering halts the progression of LVH or induces its regression.

Assadi F ; Translated by: Akbari Asbagh P

2007-04-01

282

Impact of dry weight determined by calf bioimpedance ratio on carotid stiffness and left ventricular hypertrophy in hemodialysis patients.  

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Our previous study has shown that modification of bioimpedance technique by the measurement of bioimpedance ratio in the calf (calf-BR) was a simple and practical method in assessing fluid status in hemodialysis patients. However, the consequences of periodical dry weight (DW) adjustment under the guidance of calf-BR on target organ damage have not been investigated. One hundred fifteen hemodialysis patients were enrolled in this pilot trial. Patients were divided into bioimpedance group and control group according to their dialysis schedule. In the bioimpedance group, DW was routinely adjusted under the guidance of calf-BR every 3 months. In the control group, the assessment of DW remained a clinical judgment. Carotid stiffness, left ventricular mass index (LVMI), and calf-BR were measured at baseline and at the 12th month in both groups. Home blood pressure (BP) was monitored monthly. Episodes of dialysis-related adverse events were recorded. No significant differences were observed in parameters between the two groups at baseline. Compared with the control group, the bioimpedance group had significantly lower values in terms of the annual averages of systolic home BP (147.4?±?15.3?mm?Hg vs. 152.6?±?16.9?mm?Hg, P?=?0.019), carotid stiffness index ? (10.7?±?3.3 vs. 12.2?±?3.1, P?=?0.003), LVMI (155.21?±?15.64?g/m(2) vs. 165.17?±?16.76?g/m(2) , P?ventricular hypertrophy with good tolerability in hemodialysis patients. PMID:23981096

Zhou, Yi-Lun; Liu, Jing; Ma, Lijie; Sun, Fang; Shen, Yang; Huang, Jing; Cui, Taigen

2014-04-01

283

Prevalence, pattern, and functional impact of late gadolinium enhancement in left ventricular hypertrophy due to aortic valve stenosis  

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Purpose: To assess the prevalence and pattern of myocardial late gadolinium enhancement (LGE) and its functional impact on patients with left ventricular hypertrophy caused by aortic valve stenosis. Materials and Methods: Cardiac magnetic resonance imaging of 40 patients (17 female, 23 male, mean age: 76.6 {+-} 22.5 years) with known aortic valve stenosis (mean aortic valve area: 89.8 {+-} 19.2 mm{sup 2}) and without coronary artery disease was performed at 1.5 T using steady-state free precession sequences for aortic valve planimetry and for the assessment of left ventricular (LV) volumes and mass. Ten to 15 minutes after injection of 0.2 mmol Gd-DTPA per kilogram body weight, inversion-recovery prepared spoiled gradient echo images were acquired in standard long and short axis views to detect areas of LGE. Results: LGE was observed in 32.5 % (13/40) of our patients. LGE was mainly located in the basal septal and inferior LV segments, and showed a non-ischemic pattern with sparing of the subendocardial region. Patients with LGE showed lower LV ejection fractions (55.5 {+-} 13.8 % vs. 69.1 {+-} 10.7 %, p = 0.0014), higher LV end-systolic volumes (59.8 {+-} 33.3 ml vs. 36.6 {+-} 16.0 ml, p = 0.0048), and LV masses (211.0 {+-} 13.8 vs. 157.9 {+-} 37.5 g, p = 0.0002) compared to patients without LGE. (orig.)

Nassenstein, K.; Schlosser, T. [Universitaetsklinikum Essen (Germany). Abt. fuer Diagnostische und Interventionelle Radiologie; Bruder, O. [Elisabeth-Krankenhaus Essen (Germany). Klinik fuer Kardiologie und Angiologie; Breuckmann, F.; Erbel, R. [Universitaetsklinikum Essen (Germany). Westdeutsches Herzzentrum Essen; Barkhausen, J. [Universitaetsklinikum Schleswig-Holstein, Luebeck (Germany). Klinik fuer Radiologie und Nuklearmedizin

2009-05-15

284

A model of the L-type Ca2+ channel in rat ventricular myocytes: ion selectivity and inactivation mechanisms.  

Science.gov (United States)

1. We have developed a mathematical model of the L-type Ca2+ current, which is based on data from whole-cell voltage clamp experiments on rat ventricular myocytes. Ion substitution methods were employed to investigate the ionic selectivity of the channel. Experiments were configured with Na+, Ca2+ or Ba2+ as the majority current carrier. 2. The amplitude of current through the channel is attenuated in the presence of extracellular Ca2+ or Ba2+. Our model accounts for channel selectivity by using a modified Goldman-Hodgkin-Katz (GHK) configuration that employs voltage-dependent channel binding functions for external divalent ions. Stronger binding functions were used for Ca2+ than for Ba2+. 3. Decay of the ionic current during maintained depolarization was characterized by means of voltage- and Ca2+-dependent inactivation pathways embedded in a five-state dynamic channel model. Particularly, Ca2+ first binds to calmodulin and the Ca2+-calmodulin complex is the mediator of Ca2+ inactivation. Ba2+-dependent inactivation was characterized using the ttau same scheme, but with a decreased binding to calmodulin. 4. A reduced amount of steady-state inactivation, as evidenced by a U-shaped curve at higher depolarization levels (>40 mV) in the presence of [Ca2+]o, was observed in double-pulse protocols used to study channel inactivation. To characterize this phenomenon, a mechanism was incorporated into the model whereby Ca2+ or Ba2+ also inhibits the voltage-dependent inactivation pathway. 5. The five-state dynamic channel model was also used to simulate single channel activity. Calculations of the open probability of the channel model are generally consistent with experimental data. A sixth state can be used to simulate modal activity by way of introducing long silent intervals. 6. Our model has been tested extensively using experimental data from a wide variety of voltage clamp protocols and bathing solution manipulations. It provides: (a) biophysically based explanations of putative mechanisms underlying Ca2+- and voltage-dependent channel inactivation, and (b) close fits to voltage clamp data. We conclude that the model can serve as a predictive tool in generating testable hypotheses for further investigation of this complex ion channel. PMID:11080258

Sun, L; Fan, J S; Clark, J W; Palade, P T

2000-11-15

285

Quercetin Inhibits Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats and Inhibits Angiotensin II-Induced H9C2 Cells Hypertrophy by Enhancing PPAR-? Expression and Suppressing AP-1 Activity  

Science.gov (United States)

Background Quercetin is the most abundant flavonoid in fruit and vegetables and is believed to attenuate cardiovascular disease. We hypothesized that quercetin inhibits cardiac hypertrophy by blocking AP-1 (c-fos, c-jun) and activating PPAR-? signaling pathways. Methodology/Principal Findings The aim of this study was to identify the mechanism underlying quercetin-mediated attenuation of cardiac hypertrophy. Quercetin therapy reduced blood pressure and markedly reduced the ratio of left ventricular to body weight (LVW/BW) (PSHRs)). In vitro, quercetin also significantly attenuated Ang II-induced H9C2 cells hypertrophy, as indicated by its concentration dependent inhibitory effects on [3H]leucine incorporation into H9C2 cells (64% reduction) and by the reduced hypertrophic surface area in H9C2 cells compared with the Ang II group (PSHRs or PSHRs). Additionally, both western blotting and real time-PCR demonstrated that PPAR-? protein and mRNA were increased in the myocardium and AP-1 protein and mRNA were significantly decreased in the quercetin-treated group (PSHRs). Furthermore, western blotting and real time-PCR analyses also showed that transfection with PPAR-? siRNA significantly increased AP-1 signaling and reversed the effects of quercetin inhibition on mRNA expression levels of genes such as ANP and BNP in hypertrophic H9C2 cells. Conclusions Our data indicate that quercetin may inhibit cardiac hypertrophy by enhancing PPAR-? expression and by suppressing the AP-1 signaling pathway.

Yan, Lei; Zhang, Ji Dong; Wang, Bo; Lv, Yi Jing; Jiang, Hong; Liu, Gui Lin; Qiao, Yun; Ren, Ming; Guo, Xue Feng

2013-01-01

286

Facilitation by intracellular carbonic anhydrase of Na+-HCO3? co-transport but not Na+/H+ exchange activity in the mammalian ventricular myocyte  

Science.gov (United States)

Carbonic anhydrase enzymes (CAs) catalyse the reversible hydration of CO2 to H+ and HCO3? ions. This catalysis is proposed to be harnessed by acid/base transporters, to facilitate their transmembrane flux activity, either through direct protein–protein binding (a ‘transport metabolon’) or local functional interaction. Flux facilitation has previously been investigated by heterologous co-expression of relevant proteins in host cell lines/oocytes. Here, we examine the influence of intrinsic CA activity on membrane HCO3? or H+ transport via the native acid-extruding proteins, Na+–HCO3? cotransport (NBC) and Na+/H+ exchange (NHE), expressed in enzymically isolated mammalian ventricular myocytes. Effects of intracellular and extracellular (exofacial) CA (CAi and CAe) are distinguished using membrane-permeant and –impermeant pharmacological CA inhibitors, while measuring transporter activity in the intact cell using pH and Na+ fluorophores. We find that NBC, but not NHE flux is enhanced by catalytic CA activity, with facilitation being confined to CAi activity alone. Results are quantitatively consistent with a model where CAi catalyses local H+ ion delivery to the NBC protein, assisting the subsequent (uncatalysed) protonation and removal of imported HCO3? ions. In well-superfused myocytes, exofacial CA activity is superfluous, most likely because extracellular CO2/HCO3? buffer is clamped at equilibrium. The CAi insensitivity of NHE flux suggests that, in the native cell, intrinsic mobile buffer-shuttles supply sufficient intracellular H+ ions to this transporter, while intrinsic buffer access to NBC proteins is restricted. Our results demonstrate a selective CA facilitation of acid/base transporters in the ventricular myocyte, implying a specific role for the intracellular enzyme in HCO3? transport, and hence pHi regulation in the heart.

Villafuerte, Francisco C; Swietach, Pawel; Youm, Jae-Boum; Ford, Kerrie; Cardenas, Rosa; Supuran, Claudiu T; Cobden, Philip M; Rohling, Mala; Vaughan-Jones, Richard D

2014-01-01

287

Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease  

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Invasive Doppler catheter-derived coronary flow reserve, echocardiographic measurements of left ventricular hypertrophy and intravenous dipyridamole-limited stress thallium-201 scintigraphy were compared in 48 patients (40 were hypertensive or diabetic) with clinical ischemic heart disease and no or minor coronary artery disease. Abnormal vasodilator reserve (ratio less than 3:1) occurred in 50% of the study group and markedly abnormal reserve (less than or equal to 2:1) occurred in 27%. Coronary vasodilator reserve was significantly lower (2.2 +/- 0.8 versus 3.5 +/- 1.3, p = 0.003) and indexed left ventricular mass significantly higher (152.6 +/- 42.2 versus 113.6 +/- 24.0 g, p = 0.0007) in patients with a positive (n = 11) versus a negative (n = 32) thallium perfusion scan. Coronary flow reserve was linearly related in coronary basal flow velocity as follows: y = -0.17x + 4.59; r = -0.57; p = 0.00002. The decrement in flow reserve was not linearly related to the degree of left ventricular hypertrophy. Abnormal vasodilator reserve subsets found in hypertensive patients were defined on the basis of basal flow velocity, indexed left ventricular mass and clinical factors. In this series, diabetes did not cause a detectable additional decrement in flow reserve above that found with hypertension alone. These findings demonstrate that thallium perfusion defects are associated with depressed coronary vasodilator reserve in hypertensive patients without obstructive coronary artery disease. Left ventricular hypertrophy by indexed mass criteria is predictive of which hypertensive patients are likely to have thallium defects.

Houghton, J.L.; Frank, M.J.; Carr, A.A.; von Dohlen, T.W.; Prisant, L.M. (School of Medicine, Medical College of Georgia, Augusta (USA))

1990-01-01

288

Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease  

International Nuclear Information System (INIS)

Invasive Doppler catheter-derived coronary flow reserve, echocardiographic measurements of left ventricular hypertrophy and intravenous dipyridamole-limited stress thallium-201 scintigraphy were compared in 48 patients (40 were hypertensive or diabetic) with clinical ischemic heart disease and no or minor coronary artery disease. Abnormal vasodilator reserve (ratio less than 3:1) occurred in 50% of the study group and markedly abnormal reserve (less than or equal to 2:1) occurred in 27%. Coronary vasodilator reserve was significantly lower (2.2 +/- 0.8 versus 3.5 +/- 1.3, p = 0.003) and indexed left ventricular mass significantly higher (152.6 +/- 42.2 versus 113.6 +/- 24.0 g, p = 0.0007) in patients with a positive (n = 11) versus a negative (n = 32) thallium perfusion scan. Coronary flow reserve was linearly related in coronary basal flow velocity as follows: y = -0.17x + 4.59; r = -0.57; p = 0.00002. The decrement in flow reserve was not linearly related to the degree of left ventricular hypertrophy. Abnormal vasodilator reserve subsets found in hypertensive patients were defined on the basis of basal flow velocity, indexed left ventricular mass and clinical factors. In this series, diabetes did not cause a detectable additional decrement in flow reserve above that found with hypertension alone. These findings demonstrate that thallium perfusion defects are associated with depressed coronary vasodilator reserve in hypertensive patients without obstructive coronary artery disease. Left ventricular hypertrophy by indexed mass criteria is predictive of which hypertensive patients are likely to have thallium defects

1990-01-01

289

Myocardial perfusion in type 2 diabetes with left ventricular hypertrophy: normalisation by acute angiotensin-converting enzyme inhibition  

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The purpose of this study was to assess whether acute angiotensin-converting enzyme (ACE) inhibition would improve myocardial perfusion and perfusion reserve in a subpopulation of normotensive patients with diabetes and left ventricular hypertrophy (LVH), both independent risk factors of coronary disease. Using positron emission tomography (PET), we investigated the response of regional myocardial perfusion to acute ACE inhibition with i.v. infusion of perindoprilat (vs saline infusion as control, minimum interval 3 days) in 12 diabetic patients with LVH. Myocardial perfusion was quantified with PET using nitrogen-13 ammonia infused at rest and during dipyridamole hyperaemia. Twelve healthy control subjects were included in the study, five of whom were also studied with perindoprilat. Mean blood pressure in normo-albuminuric, asymptomatic patients was 123±7/65±9 mmHg. Compared with controls, maximal perfusion was reduced in patients (1.8±0.6 vs 2.5±1.0 ml min-1 g-1; P-1 g-1, P<0.01). In the five control subjects both resting and hyperaemic perfusion remained unchanged during perindoprilat infusion. It is concluded that acute ACE inhibition with perindoprilat improves maximal achieved myocardial perfusion in non-hypertensive patients with diabetes and LVH. (orig.)

2004-03-01

290

Electrocardiographic diagnosis of left ventricular hypertrophy in aortic valve disease: evaluation of ECG criteria by cardiovascular magnetic resonance  

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Full Text Available Abstract Background Left ventricular hypertrophy (LVH is a hallmark of chronic pressure or volume overload of the left ventricle and is associated with risk of cardiovascular morbidity and mortality. The purpose was to evaluate different electrocardiographic criteria for LVH as determined by cardiovascular magnetic resonance (CMR. Additionally, the effects of concentric and eccentric LVH on depolarization and repolarization were assessed. Methods 120 patients with aortic valve disease and 30 healthy volunteers were analysed. As ECG criteria for LVH, we assessed the Sokolow-Lyon voltage/product, Gubner-Ungerleider voltage, Cornell voltage/product, Perugia-score and Romhilt-Estes score. Results All ECG criteria demonstrated a significant correlation with LV mass and chamber size. The highest predictive values were achieved by the Romhilt-Estes score 4 points with a sensitivity of 86% and specificity of 81%. There was no difference in all ECG criteria between concentric and eccentric LVH. However, the intrinsicoid deflection (V6 37 ± 1.0 ms vs. 43 ± 1.6 ms, p Conclusion By calibration with CMR, a wide range of predictive values was found for the various ECG criteria for LVH with the most favourable results for the Romhilt-Estes score. As electrocardiographic correlate for concentric LVH as compared with eccentric LVH, a shorter intrinsicoid deflection and a significant ST-segment and T-wave depression in the anterolateral leads was noted.

Feuerbach Stefan

2009-06-01

291

Tissue Doppler imaging of longitudinal movement of a fibrous ring of mitral valve during isovolumic periods in left ventricular hypertrophy  

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Full Text Available Aim. To study change of rate and duration indicators of longitudinal movement of a fibrous ring of mitral valve (MFR during isovolumic contraction (IVC and relaxation (IVR in hypertensive patients with various degree of a left ventricular hypertrophy (LVH.Material and methods. 80 hypertensive patients with moderate LVH (n=40 and severe LVH (n=40 are examined. The control group was presented by 30 healthy volunteers. Transthoracic echocardiography and Tissue Doppler imaging has been performed with ultrasonic tomograph “HDI 5000” (Philips.Results. Increase in LVH (Smm and ?/?mm associates with reduction in systolic velocity of movement of medial MFR (Smm. There is direct relation with duration of IVC-negative and IVR-positive components and myocardium mass index. Maximal velocity of IVC-positive component increases and maximal velocity of IVR-negative component decreases when LVH is growing.Conclusion. Velocities curves of IVC and IVR were bi-phase both in healthy persons and in hypertensive patients with LVH. Velocity and duration of positive and negative components of IVC and IVR depended on LVH degree.

B. Amarjagal

2007-01-01

292

Telomere length is associated with ACE I/D polymorphism in hypertensive patients with left ventricular hypertrophy  

DEFF Research Database (Denmark)

INTRODUCTION: Short telomeres are often associated with cardiovascular risk factors and age-related diseases, while the angiotensin converting enzyme (ACE) gene insertion/deletion polymorphism (DD, ID, II) has shown such associations less consistently. We hypothesized that telomere length and association of telomere length with cardiovascular risk is affected by ACE (I/D) genotype. METHODS: We measured leucocyte telomere length (LTL) by Southern blot and analysed ACE I/D genotypes in 1249 subjects with hypertension and left ventricular hypertrophy (LVH). We examined interactions of ACE I/D genotype with LTL and cardiovascular risk. RESULTS: Mean LTL in DD or ID genotype was shorter (8.15 and 8.14 kb, respectively), than in II genotype (8.27 kb, p=0.0005). This difference was significant in the younger subjects (55-64 years, p=0.02) but not in the older group (65-80 years, p=0.56 ). In DD but not I/D or II genotype, proportion of short telomeres (

Fyhrquist, Frej; Eriksson, Anders

2013-01-01

293

Angiotensin-converting enzyme gene deletion allele increases the risk of left ventricular hypertrophy: evidence from a meta-analysis.  

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Large panels of studies have examined the association between angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and risk for left ventricular hypertrophy (LVH), yet with inconclusive results. We therefore sought to evaluate this association via a comprehensive meta-analysis. A random-effects model was applied irrespective of between-study heterogeneity. Data and study quality were independently assessed by two investigators. Total 52 studies encompassing 3,663 case-patients and 8,953 controls were meta-analyzed. Overall results indicated that carriers homozygous for DD genotype conferred 1.59 times (95 % confidence interval [95 % CI]: 1.31-1.92; P hypertension, and diagnostic method of LVH were also regarded as potential sources of heterogeneity. Further, the risk estimate associated with D allele was more pronounced in studies involving males (odds ratio [OR] = 1.47; 95 % CI: 1.2-1.8; P ACE gene I/D polymorphism with LVH risk, especially in East Asians, and this association was more pronounced in studies involving males and untreated subjects. PMID:22773337

Li, Xiaobo; Li, Yuqiong; Jia, Nan; Guo, Shujie; Chu, Shaoli; Niu, Wenquan

2012-12-01

294

Paradigmas y paradojas de la hipertrofia ventricular izquierda: desde el laboratorio de investigación a la consulta clínica / Paradigms and paradoxes of left ventricular hypertrophy: from the research laboratory to the clinical consultation  

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Full Text Available SciELO Mexico | Language: Spanish Abstract in spanish La hipertrofia ventricular es considerada un mecanismo de adaptación del corazón ante diferentes sobrecargas; estas sobrecargas pueden generar a través de los mecanismos intracelulares utilizados distintas respuestas que se asocien o no con compromiso funcional del miocardio. Cuando la hipertrofia s [...] e acompaña de disfunción ventricular pudiendo ser el inicio de un proceso que conduce a la insuficiencia cardíaca, se pone en duda si ese mecanismo es realmente una adecuada adaptación a la sobrecarga. Analizando las modificaciones estructurales y funcionales del ventrículo izquierdo encontradas en ratas secundarias a hipertensión arterial, reducción del diámetro de la aorta ascendente, administración de isoproterenol y/o a infarto de miocardio y en pacientes hipertensos, con estenosis aórtica y con miocardio-patía hipertrófica se puede inferir la presencia de un mecanismo no adecuado de adaptación. Por el contrario las diferentes características de la respuesta ventricular ante la sobrecarga provocada por ejercicio o por el embarazo en humanos señalan una verdadera adaptación a la sobrecarga. En un verdadero desafío a lo conocido sería correcto especular con la necesidad de estimular el desarrollo de hipertrofia fisiológica en determinadas situaciones patológicas o llegar a modificar la respuesta patológica en fisiológica. Abstract in english Cardiac hypertrophy can occur as an adaptative response to increased cardiac workload. Different types of cardiac hypertrophy arise from a combination of genetic, physiologic, and environmental factors. When hypertophic growth of the heart leads to left ventricular dysfunction and heart failure, the [...] response is considered as maladaptive or pathological hypertrophy. After analyzed left ventricular functional and structural changes in rats induced by arterial hypertension, banding of aortic root, isoproterenol administration, or myocardial infarction, as well as in patients with arterial hypertension, aortic stenosis, or hypertrophic miocardiopathy, we found a maladaptive response considered as pathological hypertrophy. However, the adaptation of the left ventricle, found in response to physical activity or to pregnancy in humans, seems to help the heart adapt to the increase in workload acting as physiological hypertrophy. These considerations allow us to speculate for the use of future interventions to stimulate the development of physiological hypertrophy in several pathological situations or to change a pathological into a physiological response.

Eduardo Manuel, Escudero; Oscar Andrés, Pinilla.

295

Thallium myocardial perfusion scans for the assessment of right ventricular hypertrophy in patients with cystic fibrosis. A comparison with other noninvasive techniques  

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The incidence of right ventricular hypertrophy in 32 patients with cystic fibrosis was studied using thallium 201 (TI-201) myocardial perfusion scans, and compared with other noninvasive techniques including electrocardiography, vectorcardiography, and M-mode echocardiography. The patients (mean age, 17.3 yr; range, 7 to 33) had a wide range of clinical and pulmonary abnormalities (mean Shwachman-Kulczycki score, 66.6). In the total study group, TI-201 scans, like the vectorcardiograms and the M-mode echocardiograms, gave a surprisingly high proportion of positive predictions for right ventricular hypertrophy (RVH) (44%). The correlations with all other noninvasive methods were uniformly poor, so caution must be exercised in using this technique to predict early RVH in order to follow the natural history of cor pulmonale in cystic fibrosis. At the time of the study, 6 patients had clinical evidence of right ventricular failure, and in this disease setting must have had RVH. In 3 patients, RVH was confirmed at autopsy, and it was successfully predicted by TI-201 scans in 5 of the 6 patients. The false negative scan may have been due to regional myocardial ischemia secondary to severe right ventricular failure. In contrast, the vectorcardiogram, using Fowler's new criteria, made a successful prediction of RVH in all 6 patients, and the electro cardiogram in only 3. Although the M-mode echocardiogram was abnormal in all patients, it would have predicted RVH (with increased right ventricular anterior wall thickness) in only 1 patient. We concluded that TI-201 myocardial perfusion cans are good at confirming RVH in cases with established right ventricular failure, but have no advantage over vectorcardiographic assessments, which are logistically easier to perform and carry no radiation risks.

Newth, C.J.; Corey, M.L.; Fowler, R.S.; Gilday, D.L.; Gross, D.; Mitchell, I.

1981-01-01

296

Thallium myocardial perfusion scans for the assessment of right ventricular hypertrophy in patients with cystic fibrosis. A comparison with other noninvasive techniques  

International Nuclear Information System (INIS)

The incidence of right ventricular hypertrophy in 32 patients with cystic fibrosis was studied using thallium 201 (TI-201) myocardial perfusion scans, and compared with other noninvasive techniques including electrocardiography, vectorcardiography, and M-mode echocardiography. The patients (mean age, 17.3 yr; range, 7 to 33) had a wide range of clinical and pulmonary abnormalities (mean Shwachman-Kulczycki score, 66.6). In the total study group, TI-201 scans, like the vectorcardiograms and the M-mode echocardiograms, gave a surprisingly high proportion of positive predictions for right ventricular hypertrophy (RVH) (44%). The correlations with all other noninvasive methods were uniformly poor, so caution must be exercised in using this technique to predict early RVH in order to follow the natural history of cor pulmonale in cystic fibrosis. At the time of the study, 6 patients had clinical evidence of right ventricular failure, and in this disease setting must have had RVH. In 3 patients, RVH was confirmed at autopsy, and it was successfully predicted by TI-201 scans in 5 of the 6 patients. The false negative scan may have been due to regional myocardial ischemia secondary to severe right ventricular failure. In contrast, the vectorcardiogram, using Fowler's new criteria, made a successful prediction of RVH in all 6 patients, and the electro cardiogram in only 3. Although the M-mode echocardiogram was abnormal in all patients, it would have predicted RVH (with increased right ventricular anterior wall thickness) in only 1 patient. We concluded that TI-201 myocardial perfusion cans are good at confirming RVH in cases with established right ventricular failure, but have no advantage over vectorcardiographic assessments, which are logistically easier to perform and carry no radiation risks

1981-01-01

297

La hipertrofia ventricular izquierda no siempre revierte con el descenso de la presión arterial / Left ventricular hypertrophy not always reverts with the decrease in blood pressure / A hipertrofia ventricular esquerda nem sempre reverte com a diminuição da pressão arterial  

Scientific Electronic Library Online (English)

Full Text Available SciELO Argentina | Language: Spanish Abstract in portuguese Introdução. Em pacientes hipertensos considera-se que uma queda nos valores da pressão arterial é necessária para atingir a regressão da lesão em órgãos-alvo. O objetivo deste estudo é determinar o efeito obtido com a diminuição da pressão arterial em pacientes hipertensos arteriais na hipertrofia v [...] entricular esquerda em uma clínica especializada. Material e métodos. Os pacientes hipertensos na primeira consulta, segundo definição da IV Guias da Federação Argentina de Cardiologia, com hipertrofia ventricular esquerda diagnosticada pelo método ecocardiográfico de Devereux, considerando sua presença com um índice de massa ventricular esquerda igual ou superior a 110 g/m² em mulheres e 125 g/m², em homens, divididos em dois grupos: 1) a pressão arterial controlada: menos de 140 - 90 mm Hg ou inferior a 130 - 80 mm Hg em pacientes de alto risco, os pacientes com nefropatia diabética ou portadores de doença isquêmica do coração no final do seguimento, 2) pressão arterial não controlada: acima dos valores estabelecidos no final do seguimento. Aplicou-se na análise estadística o teste t de Student, considerando-se significância estatística p Abstract in spanish Introducción. En pacientes hipertensos se considera que el descenso de las cifras de presión arterial logra la regresión del daño en órgano blanco. El objetivo del presente estudio es determinar el efecto que se obtiene con el descenso de la presión arterial en pacientes hipertensos arteriales sobre [...] la hipertrofia ventricular izquierda en un consultorio especializado. Material y métodos. Pacientes hipertensos en primera consulta según definición de las IV Guías de la Federación Argentina de Cardiología, con hipertrofia ventricular izquierda diagnosticada en ecocardiografía por método de Devereux, considerándose su presencia con un índice de masa ventricular izquierda mayor o igual a 110 gramos/m² en las mujeres y 125 gramos/m² en los hombres; divididos en dos grupos: 1) presión arterial controlada: menor a 140-90 mm Hg o menor a 130-80 mm Hg en pacientes de alto riesgo, diabéticos, nefrópatas o portadores de cardiopatía isquémica al final del seguimiento; 2) presión arterial no controlada: por encima de las cifras enunciadas al final del seguimiento. En el análisis estadístico, se aplicó test t de students, considerándose significación estadística p Abstract in english Background. In hypertensive patients it is considered that a fall in blood pressure values is necessary to achieve the regression of target organ damage. The aim of this study is to determine the effect obtained with decreasing blood pressure in hypertensive patients on left ventricular hypertrophy [...] in a specialized clinic. Methods. Hypertensive patients at first consultation as defined by Argentina Cardiology Federation Guides IV, with left ventricular hypertrophy diagnosed by echocardiographic method of Devereux, considering its presence with a left ventricular mass index equal or greater than 110 g/m² in women and 125 g/m² in men, divided into two groups: 1) controlled blood pressure: less than 140 - 90 mm Hg or lower than 130 - 80 mm Hg in high risk patients, patients with diabetic nephropathy or ischemic heart disease carriers at end of follow up, 2) uncontrolled blood pressure: above the values set out at the end of follow up. In statistical analysis t students test was applied, considering statistical significance p

Piskorz, Daniel; Tommasi, Alicia.

298

Cytosolic H2O2 mediates hypertrophy, apoptosis, and decreased SERCA activity in mice with chronic hemodynamic overload.  

Science.gov (United States)

Oxidative stress in the myocardium plays an important role in the pathophysiology of hemodynamic overload. The mechanism by which reactive oxygen species (ROS) in the cardiac myocyte mediate myocardial failure in hemodynamic overload is not known. Accordingly, our goals were to test whether myocyte-specific overexpression of peroxisomal catalase (pCAT) that localizes in the sarcoplasm protects mice from hemodynamic overload-induced failure and prevents oxidation and inhibition of sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA), an important sarcoplasmic protein. Chronic hemodynamic overload was caused by ascending aortic constriction (AAC) for 12 wk in mice with myocyte-specific transgenic expression of pCAT. AAC caused left ventricular hypertrophy and failure associated with a generalized increase in myocardial oxidative stress and specific oxidative modifications of SERCA at cysteine 674 and tyrosine 294/5. pCAT overexpression ameliorated myocardial hypertrophy and apoptosis, decreased pathological remodeling, and prevented the progression to heart failure. Likewise, pCAT prevented oxidative modifications of SERCA and increased SERCA activity without changing SERCA expression. Thus cardiac myocyte-restricted expression of pCAT effectively ameliorated the structural and functional consequences of chronic hemodynamic overload and increased SERCA activity via a post-translational mechanism, most likely by decreasing inhibitory oxidative modifications. In pressure overload-induced heart failure cardiac myocyte cytosolic ROS play a pivotal role in mediating key pathophysiologic events including hypertrophy, apoptosis, and decreased SERCA activity. PMID:24633550

Qin, Fuzhong; Siwik, Deborah A; Pimentel, David R; Morgan, Robert J; Biolo, Andreia; Tu, Vivian H; Kang, Y James; Cohen, Richard A; Colucci, Wilson S

2014-05-15

299

Rate-dependent Ca2+ signalling underlying the force-frequency response in rat ventricular myocytes: a coupled electromechanical modeling study  

Science.gov (United States)

Background Rate-dependent effects on the Ca2+ sub-system in a rat ventricular myocyte are investigated. Here, we employ a deterministic mathematical model describing various Ca2+ signalling pathways under voltage clamp (VC) conditions, to better understand the important role of calmodulin (CaM) in modulating the key control variables Ca2+/calmodulin-dependent protein kinase-II (CaMKII), calcineurin (CaN), and cyclic adenosine monophosphate (cAMP) as they affect various intracellular targets. In particular, we study the frequency dependence of the peak force generated by the myofilaments, the force-frequency response (FFR). Methods Our cell model incorporates frequency-dependent CaM-mediated spatially heterogenous interaction of CaMKII and CaN with their principal targets (dihydropyridine (DHPR) and ryanodine (RyR) receptors and the SERCA pump). It also accounts for the rate-dependent effects of phospholamban (PLB) on the SERCA pump; the rate-dependent role of cAMP in up-regulation of the L-type Ca2+ channel (ICa,L); and the enhancement in SERCA pump activity via phosphorylation of PLB. Results Our model reproduces positive peak FFR observed in rat ventricular myocytes during voltage-clamp studies both in the presence/absence of cAMP mediated ?-adrenergic stimulation. This study provides quantitative insight into the rate-dependence of Ca2+-induced Ca2+-release (CICR) by investigating the frequency-dependence of the trigger current (ICa,L) and RyR-release. It also highlights the relative role of the sodium-calcium exchanger (NCX) and the SERCA pump at higher frequencies, as well as the rate-dependence of sarcoplasmic reticulum (SR) Ca2+ content. A rigorous Ca2+ balance imposed on our investigation of these Ca2+ signalling pathways clarifies their individual roles. Here, we present a coupled electromechanical study emphasizing the rate-dependence of isometric force developed and also investigate the temperature-dependence of FFR. Conclusions Our model provides mechanistic biophysically based explanations for the rate-dependence of CICR, generating useful and testable hypotheses. Although rat ventricular myocytes exhibit a positive peak FFR in the presence/absence of beta-adrenergic stimulation, they show a characteristic increase in the positive slope in FFR due to the presence of Norepinephrine or Isoproterenol. Our study identifies cAMP-mediated stimulation, and rate-dependent CaMKII-mediated up-regulation of ICa,L as the key mechanisms underlying the aforementioned positive FFR.

2013-01-01

300

Beta1-Adrenergic Receptors Promote Focal Adhesion Signaling Downregulation And Myocyte Apoptosis in Acute Volume Overload  

Science.gov (United States)

Numerous studies demonstrated increased expression of extracellular matrix (ECM) proteins and activation of focal adhesion (FA) signaling pathways in models of pressure overload-induced cardiac hypertrophy. However, little is known about FA signaling in response to volume overload where cardiac hypertrophy is associated with ECM loss. This study examines the role of beta1-adrenergic receptors (?1-ARs) in FA signaling changes and myocyte apoptosis induced during acute hemodynamic stress of volume overload. Rats with eccentric cardiac hypertrophy induced after aorto-caval fistula (ACF) develop reduced interstitial collagen content and decreased tyrosine phosphorylation of key FA signaling molecules FAK, Pyk2 and paxillin along with an increase in cardiac myocyte apoptosis. ACF also increased activation of PTEN, a dual lipid and protein phosphatase, and its interaction with FA proteins. ?1-AR blockade (extended-release of metoprolol succinate, 100 mg QD) markedly attenuated PTEN activation, restored FA signaling and reduced myocyte apoptosis induced by ACF at 2 days, but failed to reduce interstitial collagen loss and left ventricular dilatation. Treating cultured myocytes with ?1-AR agonists or adenoviral expression of ?1-ARs caused PTEN activation and interaction with FA proteins, thus leading to FA signaling downregulation and myocyte apoptosis. Adenoviral-mediated expression of a catalytically inactive PTEN mutant or wild-type FAK restored FA signaling downregulation and attenuated myocyte apoptosis induced by ?1-ARs. Collectively, these data show that ?1-AR stimulation in response to ACF induces FA signaling downregulation through an ECM-independent mechanism. This effect involves PTEN activation and may contribute to adverse cardiac remodeling and function in the course of volume overload.

Seqqat, Rachid; Guo, Xinji; Rafiq, Khadija; Kolpakov, Mikhail A; Guo, Jianfen; Koch, Walter J; Houser, Steven R; Dell'italia, Louis J; Sabri, Abdelkarim

2012-01-01

 
 
 
 
301

Myocardial perfusion in type 2 diabetes with left ventricular hypertrophy: normalisation by acute angiotensin-converting enzyme inhibition  

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The purpose of this study was to assess whether acute angiotensin-converting enzyme (ACE) inhibition would improve myocardial perfusion and perfusion reserve in a subpopulation of normotensive patients with diabetes and left ventricular hypertrophy (LVH), both independent risk factors of coronary disease. Using positron emission tomography (PET), we investigated the response of regional myocardial perfusion to acute ACE inhibition with i.v. infusion of perindoprilat (vs saline infusion as control, minimum interval 3 days) in 12 diabetic patients with LVH. Myocardial perfusion was quantified with PET using nitrogen-13 ammonia infused at rest and during dipyridamole hyperaemia. Twelve healthy control subjects were included in the study, five of whom were also studied with perindoprilat. Mean blood pressure in normo-albuminuric, asymptomatic patients was 123{+-}7/65{+-}9 mmHg. Compared with controls, maximal perfusion was reduced in patients (1.8{+-}0.6 vs 2.5{+-}1.0 ml min{sup -1} g{sup -1}; P<0.05), and perfusion reserve was also lower, at borderline significance (2.7{+-}1.0 vs 3.6{+-}1.3; P=0.059). During perindoprilat infusion, myocardial perfusion reserve in patients increased to 3.9{+-}0.9 (P<0.001) due to normalisation of maximal perfusion (2.3{+-}0.5 ml min{sup -1} g{sup -1}, P<0.01). In the five control subjects both resting and hyperaemic perfusion remained unchanged during perindoprilat infusion. It is concluded that acute ACE inhibition with perindoprilat improves maximal achieved myocardial perfusion in non-hypertensive patients with diabetes and LVH. (orig.)

Hesse, Birger; Meyer, Christian; Hove, Jens D.; Holm, Soeren; Kofoed, Klaus F. [Department of Clinical Physiology and Nuclear Medicine, KF 4011, Rigshospitalet, University of Copenhagen, Blegdamsvej 9, 2100, Copenhagen (Denmark); Nielsen, Flemming S.; Sato, Asako; Parving, Hans-Henrik [Steno Diabetes Center, Gentofte (Denmark); Bang, Lia E.; Svendsen, Tage L. [Department of Internal Medicine, Naestved County Hospital (Denmark); Opie, Lionel H. [Department of Medicine, Cape Heart Center, University of Cape Town (South Africa)

2004-03-01

302

Effects of valsartan and nebivolol on blood pressure, QT dispersion and left ventricular hypertrophy in hypertensive patients  

Directory of Open Access Journals (Sweden)

Full Text Available Objectives: The aim of this study was to analyze the antihypertensiveeffect of Valsartan and Nebivolol and their effects on QT dispersion and left ventricular hypertrophy (LVH in the treatment of naive hypertensive patients.Methods: A prospective study with a six-month follow-up was conducted on hypertensive patients with LVH and mild/ moderate essential hypertension. The patients were randomly assigned to Valsartan (80 to 160 mg/day or Nebivolol (5 to 10 mg/day groups. The study group consistedof 108 patients, 55 in the Valsartan group and 53 in the Nebivolol group.Results: The range of mean systolic blood pressure (SBP varied from 152±17 (baseline to 132±17 mmHg (follow-up in the Valsartan group (p<0.001; from 146±13 to 125±14 mmHg in the Nebivolol group (p<0.001. The decrease in mean diastolic blood pressure (DBP was 9.5±2.5 mmHg in the Valsartan group and 12.3±5.0 mmHg in the Nebivolol group. A significant reduction in QT and corrected QT (Bazett’s formula dispersion was observed in both groups, with a slightly higher reduction in the Valsartan group. Echocardiography showed a decreasein the left ventricle mass (LVM indices (p<0.05 in both groups with a greater reduction in the Valsartan group.Conclusion: Valsartan treatment was as effective as Nebivolol in reducing the 24 hour- SBP after a 6 month treatment. Nebivolol treatment proved to be superior to Valsartan in reducing DBP. Both therapies were effective in reducing the LVH; Valsartan proved to be superior to Nebivolol in reducing the QT interval indexes in relation to blood pressure and LVM reduction.

Luminita L??ea

2010-06-01

303

Shortening and intracellular Ca2+ in ventricular myocytes and expression of genes encoding cardiac muscle proteins in early onset type 2 diabetic Goto-Kakizaki rats.  

Science.gov (United States)

There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus. Cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. Contractile dysfunction, associated with disturbances in excitation-contraction coupling, has been widely demonstrated in the diabetic heart. The aim of this study was to investigate the pattern of cardiac muscle genes that are involved in the process of excitation-contraction coupling in the hearts of early onset (8-10 weeks of age) type 2 diabetic Goto-Kakizaki (GK) rats. Gene expression was assessed in ventricular muscle with real-time RT-PCR; shortening and intracellular Ca(2+) were measured in ventricular myocytes with video edge detection and fluorescence photometry, respectively. The general characteristics of the GK rats included elevated fasting and non-fasting blood glucose and blood glucose at 120 min following a glucose challenge. Expression of genes encoding cardiac muscle proteins (Myh6/7, Mybpc3, Myl1/3, Actc1, Tnni3, Tnn2, Tpm1/2/4 and Dbi) and intercellular proteins (Gja1/4/5/7, Dsp and Cav1/3) were unaltered in GK ventricle compared with control ventricle. The expression of genes encoding some membrane pumps and exchange proteins was unaltered (Atp1a1/2, Atp1b1 and Slc8a1), whilst others were either upregulated (Atp1a3, relative expression 2.61 ± 0.69 versus 0.84 ± 0.23) or downregulated (Slc9a1, 0.62 ± 0.07 versus 1.08 ± 0.08) in GK ventricle compared with control ventricle. The expression of genes encoding some calcium (Cacna1c/1g, Cacna2d1/2d2 and Cacnb1/b2), sodium (Scn5a) and potassium channels (Kcna3/5, Kcnj3/5/8/11/12, Kchip2, Kcnab1, Kcnb1, Kcnd1/2/3, Kcne1/4, Kcnq1, Kcng2, Kcnh2, Kcnk3 and Kcnn2) were unaltered, whilst others were either upregulated (Cacna1h, 0.95 ± 0.16 versus 0.47 ± 0.09; Scn1b, 1.84 ± 0.16 versus 1.11 ± 0.11; and Hcn2, 1.55 ± 0.15 versus 1.03 ± 0.08) or downregulated (Hcn4, 0.16 ± 0.03 versus 0.37 ± 0.08; Kcna2, 0.35 ± 0.03 versus 0.80 ± 0.11; Kcna4, 0.79 ± 0.25 versus 1.90 ± 0.26; and Kcnj2, 0.52 ± 0.07 versus 0.78 ± 0.08) in GK ventricle compared with control ventricle. The amplitude of ventricular myocyte shortening and the intracellular Ca(2+) transient were unaltered; however, the time-to-peak shortening was prolonged and time-to-half decay of the Ca(2+) transient was shortened in GK myocytes compared with control myocytes. The results of this study demonstrate changes in expression of genes encoding various excitation-contraction coupling proteins that are associated with disturbances in myocyte shortening and intracellular Ca(2+) transport. PMID:22581745

Salem, K A; Adrian, T E; Qureshi, M A; Parekh, K; Oz, M; Howarth, F C

2012-12-01

304

Massa ventricular e critérios eletrocardiográficos de hipertrofia: avaliação de um novo escore / Ventricular mass and electrocardiographic criteria of hypertrophy: evaluation of new score  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: Portuguese Abstract in portuguese FUNDAMENTO: A hipertrofia ventricular esquerda (HVE) é um importante e independente fator de risco cardiovascular. Inexistem, no Brasil, estudos desenhados para testar a eficácia do eletrocardiograma (ECG) no diagnóstico desse grave processo patológico. OBJETIVO: Avaliar um novo escore eletrocardiog [...] ráfico para diagnóstico de HVE pelo ECG: soma da maior amplitude da onda S com a maior da onda R no plano horizontal, multiplicando-se o resultado pela duração do QRS [(S+R) X QRS)] e comparando-o com os critérios eletrocardiográficos clássicos. MÉTODOS: Foram analisados os ecocardiogramas e ECG de 1.204 pacientes hipertensos em tratamento ambulatorial. Avaliou-se o índice de massa do ventrículo esquerdo (IMVE) pelo ecocardiograma, firmando-se o diagnóstico de HVE quando > 96 g/m² para mulheres e > 116 g/m² para homens. No ECG analisaram-se quatro critérios clássicos de HVE, além do novo escore a ser testado. RESULTADOS: Todos os índices estudados tiveram correlação estatisticamente significativa com a massa calculada do ventrículo esquerdo (VE). Porém, o novo escore foi o que apresentou maior correlação (r = 0,564). Os outros critérios apresentaram as seguintes correlações: Romhilt-Estes (r = 0,464); Sokolow-Lyon (r = 0,419); Cornell voltagem (r = 0,377); Cornell duração (r = 0,444). Para avaliação da acurácia do índice testado, utilizou-se o ponto de corte de 2,80 mm.s. Com esse valor foram obtidas as seguintes cifras para sensibilidade e especificidade: 35,2% e 88,7%, respectivamente. CONCLUSÃO: Todos os critérios eletrocardiográficos para avaliação da massa do VE apresentaram baixa sensibilidade. O novo escore foi o que apresentou melhor correlação com o IMVE em relação aos outros avaliados. Abstract in english BACKGROUND: The left ventricular hypertrophy (LVH) is an important and independent cardiovascular risk factor. There is a scarcity of studies in Brazil designed to test the efficacy of the electrocardiogram (ECG) in the diagnosis of this important pathological process. OBJECTIVE: To evaluate a new e [...] lectrocardiographic score for the diagnosis of LVH by ECG: the sum of the highest amplitude of the S wave and the highest amplitude of the R wave on the horizontal plane, multiplied by the result of the QRS duration [(S+R) X QRS)] and comparing it with the classic electrocardiographic criteria. METHODS: The echocardiograms and ECG of 1,204 hypertensive patients receiving outpatient care were evaluated. The left ventricular mass index (LVMI) was assessed by the echocardiogram, with a diagnosis of LVH when the LVMI was > 96 g/m² for women and > 116 g/m² for men. Four classic criteria of LVH were analyzed at the ECG, in addition to the new score to be tested. RESULTS: In general, the studied ECG-LVH criteria showed significant statistical correlation to the echocardiographic LVMI. The (R+S) X QRS index, using 2.80 mm.s as the cutoff value, provided test accuracy regarding sensibility and specificity of 35.2% and 88.71%, respectively, representing the best correlation to LVMI (r=0.564) when compared to the other indexes: Romhilt-Estes (r=0.464); Sokolow-Lyon (r=0.419); Cornell voltage (r=0.377); Cornell product r=0.444). CONCLUSION: All the electrocardiographic criteria used for the assessment of the LV mass presented low sensitivity. The new score presented the best correlation with LVMI when compared to the other indexes.

Mazzaro, Cléber do Lago; Costa, Francisco de Assis; Bombig, Maria Teresa Nogueira; Luna Filho, Bráulio; Paola, Ângelo Amato Vincenzo de; Carvalho, Antonio Carlos de Camargo; Costa, William da; Fonseca, Francisco Antonio Helfenstein; Póvoa, Rui Manoel dos Santos.

305

TGF-?1, Released by Myofibroblasts, Differentially Regulates Transcription and Function of Sodium and Potassium Channels in Adult Rat Ventricular Myocytes  

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Cardiac injury promotes fibroblasts activation and differentiation into myofibroblasts, which are hypersecretory of multiple cytokines. It is unknown whether any of such cytokines are involved in the electrophysiological remodeling of adult cardiomyocytes. We cultured adult cardiomyocytes for 3 days in cardiac fibroblast conditioned medium (FCM) from adult rats. In whole-cell voltage-clamp experiments, FCM-treated myocytes had 41% more peak inward sodium current (INa) density at ?40 mV than...

Kaur, Kuljeet; Zarzoso, Manuel; Ponce-balbuena, Daniela; Guerrero-serna, Guadalupe; Hou, Luqia; Musa, Hassan; Jalife, Jose?

2013-01-01

306

Association of pulse pressure with new-onset atrial fibrillation in patients with hypertension and left ventricular hypertrophy : the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study  

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Previous studies have found pulse pressure (PP), a marker of arterial stiffness, to be an independent predictor of atrial fibrillation (AF) in general and hypertensive populations. We examined whether PP predicted new-onset AF in comparison with other blood pressure components in the Losartan Intervention For Endpoint reduction in hypertension study, a double-blind, randomized (losartan versus atenolol), parallel-group study, including 9193 patients with hypertension and electrocardiographic left ventricular hypertrophy. In 8810 patients with neither a history of AF nor AF at baseline, Minnesota coding of electrocardiograms confirmed new-onset AF in 353 patients (4.0%) during mean 4.9 years of follow-up. In multivariate Cox regression analyses, baseline and in-treatment PP and baseline and in-treatment systolic blood pressure predicted new-onset AF, independent of baseline age, height, weight, and Framingham Risk Score; sex, race, and treatment allocation; and in-treatment heart rate and Cornell product. PP was the strongest single blood pressure predictor of new-onset AF determined by the decrease in the -2 Log likelihood statistic, in comparison with systolic blood pressure, diastolic blood pressure, and mean arterial pressure. When evaluated in the same model, the predictive effect of systolic and diastolic blood pressures together was similar to that of PP. In this population of patients with hypertension and left ventricular hypertrophy, PP was the strongest single blood pressure predictor of new-onset AF, independent of other risk factors.

Larstorp, Anne Cecilie K; Ariansen, Inger

2012-01-01

307

The cardiac ryanodine receptor luminal Ca2+ sensor governs Ca2+ waves, ventricular tachyarrhythmias and cardiac hypertrophy in calsequestrin-null mice.  

Science.gov (United States)

CASQ2 (cardiac calsequestrin) is commonly believed to serve as the SR (sarcoplasmic reticulum) luminal Ca2+ sensor. Ablation of CASQ2 promotes SCWs (spontaneous Ca2+ waves) and CPVT (catecholaminergic polymorphic ventricular tachycardia) upon stress but not at rest. How SCWs and CPVT are triggered by stress in the absence of the CASQ2-based luminal Ca2+ sensor is an important unresolved question. In the present study, we assessed the role of the newly identified RyR2 (ryanodine receptor 2)-resident luminal Ca2+ sensor in determining SCW propensity, CPVT susceptibility and cardiac hypertrophy in Casq2-KO (knockout) mice. We crossbred Casq2-KO mice with RyR2 mutant (E4872Q+/-) mice, which lack RyR2-resident SR luminal Ca2+ sensing, to generate animals with both deficiencies. Casq2+/- and Casq2-/- mice showed stress-induced VTs (ventricular tachyarrhythmias), whereas Casq2+/-/E4872Q+/- and Casq2-/-/E4872Q+/- mice displayed little or no stress-induced VTs. Confocal Ca2+ imaging revealed that Casq2-/- hearts frequently exhibited SCWs after extracellular Ca2+ elevation or adrenergic stimulation, whereas Casq2-/-/E4872Q+/- hearts had few or no SCWs under the same conditions. Cardiac hypertrophy developed and CPVT susceptibility increased with age in Casq2-/- mice, but not in Casq2-/-/E4872Q+/- mice. However, the amplitudes and dynamics of voltage-induced Ca2+ transients in Casq2-/- and Casq2-/-/E4872Q+/- hearts were not significantly different. Our results indicate that SCWs, CPVT and hypertrophy in Casq2-null cardiac muscle are governed by the RyR2-resident luminal Ca2+ sensor. This implies that defects in CASQ2-based lumi-nal Ca2+ sensing can be overridden by the RyR2-resident luminal Ca2+ sensor. This makes this RyR2-resident sensor a promising molecular target for the treatment of Ca2+-mediated arrhythmias. PMID:24758151

Zhang, Jingqun; Chen, Biyi; Zhong, Xiaowei; Mi, Tao; Guo, Ang; Zhou, Qiang; Tan, Zhen; Wu, Guogen; Chen, Alexander W; Fill, Michael; Song, Long-Sheng; Chen, S R Wayne

2014-07-01

308

Effects of Huoxue Qianyang Formula on expressions of proto-oncogenes c-fos and c-myc in spontaneous hypertensive rats with ventricular hypertrophy  

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Full Text Available Objective: To explore the possible mechanism of Huoxue Qianyang Formula (HXQYF, a compound traditional Chinese herbal medicine, in reversing the left ventricular hypertrophy (LVH of spontaneous hypertensive rats (SHRs by analyzing the expressions of mRNAs and proteins of proto-oncogenes c-fos and c-myc in left ventricular muscle.Methods: The experimental study was carried out in SHRs, the sex- and age-matched Wistar-Kyoto (WKY rats were served as normal control (n=5, normal saline 10 ml/kg daily. Twenty-five SHRs were randomly divided into five groups: untreated group (n=5, normal saline 10 ml/kg daily, high-dose HXQYF-treated group (n=5, 0.84 g/ml HXQYF, 10 ml/kg daily, medium-dose HXQYF-treated group (n=5, 0.42 g/ml HXQYF, 10 ml/kg daily, low-dose HXQYF-treated group (n=5, 0.21 g/ml HXQYF, 10 ml/kg daily and cilazapril-treated group (n=5, 1 mg/ml cilazapril, 10 ml/kg daily. The drugs were intragastrically administered once daily for 14 weeks. The expressions of mRNAs and proteins of proto-oncogenes c-fos and c-myc in left ventricular muscle were detected separately by in situ hybridization histochemical method and immunohistochemical method.Results: Compared with the normal control group, the expressions of mRNAs and proteins of proto-oncogenes c-fos and c-myc in left ventricular muscle were significantly increased in untreated group (P<0.01. After treatment, the expressions of c-fos and c-myc mRNAs in left ventricular muscle in HXQYF-treated groups were significantly down-regulated as compared with those of the untreated group (P<0.05. The expressions of c-myc protein were also significantly decreased in high- and medium-dose HXQYF-treated groups as compared with the untreated group (P<0.05, but it had no significant effects in protein expression of c-fos in the three HXQYF-treated groups.Conclusion: HXQYF can inhibit the expression of c-myc in ventricular hypertrophy tissue, which may be the mechanism in treating LVH of hypertention.

De-yu FU

2008-04-01

309

Valsartan in the treatment of heart failure or left ventricular dysfunction after myocardial infarction  

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The physiological role of the renin angiotensin aldosterone system (RAAS) is to maintain the integrity of the cardiovascular system. The effect of angiotensin II is mediated via the angiotensin type I receptor (AT1) resulting in vasoconstriction, sodium retention and myocyte growth changes. This causes myocardial remodeling which eventually leads to left ventricular hypertrophy, dilation and dysfunction. Inhibition of the RAAS with angiotensin converting enzyme (ACE) inhibitors after acute my...

2007-01-01

310

Angiotensin II (AT1) Receptors and NADPH Oxidase Regulate Cl? Current Elicited by ?1 Integrin Stretch in Rabbit Ventricular Myocytes  

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Direct stretch of ?1 integrin activates an outwardly rectifying, tamoxifen-sensitive Cl? current (Cl? SAC) via focal adhesion kinase (FAK) and/or Src. The characteristics of Cl? SAC resemble those of the volume-sensitive Cl? current, ICl,swell. Because myocyte stretch releases angiotensin II (AngII), which binds AT1 receptors (AT1R) and stimulates FAK and Src in an autocrine-paracrine loop, we tested whether AT1R and their downstream signaling cascade participate in mechanotransduction. Paramagnetic beads coated with mAb for ?1-integrin were applied to myocytes and pulled upward with an electromagnet while recording whole-cell anion current. Losartan (5 ?M), an AT1R competitive antagonist, blocked Cl? SAC but did not significantly alter the background Cl? current in the absence of integrin stretch. AT1R signaling is mediated largely by H2O2 produced from superoxide generated by sarcolemmal NADPH oxidase. Diphenyleneiodonium (DPI, 60 ?M), a potent NADPH oxidase inhibitor, rapidly and completely blocked both Cl? SAC elicited by stretch and the background Cl? current. A structurally unrelated NADPH oxidase inhibitor, 4-(2-aminoethyl) benzenesulfonyl fluoride (AEBSF, 0.5 and 2 mM), also rapidly and completely blocked Cl? SAC as well as a large fraction of the background Cl? current. With continuing integrin stretch, Cl? SAC recovered upon washout of AEBSF (2 mM). In the absence of stretch, exogenous AngII (5 nM) activated an outwardly rectifying Cl? current that was rapidly and completely blocked by DPI (60 ?M). Moreover, exogenous H2O2 (10, 100, and 500 ?M), the eventual product of NADPH oxidase activity, also activated Cl? SAC in the absence of stretch, whereas catalase (1,000 U/ml), an H2O2 scavenger, attenuated the response to stretch. Application of H2O2 during NADPH oxidase inhibition by either DPI (60 ?M) or AEBSF (0.5 mM) did not fully reactivate Cl? SAC, however. These results suggest that stretch of ?1-integrin in cardiac myocytes elicits Cl? SAC by activating AT1R and NADPH oxidase and, thereby, producing reactive oxygen species. In addition, NADPH oxidase may be intimately coupled to the channel responsible for Cl? SAC, providing a second regulatory pathway.

Browe, David M.; Baumgarten, Clive M.

2004-01-01

311

Increase in cardiac myosin heavy-chain (MyHC) alpha protein isoform in hibernating ground squirrels, with echocardiographic visualization of ventricular wall hypertrophy and prolonged contraction.  

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Deep hibernators such as golden-mantled ground squirrels (Callospermophilus lateralis) have multiple challenges to cardiac function during low temperature torpor and subsequent arousals. As heart rates fall from over 300 beats min(-1) to less than 10, chamber dilation and reduced cardiac output could lead to congestive myopathy. We performed echocardiography on a cohort of individuals prior to and after several months of hibernation. The left ventricular chamber exhibited eccentric and concentric hypertrophy during hibernation and thus calculated ventricular mass was ~30% greater. Ventricular ejection fraction was mildly reduced during hibernation but stroke volumes were greater due to the eccentric hypertrophy and dramatically increased diastolic filling volumes. Globally, the systolic phase in hibernation was ~9.5 times longer, and the diastolic phase was 28× longer. Left atrial ejection generally was not observed during hibernation. Atrial ejection returned weakly during early arousal. Strain echocardiography assessed the velocity and total movement distance of contraction and relaxation for regional ventricular segments in active and early arousal states. Myocardial systolic strain during early arousal was significantly greater than the active state, indicating greater total contractile movement. This mirrored the increased ventricular ejection fraction noted with early arousal. However, strain rates were slower during early arousal than during the active period, particularly systolic strain, which was 33% of active, compared with the rate of diastolic strain, which was 67% of active. As heart rate rose during the arousal period, myocardial velocities and strain rates also increased; this was matched closely by cardiac output. Curiously, though heart rates were only 26% of active heart rates during early arousal, the cardiac output was nearly 40% of the active state, suggesting an efficient pumping system. We further analyzed proportions of cardiac myosin heavy-chain (MyHC) isoforms in a separate cohort of squirrels over 5 months, including time points before hibernation, during hibernation and just prior to emergence. Hibernating individuals were maintained in both a 4°C cold room and a 20°C warm room. Measured by SDS-PAGE, relative percentages of cardiac MyHC alpha were increased during hibernation, at both hibernacula temperatures. A potential increase in contractile speed, and power, from more abundant MyHC alpha may aid force generation at low temperature and at low heart rates. Unlike many models of cardiomyopathies where the alpha isoform is replaced by the beta isoform in order to reduce oxygen consumption, ground squirrels demonstrate a potential cardioprotective mechanism to maintain cardiac output during torpor. PMID:24072796

Nelson, O Lynne; Rourke, Bryan C

2013-12-15

312

Calcium-sensing receptor activation contributed to apoptosis stimulates TRPC6 channel in rat neonatal ventricular myocytes  

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Capacitative calcium entry (CCE) refers to the influx of calcium through plasma membrane channels activated on depletion of endoplasmic sarcoplasmic/reticulum (ER/SR) Ca2+ stores, which is performed mainly by the transient receptor potential (TRP) channels. TRP channels are expressed in cardiomyocytes. Calcium-sensing receptor (CaR) is also expressed in rat cardiac tissue and plays an important role in mediating cardiomyocyte apoptosis. However, there are no data regarding the link between CaR and TRP channels in rat heart. In this study, in rat neonatal myocytes, by Ca2+ imaging, we found that the depletion of ER/SR Ca2+ stores by thapsigargin (TG) elicited a transient rise in cytoplasmic Ca2+ ([Ca2+]i), followed by sustained increase depending on extracellular Ca2+. But, TRP channels inhibitor (SKF96365), not L-type channels or the Na+/Ca2+ exchanger inhibitors, inhibited [Ca2+]i relatively high. Then, we found that the stimulation of CaR with its activator gadolinium chloride (GdCl3) or by an increased extracellular Ca2+([Ca2+]o) increased the concentration of intracelluar Ca2+, whereas, the sustained elevation of [Ca2+]i was reduced in the presence of SKF96365. Similarly, the duration of [Ca2+]i increase was also shortened in the absence of extracellular Ca2+. Western blot analysis showed that GdCl3 increased the expression of TRPC6, which was reversed by SKF96365. Additionally, SKF96365 reduced cardiomyocyte apoptosis induced by GdCl3. Our results suggested that CCE exhibited in rat neonatal myocytes and CaR activation induced Ca2+-permeable cationic channels TRPCs to gate the CCE, for which TRPC6 was one of the most likely candidates. TRPC6 channel was functionally coupled with CaR to enhance the cardiomyocyte apoptosis.

2010-04-16

313

Outcomes in atrial fibrillation patients with and without left ventricular hypertrophy when treated with a lenient rate-control or rhythm-control strategy.  

Science.gov (United States)

Although left ventricular (LV) hypertrophy has been proposed as a factor predisposing to atrial fibrillation (AF), its relevance to prognosis and selection of therapeutic strategies is unclear. We identified 2,105 patients with echocardiographic data on LV mass enrolled in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial. LV hypertrophy was defined as increased LV mass, stratified by American Society of Echocardiography criteria. The primary end point was all-cause mortality, secondary end point was as per AFFIRM trial definition, and tertiary end point was cardiovascular hospitalizations. We compared "strict" versus "lenient" rate control in patients with increased LV mass, and studied association of heart failure (HF) with preserved and decreased systolic function in patients with increased LV mass. Over 6 years, 332 deaths (15.7%) were reported. Adjusted hazard ratio (HR) of severely increased LV mass for all-cause mortality was 1.34 (95% confidence interval [CI] 1.01 to 1.79, p=0.045) for the overall population and 1.61 (95% CI 1.09 to 2.37, p=0.016) for the rhythm-control arm. Increased LV mass was a predictor of cardiovascular hospitalizations in the lenient rate-control group (HR 1.72, 95% CI 1.05 to 2.82, p=0.03) but not in the strict rate-control group. Severely increased LV mass was predictive of cardiovascular hospitalizations in patients with HF with preserved (HR 1.8, 95% CI 1.0 to 3.2, p=0.03) and decreased LV systolic function (HR 2.4, 95% CI 1.1 to 5.2, p=0.02). Thus, LV hypertrophy is a significant independent predictor of mortality in patients with AF, especially those managed with rhythm control. In patients with LV hypertrophy, strict rate control may be associated with better outcomes than lenient rate control. LV hypertrophy portends higher cardiovascular morbidity in patients with AF and HF. PMID:24507168

Badheka, Apurva O; Shah, Neeraj; Grover, Peeyush M; Patel, Nileshkumar J; Chothani, Ankit; Mehta, Kathan; Singh, Vikas; Deshmukh, Abhishek; Savani, Ghanshyambhai T; Rathod, Ankit; Panaich, Sidakpal S; Patel, Nilay; Arora, Shilpkumar; Bhalara, Vipulkumar; Coffey, James O; Mitrani, Raul D; Halperin, Jonathan L; Viles-Gonzalez, Juan F

2014-04-01

314

Loss of T-tubules and other changes to surface topography in ventricular myocytes from failing human and rat heart  

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T-tubular invaginations of the sarcolemma of ventricular cardiomyocytes contain junctional structures functionally coupling L-type calcium channels to the sarcoplasmic reticulum calcium-release channels (the ryanodine receptors), and therefore their configuration controls the gain of calcium-induced calcium release (CICR). Studies primarily in rodent myocardium have shown the importance of T-tubular structures for calcium transient kinetics and have linked T-tubule disruption to delayed CICR....

2009-01-01

315

Effects of PP1/PP2A inhibitor calyculin A on the E-C coupling cascade in murine ventricular myocytes.  

Science.gov (United States)

Calyculin A was used to examine the importance of phosphatases in the modulation of cardiac contractile magnitude in the absence of any neural or humoral stimulation. Protein phosphatase (PP)1 and PP2A activity, twitch contractions, intracellular Ca(2+) concentration ([Ca(2+)](i)) transients, action potentials, membrane currents, and myofilament Ca(2+) sensitivity were measured in isolated mouse ventricular myocytes. Calyculin A (125 nM) inhibited PP1 and PP2A by 50% and 85%, respectively, whereas it doubled the twitch magnitude and increased twitch duration by 50% in field-stimulated cells. Calyculin A-evoked increases in L-type Ca(2+) current (70%) and the resulting [Ca(2+)](i) transient (83%) explain the positive inotropic response. However, increases in twitch and action potential durations did not result from increased myofilament Ca(2+) sensitivity or K(+) current inhibition, respectively. Comparison of the effects of calyculin A and isoproterenol on [Ca(2+)](i) transients and twitch contractions revealed that calyculin A had a much smaller lusitropic effect than the beta-agonist, indicating that calyculin A did not significantly increase sarcoplasmic reticulum Ca(2+) reuptake. Thus while cardiac contractile magnitude is controlled by a steady-state kinase/phosphatase balance, this regulation is not equally operative at all of the steps in the excitation-contraction coupling pathway and may in fact be most important to the regulation of the L-type Ca(2+) channel. PMID:11748045

duBell, William H; Gigena, Marisa S; Guatimosim, Silvia; Long, Xilin; Lederer, W J; Rogers, Terry B

2002-01-01

316

Diagnóstico electrocardiográfico de la Hipertrofia Ventricular Izquierda en pacientes hipertensos. Utilidad del producto duración por voltaje del QRS / Electrocardiography Diagnosis of the Left Ventricular Hypertrophy in hypertensive patients. Usefulness of the product of the duration of voltage of QRS  

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Full Text Available SciELO Cuba | Language: Spanish Abstract in spanish Introducción: las enfermedades cardiovasculares provocan la muerte de uno de cada tres cubanos. La Hipertensión arterial (HTA) y consecuentemente la Hipertrofia Ventricular Izquierda (HVI) constituye un factor de riesgo prevalente y capaz de desencadenar serias complicaciones. Objetivo: identificar [...] el comportamiento de los criterios electrocardiográficos de Sokolow, Cornell y el Producto de la Duración por el Voltaje (PDV) del QRS en pacientes con HVI ecocardiográfica. Material y Método: la muestra seleccionada coincide con el universo y consta de 76 pacientes portadores de hipertensión arterial (HTA) atendidos en la consulta de Cardiología. Se les realizó una encuesta sobre la presencia de factores de riesgo, determinación del índice de masa corporal, realización de electrocardiograma y ecocardiograma para establecer la HVI. Resultados: el 61% de los pacientes eran portadores del HVI ecocardiográfica (Prueba de Oro diagnóstica). Para los índices electrocardiográficos de Sokolow y Cornell la sensibilidad (S) fue respectivamente de 22%, y 24%, existiendo en ambos una especificidad (E) de 93%. La (S) para el PDV-Sokolow alcanzó 33%, 22% entre los hombres y 11% entre las mujeres con una (E) total de 97%, mientras el PDV-Cornell tuvo una (S) de 35%, 11% entre los hombres y 24% entre las mujeres, con una (E) total para este índice de 93%. Conclusiones: el ECG es indispensable para el diagnóstico de HVI; el PDV-C y el PDV-S son de mayor sensibilidad diagnóstica que los índices de voltaje aislados; el primero es más útil en mujeres con características epidemiológicas bien definidas. Abstract in english Introduction: cardiovascular diseases cause the death of one out of three Cubans. High Blood Pressure and consequently Left Ventricular Hyperthrophty constitutes a prevalent risk factor able to trigger serious complications. Objective: to identify the behavior of the electrocardiographic approaches [...] of Sokolow, Cornell and the Product of the Duration of Voltage of QRS in patients with Echocardiography Left Ventricular Hypertrophy. Material and Method: the sample coincides with the universe which consists of 76 patients suffering from High Blood Pressure and treated at the Consultation of Cardiology. The patients were surveyed about the presence of risk factors, body mass index and records of electrocardiogram and echocardiogram to confirm their left ventricular hypertrophy. Results: 61% of the patients had echocardiograph left ventricular hypertrophy. For the electrocardiographic indexes of Sokolow and Cornell the sensitivity was 26% and 24% respectively, both tests showed a specificity of 93%. The sensitivity for the Product of the Duration of Voltage for Sokolow reached 33% with a specificity of 97% while the Product of the Duration of Voltage for Cornell had a sensitivity of 35% and a specificity of 93%. Conclusions: ECG is essential in the diagnosis of Left Ventricular Hypertrophy, the Product of the Duration of Voltage for Cornell and the Product of the Duration of Voltage for Sokolow have a higher diagnostic sensitivity than isolated voltage indexes, the former is more useful in women with well defined epidemiological features.

Juan Lázaro, González Moreno; Belkis, Martínez Martínez; Olga María, Rivero González; Adys H, Salgado Friol; Pablo José, Díaz San Jorge.

317

Calcium-sensing receptor activation contributed to apoptosis stimulates TRPC6 channel in rat neonatal ventricular myocytes  

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Capacitative calcium entry (CCE) refers to the influx of calcium through plasma membrane channels activated on depletion of endoplasmic sarcoplasmic/reticulum (ER/SR) Ca{sup 2+} stores, which is performed mainly by the transient receptor potential (TRP) channels. TRP channels are expressed in cardiomyocytes. Calcium-sensing receptor (CaR) is also expressed in rat cardiac tissue and plays an important role in mediating cardiomyocyte apoptosis. However, there are no data regarding the link between CaR and TRP channels in rat heart. In this study, in rat neonatal myocytes, by Ca{sup 2+} imaging, we found that the depletion of ER/SR Ca{sup 2+} stores by thapsigargin (TG) elicited a transient rise in cytoplasmic Ca{sup 2+} ([Ca{sup 2+}]{sub i}), followed by sustained increase depending on extracellular Ca{sup 2+}. But, TRP channels inhibitor (SKF96365), not L-type channels or the Na{sup +}/Ca{sup 2+} exchanger inhibitors, inhibited [Ca{sup 2+}]{sub i} relatively high. Then, we found that the stimulation of CaR with its activator gadolinium chloride (GdCl{sub 3}) or by an increased extracellular Ca{sup 2+}([Ca{sup 2+}]{sub o}) increased the concentration of intracelluar Ca{sup 2+}, whereas, the sustained elevation of [Ca{sup 2+}]{sub i} was reduced in the presence of SKF96365. Similarly, the duration of [Ca{sup 2+}]{sub i} increase was also shortened in the absence of extracellular Ca{sup 2+}. Western blot analysis showed that GdCl{sub 3} increased the expression of TRPC6, which was reversed by SKF96365. Additionally, SKF96365 reduced cardiomyocyte apoptosis induced by GdCl{sub 3}. Our results suggested that CCE exhibited in rat neonatal myocytes and CaR activation induced Ca{sup 2+}-permeable cationic channels TRPCs to gate the CCE, for which TRPC6 was one of the most likely candidates. TRPC6 channel was functionally coupled with CaR to enhance the cardiomyocyte apoptosis.

Sun, Yi-hua [Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086 (China); Li, Yong-quan [Harbin Medical University, Harbin 150086 (China); Feng, Shan-li [Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086 (China); Li, Bao-xin; Pan, Zhen-wei [Department of Pharmacology, Harbin Medical University, Harbin 150086 (China); Xu, Chang-qing [Department of Pathophysiology, Harbin Medical University, Harbin 150086 (China); Li, Ting-ting [Department of Clinical Laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086 (China); Yang, Bao-feng, E-mail: syh200415@yahoo.com.cn [Department of Pharmacology, Harbin Medical University, Harbin 150086 (China)

2010-04-16

318

Association of the beta-1 adrenergic receptor carboxyl terminal variants with left ventricular hypertrophy among diabetic and non-diabetic survivors of acute myocardial infarction  

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Full Text Available Abstract Background The beta-1 adrenergic receptor (?1AR plays a fundamental role in the regulation of cardiovascular functions. It carries a nonsynonymous single nucleotide polymorphism in its carboxyl terminal tail (Arg389Gly, which has been shown to associate with various echocardiographic parameters linked to left ventricular hypertrophy (LVH. Diabetes mellitus (DM, on the other hand, represents a risk factor for LVH. We investigated the possible association between the Arg389Gly polymorphism and LVH among non-diabetic and diabetic acute myocardial infarction (AMI survivors. Methods The study population consisted of 452 AMI survivors, 20.6% of whom had diagnosed DM. Left ventricular parameters were measured with two-dimensional guided M-mode echocardiography 2-7 days after AMI, and the Arg389Gly polymorphism was determined using a polymerase chain reaction-restriction fragment length polymorphism assay. Results The Arg389 homozygotes in the whole study population had a significantly increased left ventricular mass index (LVMI when compared to the Gly389 carriers (either Gly389 homozygotes or Arg389/Gly389 heterozygotes [62.7 vs. 58.4, respectively (p = 0.023]. In particular, the Arg389 homozygotes displayed thicker diastolic interventricular septal (IVSd measures when compared to the Gly389 carriers [13.2 vs. 12.3 mm, respectively (p = 0.004]. When the euglycemic and diabetic patients were analyzed separately, the latter had significantly increased LVMI and diastolic left ventricular posterior wall (LVPWd values compared to the euglycemic patients [LVMI = 69.1 vs. 58.8 (p = 0.001 and LVPWd = 14.2 vs. 12.3 mm (p Conclusions The data suggest an association between the ?1AR Arg389Gly polymorphism and LVH, particularly the septal hypertrophy. The Arg389 variant appears to confer a higher risk of developing LVH than the corresponding Gly389 variant among patients who have suffered AMI. This association cannot be considered to be universal, however, since it does not appear to exist among diabetic AMI survivors.

Hakalahti Anna E

2010-08-01

319

IGF-1 response to arm exercise with eccentric and concentric muscle contractions in resistance-trained athletes with left ventricular hypertrophy.  

Science.gov (United States)

The study aimed at evaluating changes in plasma levels of insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), testosterone, growth hormone (GH), cortisol, and insulin in resistance-trained male athletes with (n=9) and without (n=9) left ventricular hypertrophy (LVH) in response to eccentric (ECC) and concentric (CON) arm exercise. 10 age-matched healthy non-trained subjects served as controls. M-mode and 2D Doppler echocardiography were used to estimate LV mass.Resting IGF-1 concentration was higher in LVH athletes compared to controls (52 ± 5 nM vs. 46 ± 7 nM, pconcentrations in athletes with LVH (70 ± 11 nM, n=9) compared to those without LVH (62 ± 10 nM, n=9), and to untrained controls (54 ± 6 nM). Both CON and ECC exercise resulted in higher serum IGFBP-3 levels in LVH athletes compared to controls (242 ± 57 and 274 ± 58, athletes, vs. 215 ± 63 and 244 ± 67, controls, nM, pconcentrations were lower in LVH than in non-LVH athletes (4.7 ± 2.1 vs. 6.1 ± 1.8 ng ?mL(-1), peccentric arm exercise. These findings suggest a role of IGF-1, possibly released from contracting muscle, in stimulating LV hypertrophy in resistance training. PMID:22960989

?ebrowska, A; Wa?kiewicz, Z; Zaj?c, A; G?sior, Z; Galbo, H; Langfort, J

2013-02-01

320

La disfunción diastólica en pacientes hipertensos no es debida a hipertrofia ventricular izquierda / Diastolic dysfunction in hypertensive patients is not due to left ventricular hypertrophy / A disfunção diastólica em pacientes hipertensos não é devida à hipertrofia ventricular esquerda  

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Full Text Available SciELO Argentina | Language: Spanish Abstract in portuguese Introdução. .A hipertrofia ventricular esquerda (HVE) é uma complicação comum da hipertensão e pode estar associada com disfunção diastólica (DD). Objetivos. Determinar a prevalência de DD em pacientes hipertensos (HT) sem HVE. Material e métodos. Foram incluídos 98 pacientes HT, 66 pacientes sem HV [...] E e 32 pacientes com HVE medida pelo método de Devereux, considerando HVE um índice de massa ventricular esquerda >110 g/m2 em mulheres e 125 g/m2 em homens. Foi realizado Doppler pulsado do orifício da válvula mitral, e foi medida a razão velocidade instantânea pico E / velocidade instantânea pico A (VE/VA) e tempo de relaxamento isovolumétrico (TRIV), ambos foram corrigidos pela idade; e Doppler tecidual do septo interventricular, e foi medida a taxa de pico de velocidade instantânea E'/ pico de velocidade instantânea A' (VE'/VA') e de pico e velocidade instantânea E / pico de velocidade instantânea E' (VE/VE'). Resultados. A média de idade 60,3 ± 36,7 anos, 45 pacientes do sexo masculino (45,9%), 8 pacientes diabéticos (8,2%). A tabela apresenta os resultados da avaliação da função diastólica Conclusões. 1) Alta freqüência de DD em pacientes com hipertensão sem HVE; 2) A única diferença na função diastólica entre pacientes com hipertensão sem e com HVE é maior a pressão diastólica ventricular esquerda expressa por VE/VE'; 3) HVE não é causa do DD em pacientes com hipertensão. Abstract in spanish Introducción. La hipertrofia ventricular izquierda (HVI) es una complicación frecuente en hipertensión arterial y se puede acompañar de disfunción diastólica (DD). Objetivos. Determinar la prevalencia de DD en pacientes hipertensos (HT) sin HVI. Material y métodos. Se incluyeron 98 pacientes con HT, [...] 66 pacientes sin HVI y 32 pacientes con HVI medida por método de Devereux, considerándose HVI un índice de masa ventricular izquierda >110 g/m2 en mujeres y 125 g/m2 en hombres. Se efectuó Doppler pulsado del orificio valvular mitral y se midió la relación velocidad instantánea pico E/velocidad instantánea pico A (VE/VA) y el tiempo de relajación isovolumétrica (TRIV), ambos fueron corregidos por edad, y Doppler tisular del septum interventricular, midiéndose la relación velocidad instantánea pico E´/velocidad instantánea pico A´ (VE´/VA´) y velocidad instantánea pico E/velocidad instantánea pico E´ (VE/VE´). Resultados. Edad media: 60,3±36,7 años; sexo masculino: 45 pacientes (45,9 %); 8 pacientes diabéticos (8,2%). La tabla presenta los resultados de la evaluación de función diastólica. Conclusiones. 1) Alta frecuencia de DD en pacientes HT sin HVI. 2) La única diferencia en la función diastólica entre pacientes HT sin y con HVI es la mayor presión de fin de diástole del ventrículo izquierdo expresada por VE/VE´. 3) La HVI no es la causa de DD en pacientes HT. Abstract in english Background. Left ventricular hypertrophy (LVH) is a common complication of hypertension and may be associated with diastolic dysfunction (DD). Objectives. To determine the prevalence of DD in hypertensive (HT) patients without LVH. Methods and material. 98 HT patients were included, 66 with LVH and [...] 32 without LVH measured by the method ofDevereux, LVH was considered a left ventricular mass index >110 g/m2 in women and 125 g/m2 in men. Mitral valve orifice pulsed Doppler was performed and it was measured the peak instantaneous velocity ratio E/A (VE/VA) and isovolumetric relaxation time (IVRT), both were corrected by age; and tissue Doppler of the interventricular septum was also preformed, and it was measured the peak instantaneous velocity ratio E'/A' (VE'/ VA') and instantaneous velocity peak E/E' (VE/VE'). Results. Mean age 60.3±36.7 years, male 45 patients (45,9%), 8 diabetic patients (8.2%). The table presents the results of the assessment of diastolic function. Conclusions. 1) High frequency of DD in HT patients without LVH, 2) The only one difference between patients

Piskorz, Daniel; Tommasi, Alicia.

 
 
 
 
321

Differential expression of small-conductance Ca2+-activated K+ channels SK1, SK2, and SK3 in mouse atrial and ventricular myocytes.  

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Small-conductance Ca2+-activated K+ channels (SK channels, KCa channels) have been reported in excitable cells, where they aid in integrating changes in intracellular Ca2+ with membrane potential. We recently reported for the first time the functional existence of SK2 (KCa2.2) channels in human and mouse cardiac myocytes. Here, we report cloning of SK1 (KCa2.1) and SK3 (KCa2.3) channels from mouse atria and ventricles using RT-PCR. Full-length transcripts and their variants were detected for both SK1 and SK3 channels. Variants of mouse SK1 channel (mSK1) differ mainly in the COOH-terminal structure, affecting a portion of the sixth transmembrane segment (S6) and the calmodulin binding domain (CaMBD). Mouse SK3 channel (mSK3) differs not only in the number of polyglutamine repeats in the NH2 terminus but also in the intervening sequences between the polyglutamine repeats. Full-length cardiac mSK1 and mSK3 show 99 and 91% nucleotide identity with those of mouse colon SK1 and SK3, respectively. Quantification of SK1, SK2, and SK3 transcripts between atria and ventricles was performed using real-time quantitative RT-PCR from single, isolated cardiomyocytes. SK1 transcript was found to be more abundant in atria compared with ventricles, similar to the previously reported finding for SK2 channel. In contrast, SK3 showed similar levels of expression in atria and ventricles. Together, our data are the first to indicate the presence of the three different isoforms of SK channels in heart and the differential expression of SK1 and SK2 in mouse atria and ventricles. Because of the marked differential expression of SK channel isoforms in heart, specific ligands for Ca2+-activated K+ currents may offer a unique therapeutic opportunity to modify atrial cells without interfering with ventricular myocytes. PMID:16055520

Tuteja, Dipika; Xu, Danyan; Timofeyev, Valeriy; Lu, Ling; Sharma, Dipika; Zhang, Zhao; Xu, Yanfang; Nie, Liping; Vázquez, Ana E; Young, J Nilas; Glatter, Kathryn A; Chiamvimonvat, Nipavan

2005-12-01

322

Remodeling of the sarcomeric cytoskeleton in cardiac ventricular myocytes during heart failure and after cardiac resynchronization therapy.  

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Sarcomeres are the basic contractile units of cardiac myocytes. Recent studies demonstrated remodeling of sarcomeric proteins in several diseases, including genetic defects and heart failure. Here we investigated remodeling of sarcomeric ?-actinin in two models of heart failure, synchronous (SHF) and dyssynchronous heart failure (DHF), as well as a model of cardiac resynchronization therapy (CRT). We applied three-dimensional confocal microscopy and quantitative methods of image analysis to study isolated cells from our animal models. 3D Fourier analysis revealed a decrease of the spatial regularity of the ?-actinin distribution in both SHF and DHF versus control cells. The spatial regularity of ?-actinin in DHF cells was reduced when compared with SHF cells. The spatial regularity of ?-actinin was partially restored after CRT. We found longitudinal depositions of ?-actinin in SHF, DHF and CRT cells. These depositions spanned adjacent Z-disks and exhibited a lower density of ?-actinin than in the Z-disk. Differences in the occurrence of depositions between the SHF, CRT and DHF models versus control were significant. Also, CRT cells exhibited a higher occurrence of depositions versus SHF, but not DHF cells. Other sarcomeric proteins did not accumulate in the depositions to the same extent as ?-actinin. We did not find differences in the expression of ?-actinin protein and its encoding gene in our animal models. In summary, our studies indicate that HF is associated with two different types of remodeling of ?-actinin and only one of those was reversed after CRT. We suggest that these results can guide us to an understanding of remodeling of structures and function associated with sarcomeres. PMID:24657727

Lichter, Justin G; Carruth, Eric; Mitchell, Chelsea; Barth, Andreas S; Aiba, Takeshi; Kass, David A; Tomaselli, Gordon F; Bridge, John H; Sachse, Frank B

2014-07-01

323

Detection of incipient left ventricular hypertrophy in mild to moderate arterial hypertension with normal electrocardiogram and echocardiogram: a new use for signal-averaged electrocardiography  

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Full Text Available SciELO Brazil | Language: English Abstract in english OBJECTIVE: To assess signal-averaged electrocardiogram (SAECG) for diagnosing incipient left ventricular hypertrophy (LVH). METHODS: A study with 115 individuals was carried out. The individuals were divided as follows: GI - 38 healthy individuals; GII - 47 individuals with mild to moderate hyperten [...] sion and normal findings on echocardiogram and ECG; and GIII - 30 individuals with hypertension and documented LVH. The magnitude vector of the SAECG was analyzed with the high-pass cutoff frequency of 40 Hz through the bidirectional four-pole Butterworth high-pass digital filter. The mean quadratic root of the total QRS voltage (RMST) and the two-dimensional integral of the QRS area of the spectro-temporal map were analyzed between 0 and 30 Hz for the frequency domain (Int FD), and between 40 and 250 Hz for the time domain (Int TD). The electrocardiographic criterion for LVH was based on the Cornell Product. Left ventricular mass was calculated with the Devereux formula. RESULTS: All parameters analyzed increased from GI to GIII, except for Int FD (GII vs GIII) and RMST log (GII vs GIII). Int TD showed greater accuracy for detecting LVH with an appropriate cutoff > 8 (sensitivity of 55%, specificity of 81%). Positive values (> 8) were found in 56.5% of the G II patients and in 18.4% of the GI patients (p

Paulo, Ginefra; Eduardo C., Barbosa; P. R., Benchimol-Barbosa; Alfredo S., Bomfim; Sílvia H., Boghossian; Angelo A., Salgado; Flávia G., Brasil; Elizabete A., Freitas; Francisco M., Albanesi Filho.

324

Detection of incipient left ventricular hypertrophy in mild to moderate arterial hypertension with normal electrocardiogram and echocardiogram: a new use for signal-averaged electrocardiography  

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Full Text Available OBJECTIVE: To assess signal-averaged electrocardiogram (SAECG for diagnosing incipient left ventricular hypertrophy (LVH. METHODS: A study with 115 individuals was carried out. The individuals were divided as follows: GI - 38 healthy individuals; GII - 47 individuals with mild to moderate hypertension and normal findings on echocardiogram and ECG; and GIII - 30 individuals with hypertension and documented LVH. The magnitude vector of the SAECG was analyzed with the high-pass cutoff frequency of 40 Hz through the bidirectional four-pole Butterworth high-pass digital filter. The mean quadratic root of the total QRS voltage (RMST and the two-dimensional integral of the QRS area of the spectro-temporal map were analyzed between 0 and 30 Hz for the frequency domain (Int FD, and between 40 and 250 Hz for the time domain (Int TD. The electrocardiographic criterion for LVH was based on the Cornell Product. Left ventricular mass was calculated with the Devereux formula. RESULTS: All parameters analyzed increased from GI to GIII, except for Int FD (GII vs GIII and RMST log (GII vs GIII. Int TD showed greater accuracy for detecting LVH with an appropriate cutoff > 8 (sensitivity of 55%, specificity of 81%. Positive values (> 8 were found in 56.5% of the G II patients and in 18.4% of the GI patients (p< 0.0005. CONCLUSION: SAECG can be used in the early diagnosis of LVH in hypertensive patients with normal ECG and echocardiogram.

Ginefra Paulo

2003-01-01

325

Longitudinal Evaluation of Left Ventricular Substrate Metabolism, Perfusion, and Dysfunction in the Spontaneously Hypertensive Rat Model of Hypertrophy Using Small-Animal PET/CT Imaging  

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Myocardial metabolic and perfusion imaging is a vital tool for understanding the physiologic consequences of heart failure. We used PET imaging to examine the longitudinal kinetics of 18F-FDG and 14(R,S)-18F-fluoro-6-thia-heptadecanoic acid (18F-FTHA) as analogs of glucose and fatty acid (FA) to quantify metabolic substrate shifts with the spontaneously hypertensive rat (SHR) as a model of left ventricular hypertrophy (LVH) and failure. Myocardial perfusion and left ventricular function were also investigated using a newly developed radiotracer 18F-fluorodihydrorotenol (18F-FDHROL). Methods Longitudinal dynamic electrocardiogram-gated small-animal PET/CT studies were performed with 8 SHR and 8 normotensive Wistar-Kyoto (WKY) rats over their life cycle. We determined the myocardial influx rate constant for 18F-FDG and 18F-FTHA (KiFDG and KiFTHA, respectively) and the wash-in rate constant for 18F-FDHROL (K1FDHROL). 18F-FDHROL data were also used to quantify left ventricular ejection fraction (LVEF) and end-diastolic volume (EDV). Blood samples were drawn to independently measure plasma concentrations of glucose, insulin, and free fatty acids (FFAs). Results KiFDG and KiFTHA were higher in SHRs than WKY rats (P SHRs than controls (P SHRs than controls (P < 3 × 10?3), with an age-dependent decrease when models were combined (P = 0.046). FFA levels were similar between models (P = 0.374), but an increase with age was evident only in SHR (P < 7 × 10?6). Conclusion The SHR exhibited alterations in myocardial substrate use at 8 mo characterized by increased glucose and FA utilizations. At 20 mo, the SHR had LVH characterized by decreased LVEF and increased EDV, while simultaneously sustaining higher glucose and similar FA utilizations (compared with WKY rats), which indicates maladaptation of energy substrates in the failing heart. Elevated K1FDHROL in the SHR may reflect elevated oxygen consumption and decreased capillary density in the hypertrophied heart. From our findings, metabolic changes appear to precede mechanical changes of LVH progression in the SHR model.

Hernandez, Andrew M.; Huber, Jennifer S.; Murphy, Stephanie T.; Janabi, Mustafa; Zeng, Gengsheng L.; Brennan, Kathleen M.; O'Neil, James P.; Seo, Youngho; Gullberg, Grant T.

2014-01-01

326

Determinants of left ventricular hypertrophy in hypertensive patients: identification of high-risk patients by metabolic, vascular, and inflammatory risk factors.  

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Left ventricular hypertrophy (LVH) is recognized as an independent predictor of cardiovascular morbidity and mortality in hypertensive patients. Thus, it is critical to understand the mechanisms underlying the development of LVH for formulation screening and treatment strategies. This study was designed to determine the association between echographically determined LVH measures and markers of inflammation, neurohormonal activity, glomerular function, oxidative stress, insulin resistance, and vascular endothelial function. In this study, 129 hypertensive subjects were evaluated for lipids, glucose, HbA1C, insulin, homeostasis model assessment-insulin resistance, C-reactive protein (CRP), urinary microalbumin, homocysteine, aldosterone, renin, and endothelin. LVH parameters including interventricular septum thickness, posterior wall thickness (PWT), and left ventricular mass index (LVMI) were assessed echographically. Serum aldosterone levels were significantly positively associated with left ventricular mass (LVM) and marginally positively associated with LVMI and PWT. Both LVM and LVMI were significantly elevated in subjects with high versus normal serum aldosterone levels (p?=?0.018 for LVM and p?=?0.050 for LVMI). Serum endothelin was positively associated with LVM and LVMI. In multiple linear regression analysis, aldosterone remained a significant predictor of LVM (standardized ??=?0.229, p?=?0.024), and endothelin a marginally significant predictor of LVM (standardized ??=?0.178, p?=?0.077). Among serum lipids, high-density lipoprotein cholesterol only had a significant inverse association with LVM and PWT. Homocysteine as well as CRP were significantly positively associated with LVM and LVMI in females. This study found that aldosterone and endothelin levels are the most important independent determinants of LVH in hypertensive subjects. These markers may be useful to identify asymptomatic hypertensive subjects at risk for heart failure. PMID:24436616

Peer, Maya; Boaz, Mona; Zipora, Matas; Shargorodsky, Marina

2013-12-01

327

Inhibition of the sarcoplasmic reticulum Ca2+ pump with thapsigargin to estimate the contribution of Na+-Ca2+ exchange to ventricular myocyte relaxation  

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Full Text Available Relaxation in the mammalian ventricle is initiated by Ca2+ removal from the cytosol, which is performed by three main transport systems: sarcoplasmic reticulum Ca2+-ATPase (SR-A, Na+-Ca2+ exchanger (NCX and the so-called slow mechanisms (sarcolemmal Ca2+-ATPase and mitochondrial Ca2+ uptake. To estimate the relative contribution of each system to twitch relaxation, SR Ca2+ accumulation must be selectively inhibited, usually by the application of high caffeine concentrations. However, caffeine has been reported to often cause changes in membrane potential due to NCX-generated inward current, which compromises the reliability of its use. In the present study, we estimated integrated Ca2+ fluxes carried by SR-A, NCX and slow mechanisms during twitch relaxation, and compared the results when using caffeine application (Cf-NT and an electrically evoked twitch after inhibition of SR-A with thapsigargin (TG-TW. Ca2+ transients were measured in 20 isolated adult rat ventricular myocytes with indo-1. For transients in which one or more transporters were inhibited, Ca2+ fluxes were estimated from the measured free Ca2+ concentration and myocardial Ca2+ buffering characteristics. NCX-mediated integrated Ca2+ flux was significantly higher with TG-TW than with Cf-NT (12 vs 7 µM, whereas SR-dependent flux was lower with TG-TW (77 vs 81 µM. The relative participations of NCX (12.5 vs 8% with TG-TW and Cf-NT, respectively and SR-A (85 vs 89.5% with TG-TW and Cf-NT, respectively in total relaxation-associated Ca2+ flux were also significantly different. We thus propose TG-TW as a reliable alternative to estimate NCX contribution to twitch relaxation in this kind of analysis.

R.A. Bassani

2003-12-01

328

Inhibition of the sarcoplasmic reticulum Ca2+ pump with thapsigargin to estimate the contribution of Na+-Ca2+ exchange to ventricular myocyte relaxation  

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Full Text Available SciELO Brazil | Language: English Abstract in english Relaxation in the mammalian ventricle is initiated by Ca2+ removal from the cytosol, which is performed by three main transport systems: sarcoplasmic reticulum Ca2+-ATPase (SR-A), Na+-Ca2+ exchanger (NCX) and the so-called slow mechanisms (sarcolemmal Ca2+-ATPase and mitochondrial Ca2+ uptake). To e [...] stimate the relative contribution of each system to twitch relaxation, SR Ca2+ accumulation must be selectively inhibited, usually by the application of high caffeine concentrations. However, caffeine has been reported to often cause changes in membrane potential due to NCX-generated inward current, which compromises the reliability of its use. In the present study, we estimated integrated Ca2+ fluxes carried by SR-A, NCX and slow mechanisms during twitch relaxation, and compared the results when using caffeine application (Cf-NT) and an electrically evoked twitch after inhibition of SR-A with thapsigargin (TG-TW). Ca2+ transients were measured in 20 isolated adult rat ventricular myocytes with indo-1. For transients in which one or more transporters were inhibited, Ca2+ fluxes were estimated from the measured free Ca2+ concentration and myocardial Ca2+ buffering characteristics. NCX-mediated integrated Ca2+ flux was significantly higher with TG-TW than with Cf-NT (12 vs 7 µM), whereas SR-dependent flux was lower with TG-TW (77 vs 81 µM). The relative participations of NCX (12.5 vs 8% with TG-TW and Cf-NT, respectively) and SR-A (85 vs 89.5% with TG-TW and Cf-NT, respectively) in total relaxation-associated Ca2+ flux were also significantly different. We thus propose TG-TW as a reliable alternative to estimate NCX contribution to twitch relaxation in this kind of analysis.

R.A., Bassani; J.W.M., Bassani.

329

The H{sub 1}–H{sub 2} domain of the ?{sub 1} isoform of Na{sup +}–K{sup +}–ATPase is involved in ouabain toxicity in rat ventricular myocytes  

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The composition of different isoforms of Na{sup +}-K{sup +}-ATPase (NKA, Na/K pump) in ventricular myocytes is an important factor in determining the therapeutic effect and toxicity of cardiac glycosides (CGs) on heart failure. The mechanism whereby CGs cause these effects is still not completely clear. In the present study, we prepared two site-specific antibodies (SSA78 and WJS) against the H{sub 1}–H{sub 2} domain of ?{sub 1} and ?{sub 2} isoforms of NKA in rat heart, respectively, and compared their influences on the effect of ouabain (OUA) in isolated rat ventricular myocytes. SSA78 or WJS, which can specifically bind with the ?{sub 1} or ?{sub 2} isoform, were assessed with enzyme linked immunosorbent assay (ELISA), Western blot and immunofluorescent staining methods. Preincubation of myocytes with SSA78 inhibited low OUA affinity pump current but not high OUA affinity pump current, reduced the rise in cytosolic calcium concentration ([Ca{sup 2+}]{sub i}), attenuated mitochondrial Ca{sup 2+} overload, restored mitochondrial membrane potential reduction, and delayed the decrease of the myocardial contractile force as well as the occurrence of arrhythmic contraction induced by high concentrations (1 mM) but not low concentrations (1 ?M) of OUA. Similarly, preincubation of myocytes with WJS inhibited high OUA affinity pump current, reduced the increase of [Ca{sup 2+}]{sub i} and the contractility induced by 1 ?M but not that induced by 1 mM OUA. These results indicate that the H{sub 1}–H{sub 2} domain of the NKA ?{sub 1} isoform mediates OUA-induced cardiac toxicity in rat ventricular myocytes, and inhibitors for this binding site may be used as an adjunct to CGs treatment for cardiovascular disease. -- Highlights: ? We prepared two antibodies against the H{sub 1}-H{sub 2} domain of ?{sub 1} and ?{sub 2} isoforms of NKA. ? The H{sub 1}-H{sub 2} domain of the NKA ?{sub 1} isoform mediates OUA-induced cardiac toxicity. ? The H{sub 1}-H{sub 2} domain of the NKA ?{sub 2} isoform mediates OUA-induced positive inotropic.

Xiong, Chen; Li, Jun-xia; Guo, Hui-cai; Zhang, Li-nan; Guo, Wei; Meng, Jing; Wang, Yong-li, E-mail: wangyongli@gmail.com

2012-07-01

330

A new method of attachment of isolated mammalian ventricular myocytes for tension recording: length dependence of passive and active tension.  

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The study of the Frank-Starling's law in mammalian single cells has been hindered by a lack of an easily performed method of stretching cells. Some authors have succeeded in this but their methods required a great deal of technical expertise and in most cases they have not had much success. We have developed an easy method of stretching mammalian ventricular cells from slack sarcomere length (S.L.) (Lo, 1.77 +/- 0.05 microns) to about 117% of this length. Thin carbon fibers (12 microns in diameter) which can be bound electrochemically to the cell membrane surface have been used. A flexible long fiber of known compliance (80 microns/microN) was attached to one end of the cell and a stiff double fiber (4 microns/microN) to the other end. The cell attachment was relatively easy to perform and successful results were obtained in 80% of the attempts. The displacement of the flexible fiber allows the quantitative measurements of the resting tension in a group of non-stimulated cells and of auxotonic contractions developed upon stimulation in another group of cells. Increasing S.L. from Lo to 105-106% of Lo, an increase in active tension from 0.21 +/- 0.03 mN/mm to 0.26 +/- 0.01 mN/mm (n = 4) could be noticed with a stimulation frequency of 0.5 Hz. An increase in active tension was also observed at 1 Hz. Staircase kinetics were accelerated with stretching; this confirms at the single cell level the hypothesis of an effect of length-dependent activation on the staircase. Eulerian differential stiffness constant was calculated and found to be 13.5 +/- 1.2, a value which is comparable to that described in intact heart. Thus the important stiffness found in the whole heart may be due to intracellular component(s) such as myofilament and/or connectin. PMID:2095433

Le Guennec, J Y; Peineau, N; Argibay, J A; Mongo, K G; Garnier, D

1990-10-01

331

Cardiac MRI in a Patient with Coincident Left Ventricular Non-Compaction and Hypertrophic Cardiomyopathy  

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Full Text Available Left ventricular non-compaction cardiomyopathy is a rare congenital cardiomyopathy that affects both children and adults. Since the clinical manifestations are not sufficient to establish diagnosis, echocardiography is the diagnostic tool that makes it possible to document ventricular non-compaction and establish prognostic factors. We report a 47-year-old woman with a history of dilated cardiomyopathy with unknown etiology. Echocardiography showed mild left ventricular enlargement with severe systolic dysfunction (EF = 20-25%. According to cardiac magnetic resonance imaging findings non-compaction left ventricle with hypertrophic cardiomyopathy was considered, and right ventricular septal biopsy was recommended. Right ventricular endomyocardial biopsy showed moderate hypertrophy of cardiac myocytes with foci of myocytolysis and moderate interstitial fibrosis. No evidence of infiltrative deposition was seen.

Zahra Alizadeh-Sani

2011-12-01

332

Echocardiographic assessment of subclinical left ventricular eccentric hypertrophy in adult-onset GHD patients by geometric remodeling: an observational case-control study  

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Full Text Available Abstract Background Most patients with growth hormone deficiency (GHD show high body mass index. Overweight subjects, but GHD patients, were demonstrated to have high left ventricular mass index (LVMi and abnormal LV geometric remodeling. We sought to study these characteristics in a group of GHD patients, in an attempt to establish the BMI-independent role of GHD. Methods Fifty-four patients, 28 F and 26 M, aged 45.9 ± 13.1, with adult-onset GHD (pituitary adenomas 48.2%, empty sella 27.8%, pituitary inflammation 5.5%, cranio-pharyngioma 3.7%, not identified pathogenesis 14.8% were enrolled. To minimize any possible interferences of BMI on the aim of this study, the control group included 20 age- and weight-matched healthy subjects. The LV geometry was identified by the relationship between LVMi (cut-off 125 g/m2 and relative wall thickness (cut-off 0.45 at echocardiography. Results There was no significant between-group difference in resting cardiac morphology and function, nor when considering age-related discrepancy. The majority of patients had normal-low LVM/LVMi, but about one fourth of them showed higher values. These findings correlated to relatively high circulating IGF-1 and systolic blood pressure at rest. The main LV geometric pattern was eccentric hypertrophy in 22% of GHD population (26% of with severe GHD and in 15% of controls (p = NS. Conclusion Though the lack of significant differences in resting LV morphology and function, about 25% of GHD patients showed high LVMi (consisting of eccentric hypertrophy, not dissimilarly to overweight controls. This finding, which prognostic role is well known in obese and hypertensive patients, is worthy to be investigated in GHD patients through wider controlled trials.

Trimarchi Francesco

2006-02-01

333

Hyperglycemia and nocturnal systolic blood pressure are associatedwith left ventricular hypertrophy and diastolic dysfunction in hypertensive diabetic patients  

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Abstract Background The aim of this study was to determine if hypertensive type 2 diabetic patients, when compared to patients with essential hypertension have an increased left ventricular mass index (LVMI) and a worse diastolic function, and if this fact would be related to 24-h pressoric levels changes. Methods Ninety-one hypertensive patients with type 2 diabetes mellitus (DM) (group-1 [G1]), 59 essential hypertensive patients (group-2 [G2]) and 26 healthy c...

Felício João S; Pacheco Juliana T; Ferreira Sandra R; Plavnik Frida; Moisés Valdir A; Kohlmann Oswaldo; Ribeiro Artur B; Zanella Maria T

2006-01-01

334

Vitamin D therapy to reduce blood pressure and left ventricular hypertrophy in resistant hypertension: randomized, controlled trial.  

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Low 25-hydroxyvitamin D levels are associated with higher prevalent blood pressure. We tested whether high-dose intermittent oral vitamin D therapy could reduce blood pressure and left ventricular mass in patients with hypertension resistant to conventional treatment. We conducted a parallel-group, double-blind, randomized placebo-controlled trial. Patients with supine office blood pressure >140/90 mm Hg on ?3 antihypertensive agents received 100 000 U oral vitamin D3 or matching placebo every 2 months. Office and 24-hour ambulatory blood pressure, glucose, and cholesterol were measured at baseline, 2, 4, and 6 months; left ventricular mass index was measured by cardiac MRI on a subgroup at baseline and 6 months. The primary outcome was mean 24-hour ambulatory blood pressure at 6 months. A total of 68 participants were randomized, 34 in each group. Mean age was 63 (SD 11) years, mean baseline office blood pressure was 154/84 (13/10) mm Hg, and mean baseline 25-hydroxyvitamin D level was 42 (16) nmol/L. Treatment with vitamin D did not reduce 24-hour ambulatory blood pressure (adjusted treatment effects: systolic, +3 mm Hg; 95% confidence interval, -4 to +11; P=0.33; diastolic, -2 mm Hg; 95% confidence interval, -6 to +2; P=0.29); similar results were seen for office blood pressure. Left ventricular mass index was measured in a subgroup (n=25); no reduction was seen with vitamin D treatment (adjusted treatment effect, +4 g/m(2); 95% confidence interval, 0 to +7; P=0.04). There was no significant change in cholesterol or glucose levels. Thus, 6 months of intermittent, high-dose oral vitamin D3 did not reduce blood pressure or left ventricular mass in patients with resistant hypertension. PMID:24420547

Witham, Miles D; Ireland, Sheila; Houston, J Graeme; Gandy, Stephen J; Waugh, Shelley; Macdonald, Thomas M; Mackenzie, Isla S; Struthers, Allan D

2014-04-01

335

Negative association of endothelial nitric oxide gene polymorphism with hypertension in Turkish patients: effect of ecNOS polymorphism on left ventricular hypertrophy  

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Full Text Available Abstract Background Endothelial nitric oxide synthase produces nitric oxide which is involved in many physiologic regulatory functions. Variable number of tandem repeats in intron 4 of endothelial nitric oxide synthase gene are reported to be associated with blood pressure regulation. Nitric oxide is involved in regulation of cardiomyocyte genes but it is not known If endothelial nitric oxide synthase 4 gene polymorphisms are related with left ventricular hypertrophy. We studied endothelial nitric oxide synthase 4a/b allele status in hypertensive and normotensive patients and echocardiographic parameters in a subgroup of hypertensive group. Methods We performed a case-control study involving 110 Turkish hypertensive patients and 87 controls. All subjects were genotyped for endothelial nitric oxide synthase 4a/b polymorphism. Echocardiographic measurements were obtained in 94 of the hypertensive patients. Results Endothelial nitric oxide synthase 4a/b genotype frequencies were 6.4%, 23.6%, 70% in hypertensives and 1.1%, 18.4%, 80.5% in controls for a/a, a/b, b/b, respectively. Left ventricular dimensions, mass and diastolic indices were not different across endothelial nitric oxide synthase 4 genotypes. Patients with 4a/a genotype had higher interventricular septal thickness than the other group; 14.83(1.6, 11.91(1.51, 12.21(1.56 for a/a, a/b, b/b, respectively and p = 0.0001. Conclusion Endothelial nitric oxide synthase 4a/b gene polymorphism is not associated with hypertension in Turkish patients. 4a/a genotype was associated with higher interventricular septal thickness in hypertensive patients.

Arslan Erol

2006-08-01

336

Índice tornozelo-braquial e hipertrofia ventricular na hipertensão arterial Índice tobillo-braquial y hipertrofia ventricular en la hipertensión arterial Ankle-brachial index and ventricular hypertrophy in arterial hypertension  

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Full Text Available O Índice Tornozelo-Braquial (ITB é marcador de doença arterial obstrutiva periférica. Raros relatos correlacionam esse índice com hipertrofia ventricular esquerda (HVE, capacidade funcional (CF e escore de risco coronariano de Framingham (ERCF. O objetivo do trabalho foi verificar a correlação entre ITB, HVE, CF e ERCF em homens com hipertensão arterial (HA. Estudo prospectivo e transversal de pacientes do sexo masculino (n = 40, com idade média de 57,92 ± 7,61 anos, sem complicações cardiovasculares. Essa população foi submetida às medidas de ITB, ecocardiograma (ECO, teste ergométrico (TE e exames laboratoriais. O ITB (direito e esquerdo foi considerado anormal quando a relação entre a maior média das pressões sistólicas dos tornozelos e dos braços foi inferior ou igual a 0,9 ou superior a 1,3 mmHg. A HVE foi identificada pelo ECO transtorácico; e a CF, pelo TE. Amostras sanguíneas periféricas foram colhidas para o cálculo do ERCF. Valores normais de ITB foram encontrados em 33 pacientes (82,5%, os quais foram incluídos no Grupo I; sete pacientes (17,5% com ITB anormal constituíram o Grupo II. Os índices de massa do índice de massa do ventrículo esquerdo (IMVE ao ECO foram de 111,18 ± 34,34 g/m² (Grupo I e de 150,29 ± 34,06 g/m2 (Grupo II (p = 0,009. A prevalência de HVE foi de 4% (Grupo I e de 35,3% (Grupo II (p = 0,01, constatando-se diferenças significativas entre os grupos. Quanto à CF no TE, não se registrou diferença entre os grupos. Em relação ao ERCF, a média do Grupo I foi inferior à média do Grupo II: 13,18 ± 2,11 versus 15,28±1,79 (p = 0,019. Em HA, a presença de HVE definida pelo IMVE esteve mais presente nos casos com ITB anormal, identificando maior risco cardiovascular.El Índice Tobillo-Braquial (ITB es un marcador de enfermedad arterial obstructiva periférica. Raros relatos correlacionan ese índice con la hipertrofia ventricular izquierda (HVI, capacidad funcional (CF y puntación de riesgo coronario de Framingham (PRCF. El objetivo de este estudio fue verificar la correlación entre ITB, HVI, CF y PRCF en hombres con hipertensión arterial (HA. Estudio prospectivo y transversal de pacientes del sexo masculino (n = 40, con edad promedio de 57,92 ± 7,61 años, sin complicaciones cardiovasculares. Esa población fue sometida a las medidas de ITB, ecocardiograma (ECO, test ergométrico (TE y exámenes de laboratorio. El ITB (derecho e izquierdo, se consideró anormal cuando la relación entre la mayor media de las presiones sistólicas de los tobillos y de los brazos fue inferior o igual a 0,9 o superior a 1,3 mmHg. La HVI fue identificada por el ECO transtorácico; y la CF por el TE. Muestras sanguíneas periféricas se recogieron para el cálculo del PRCF. Valores normales de ITB fueron encontrados en 33 pacientes (82,5%, los cuales se incluyeron en el Grupo I; siete pacientes (17,5% con ITB anormal formaron el Grupo II. Los índices de masa del índice de masa del ventrículo izquierdo (IMVI al ECO fueron de 111,18 ± 34,34 g/m² (Grupo I y de 150,29 ± 34,06 g/m² (Grupo II (p = 0,009. La prevalencia de HVI fue de 4% (Grupo I y de 35,3% (Grupo II (p = 0,01, siendo comprobadas las diferencias significativas entre los grupos. En cuanto a la CF en el TE, no se registró ninguna diferencia entre los grupos. Con relación al PRCF, el promedio del Grupo I quedó por debajo del promedio del Grupo II: 13,18 ± 2,11 versus 15,28±1,79 (p = 0,019. En HA, la presencia de HVI definida por el IMVI estuvo más presente en los casos con ITB anormal, identificando un mayor riesgo cardiovascular.The ankle-brachial index (ABI is a marker of peripheral arterial disease. Very few reports have correlated this index with left ventricular hypertrophy (LVH, functional capacity (FC and Framingham risk score (FRS. The objective of this study was to verify the correlation between ABI, LVH, FC and FRS in men with arterial hypertension (AH. Prospective and cross-sectional study of male patients (n = 40 with a mean age of 57.92 ± 7.61 years and no cardiovascula

Pedro Ferreira de Albuquerque

2012-01-01

337

Índice tornozelo-braquial e hipertrofia ventricular na hipertensão arterial / Ankle-brachial index and ventricular hypertrophy in arterial hypertension / Índice tobillo-braquial y hipertrofia ventricular en la hipertensión arterial  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: Portuguese Abstract in portuguese O Índice Tornozelo-Braquial (ITB) é marcador de doença arterial obstrutiva periférica. Raros relatos correlacionam esse índice com hipertrofia ventricular esquerda (HVE), capacidade funcional (CF) e escore de risco coronariano de Framingham (ERCF). O objetivo do trabalho foi verificar a correlação e [...] ntre ITB, HVE, CF e ERCF em homens com hipertensão arterial (HA). Estudo prospectivo e transversal de pacientes do sexo masculino (n = 40), com idade média de 57,92 ± 7,61 anos, sem complicações cardiovasculares. Essa população foi submetida às medidas de ITB, ecocardiograma (ECO), teste ergométrico (TE) e exames laboratoriais. O ITB (direito e esquerdo) foi considerado anormal quando a relação entre a maior média das pressões sistólicas dos tornozelos e dos braços foi inferior ou igual a 0,9 ou superior a 1,3 mmHg. A HVE foi identificada pelo ECO transtorácico; e a CF, pelo TE. Amostras sanguíneas periféricas foram colhidas para o cálculo do ERCF. Valores normais de ITB foram encontrados em 33 pacientes (82,5%), os quais foram incluídos no Grupo I; sete pacientes (17,5%) com ITB anormal constituíram o Grupo II. Os índices de massa do índice de massa do ventrículo esquerdo (IMVE) ao ECO foram de 111,18 ± 34,34 g/m² (Grupo I) e de 150,29 ± 34,06 g/m2 (Grupo II) (p = 0,009). A prevalência de HVE foi de 4% (Grupo I) e de 35,3% (Grupo II) (p = 0,01), constatando-se diferenças significativas entre os grupos. Quanto à CF no TE, não se registrou diferença entre os grupos. Em relação ao ERCF, a média do Grupo I foi inferior à média do Grupo II: 13,18 ± 2,11 versus 15,28±1,79 (p = 0,019). Em HA, a presença de HVE definida pelo IMVE esteve mais presente nos casos com ITB anormal, identificando maior risco cardiovascular. Abstract in spanish El Índice Tobillo-Braquial (ITB) es un marcador de enfermedad arterial obstructiva periférica. Raros relatos correlacionan ese índice con la hipertrofia ventricular izquierda (HVI), capacidad funcional (CF) y puntación de riesgo coronario de Framingham (PRCF). El objetivo de este estudio fue verific [...] ar la correlación entre ITB, HVI, CF y PRCF en hombres con hipertensión arterial (HA). Estudio prospectivo y transversal de pacientes del sexo masculino (n = 40), con edad promedio de 57,92 ± 7,61 años, sin complicaciones cardiovasculares. Esa población fue sometida a las medidas de ITB, ecocardiograma (ECO), test ergométrico (TE) y exámenes de laboratorio. El ITB (derecho e izquierdo), se consideró anormal cuando la relación entre la mayor media de las presiones sistólicas de los tobillos y de los brazos fue inferior o igual a 0,9 o superior a 1,3 mmHg. La HVI fue identificada por el ECO transtorácico; y la CF por el TE. Muestras sanguíneas periféricas se recogieron para el cálculo del PRCF. Valores normales de ITB fueron encontrados en 33 pacientes (82,5%), los cuales se incluyeron en el Grupo I; siete pacientes (17,5%) con ITB anormal formaron el Grupo II. Los índices de masa del índice de masa del ventrículo izquierdo (IMVI) al ECO fueron de 111,18 ± 34,34 g/m² (Grupo I) y de 150,29 ± 34,06 g/m² (Grupo II) (p = 0,009). La prevalencia de HVI fue de 4% (Grupo I) y de 35,3% (Grupo II) (p = 0,01), siendo comprobadas las diferencias significativas entre los grupos. En cuanto a la CF en el TE, no se registró ninguna diferencia entre los grupos. Con relación al PRCF, el promedio del Grupo I quedó por debajo del promedio del Grupo II: 13,18 ± 2,11 versus 15,28±1,79 (p = 0,019). En HA, la presencia de HVI definida por el IMVI estuvo más presente en los casos con ITB anormal, identificando un mayor riesgo cardiovascular. Abstract in english The ankle-brachial index (ABI) is a marker of peripheral arterial disease. Very few reports have correlated this index with left ventricular hypertrophy (LVH), functional capacity (FC) and Framingham risk score (FRS). The objective of this study was to verify the correlation between ABI, LVH, FC and [...] F

Albuquerque, Pedro Ferreira de; Albuquerque, Pedro Henrique Oliveira de; Albuquerque, Gustavo Oliveira de; Servantes, Denise Maria; Carvalho, Saskya Meneses de; Oliveira Filho, Japy Angelini.

338

Fixed combination of valsartan and amlodipine: effects on the left ventricular hypertrophy regression, albuminuria reduction and endothelium function in hypertensive patients with metabolic syndrome  

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Full Text Available Aim. To study effects of fixed combination of valsartan and amlodipine on of left ventricular hypertrophy (LVH regression, microalbuminuria reduction and endothelium function in hypertensive patients with metabolic syndrome (MS.Materials and methods. 20 hypertensive patients (15 females and 5 males with metabolic syndrome and a history of previous ineffective antihypertensive therapy were studied. Combined antihypertensive therapy was applied during 12-24 weeks. Amlodipine and valsartan dose was 5/160 or 10/160 mg/day depending on blood pressure level. Endothelial function, blood pressure level, urinary albumin excretion and LVH regression were estimated.Results. Blood pressure reduction to the target level was revealed. There was a significant reduction in microalbuminuria by -55.3±39.2% (?=0.022 in comparison with the baseline. Endothelium-dependent vasodilation increased in 3.6±7.2% (?=0.05 in comparison with baseline, LVH decreased by -9.1±12.4 g/m2 (?=0.021.Conclusion. Therapy with fixed combination of valsartan and amlodipine results in blood pressure and microalbuminuria reduction, endothelium-dependent vasodilation improvement, LVH regression in hypertensive patients with MS. These findings show that the fixed combination of these antihypertensives has a multifaceted impact on cardiovascular risk.

Ye.I. Tarlovskaya

2010-01-01

339

Fatores e mecanismos envolvidos na hipertrofia ventricular esquerda e o papel anti-hipertrófico do óxido nítrico / Factors and mechanisms involved in left ventricular hypertrophy and the anti-hypertrophic role of nitric oxide  

Scientific Electronic Library Online (English)

Full Text Available SciELO Brazil | Language: Portuguese Abstract in portuguese A hipertrofia ventricular esquerda (HVE) ocorre em reposta à sobrecarga hemodinâmica relatada em várias condições fisiológicas e patológicas. Entretanto, ainda não está completamente elucidado se o estímulo primário para a hipertrofia é o estiramento mecânico do coração, fatores neuro-humorais, ou m [...] esmo a interação de ambos. Esses fatores são traduzidos no interior da célula como alterações bioquímicas que levam à ativação de segundos (citosólicos) e terceiros (nucleares) mensageiros que irão agir no núcleo da célula, regulando a transcrição, e finalmente determinarão a expressão gênica que induza HVE. A HVE é caracterizada por alterações estruturais decorrentes do aumento das dimensões dos cardiomiócitos, da proliferação do tecido conjuntivo intersticial e da rarefação da microcirculação coronariana. Nos últimos anos, o óxido nítrico (•NO) surgiu como um importante regulador do remodelamento cardíaco, especificamente reconhecido como um mediador anti-hipertrófico. Vários estudos têm demonstrado os alvos celulares, as vias de sinalização anti-hipertrófica e o papel funcional do •NO. Portanto, a HVE parece desenvolver-se em decorrência da perda do balanço entre as vias de sinalização pró e anti-hipertróficas. Esses novos conhecimentos sobre as vias de sinalização pró e anti-hipertróficas permitirão desenvolver novas estratégicas no tratamento das HVE patológicas. Abstract in english The left ventricular hypertrophy (LVH) occurs in response to the hemodynamic overload in some physiological and pathological conditions. However, it has not been completely elucidated whether the primary stimulation for the hypertrophy is the mechanical stretching of the heart, neurohumoral factors, [...] or even the interaction of both. These factors are translated inside the cell as biochemical alterations that lead to the activation of second (cytosolic) and third (nuclear) messengers that will act in the cell nucleus, regulating transcription, and will finally determine the genic expression that induces LVH. The LVH is characterized by structural alterations due to the increase in the cardiomyocyte dimensions, the proliferation of the interstitial connective tissue and the rarefaction of the coronary microcirculation. Recently, nitric oxide (•NO) has appeared as an important regulator of cardiac remodeling, specifically recognized as an anti-hypertrophic mediator. Some studies have demonstrated the cellular targets, the anti-hypertrophic signaling pathways and the functional role of •NO. Thus, the LVH seems to develop as a result of the loss of the balance between the pro and the anti-hypertrophic signaling pathways. This new knowledge about the pro and anti-hypertrophic signaling pathways will allow the development of new strategies in the treatment of pathological LVH.

José Antonio Dias, Garcia; Erika Kristina, Incerpi.

340

Membrane proteins of the myocytes in cardiac overload  

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1 Hypertrophy of the cardiac myocytes resulting from a mechanical overload may be responsible for major membraneous modifications, either at the sarcolemmal or at the sarcoplasmic level. In this study several sarcolemmal markers such as ?-adrenoceptors, muscarinic receptors or (Na+,K+)-ATPase were investigated in an experimental model of cardiac hypertrophy, the chronic aortic stenosis in adult rats.

Mansier, Pascal; Chevalier, Brigitte; Mayoux, Eric; Charlemagne, Danie?le; Ollivier, Laurence; Amrani, Francine Callens-el; Swynghedauw, Bernard

1990-01-01

 
 
 
 
341

Left ventricular mechanical and energetic changes in long-term isoproterenol-induced hypertrophied hearts of SERCA2a transgenic rats.  

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Overexpression of cardiac sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) has been suggested as a strategic intervention for cardiac failure. However, its benefit in wild-type (WT) rats with normal SERCA2a levels seems to be small. To investigate whether it would be beneficial in a cardiac failure model with down-regulated SERCA2a levels, we made a cardiac hypertrophy model using isoproterenol infusion (1.2mgkg(-1)day(-1) for 1 or 4weeks; TG-ISO1w and TG-ISO4w, respectively) in SERCA2a transgenic (TG) rats and compared these rats with littermate WT rats that underwent the same treatments (WT-ISO1w and WT-ISO4w). We analyzed the left ventricular (LV) mechanoenergetics in the excised heart using our original cross-circulation system. The downward shift of curvilinear LV end-systolic pressure-volume relations (ESPVRs) observed in WT-ISO4w rats was abolished in TG-ISO4w rats. The slope and VO2 intercept of the VO2 (myocardial oxygen consumption per beat)-PVA (systolic pressure-volume area: total mechanical energy per beat) linear relation did not differ in any of the groups. The most important finding was a significantly smaller O2 cost of LV contractility in the TG-ISO4w group, which means that less O2 is needed to exert the same LV contractility, compared with the other groups. The increased ratio of SERCA2a/phospholamban returned to the level of the WT-control group only in the TG-ISO4w group. Longer-term up-regulation of mitochondrial transcription factor A for genes of mitochondrial enzymes producing ATP was observed in TG rats. In conclusion, longer-term overexpression of SERCA2a will be beneficial in the present cardiac failure model with down-regulated SERCA2a levels. PMID:23458361

Mitsuyama, Shinichi; Takeshita, Daisuke; Obata, Koji; Zhang, Guo-Xing; Takaki, Miyako

2013-06-01

342

Prognostic usefulness of left ventricular hypertrophy by electrocardiography in patients with atrial fibrillation (from the Randomized Evaluation of Long-Term Anticoagulant Therapy Study).  

Science.gov (United States)

It is unknown whether left ventricular hypertrophy (LVH) diagnosis by electrocardiography improves risk stratification in patients with atrial fibrillation (AF). We investigated the prognostic impact of LVH diagnosis by electrocardiography in a large sample of anticoagulated patients with AF included in the Randomized Evaluation of Long-Term Anticoagulant Therapy (RE-LY) Study. We defined electrographic LVH (ECG-LVH) by strain pattern or Cornell voltage (R wave in aVL plus S wave in V3) >2.0 mV (women) or >2.4 mV (men). LVH prevalence was 22.7%. During a median follow-up of 2.0 years, 303 patients developed a stroke, 778 died (497 from cardiovascular causes), and 140 developed a myocardial infarction. LVH was associated with a greater risk of stroke (1.99% vs 1.32% per year, hazard ratio [HR] 1.51, 95% confidence interval [CI] 1.18 to 1.93, p <0.001), cardiovascular death (4.52% vs 1.80% per year, HR 2.56, 95% CI 2.14 to 3.06, p <0.0001), all-cause death (6.03% vs 3.11% per year, HR 1.95, 95% CI 1.68 to 2.26, p <0.0001), and myocardial infarction (1.11% vs 0.55% per year, HR 2.07, 95% CI 1.47 to 2.92, p <0.0001). In multivariate analysis, the prognostic value of LVH was additive to CHA2DS2-VASc score and other covariates. The category-free net reclassification index and integrated discrimination improvement increased significantly after adding LVH to multivariate models. In conclusion, our study demonstrates for the first time that ECG-LVH, a simple and easily accessible prognostic indicator, improves risk stratification in anticoagulated patients with AF. PMID:24359765

Verdecchia, Paolo; Reboldi, Gianpaolo; Di Pasquale, Giuseppe; Mazzotta, Giovanni; Ambrosio, Giuseppe; Yang, Sean; Pogue, Janice; Wallentin, Lars; Ezekowitz, Michael D; Connolly, Stuart J; Yusuf, Salim

2014-02-15

343

False-positive defects in technetium-99m sestamibi myocardial single-photon emission tomography in healthy athletes with left ventricular hypertrophy  

International Nuclear Information System (INIS)

Exercise ECG and myocardial single-photon emission tomography (SPET) are fundamental in the non-invasive evaluation of patients suspected of having coronary artery disease (CAD). The purpose of the present study was to investigate the influence of physiological left ventricular hypertrophy (LVH) on myocardial sestamibi SPET in healthy young and old athletes. Eighteen young male elite athletes (ten rowers, five power/weight lifters and three triathletes) and 14 well-trained elderly rowers were studied. All underwent a bicycle test as part of a 2-day sestamibi SPET protocol. Attenuation correction was not performed. The studies were evaluated visually and quantitatively analysed by the CEqual program with its reference files and with a file from a local non-athletic age-matched population. Echocardiographic LVH was an inclusion criterion in the young athletes. Exercise ECG was normal in all subjects. In at least three of the young athletes a reversible defect was observed by visual analysis. On quantitative analysis one-third of the young athletes had ''significant'' (>10 pixels) defects compared with both the local reference base and the CEqual reference population. Nearly all defects were found in the anterior or inferior wall. The remaining subjects, including all old rowers, had normal SPET findings. Anterior and inferior wall defects are so common in healthy athletes with physiological LVH that the specificity of myocardial SPET, in contrast to exercise ECG, seems to be too low for evaluation of chest pain in this group. The mechanism of anterior and inferior defects may be related to hot spots (papillary muscles?) in the lateral wall. The specificity of SPET is maintained in athletes without LVH. (orig.)

1998-09-01

344

Cardiac-specific Traf2 overexpression enhances cardiac hypertrophy through activating AKT/GSK3? signaling.  

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Tumor necrosis factor superfamily ligands provoke a dilated cardiac phenotype signal through a common scaffolding protein termed tumor necrosis factor receptor-associated factor 2 (Traf2); however, Traf2 signaling in the adult mammalian cardiac hypertrophy is not fully understood. This study was aimed to identify the effect of Traf2 on cardiac hypertrophy and the underlying mechanisms. A significant up-regulation of Traf2 expression was observed in mice failing hearts. To further investigate the role of Traf2 in cardiac hypertrophy, we used cultured neonatal rat cardiomyocytes with gain and loss of Traf2 function and cardiac-specific Traf2-overexpressing transgenic (TG) mice. In cultured cardiomyocytes, Traf2 positively regulated angiotensin II (Ang II)-mediated hypertrophic growth, as detected by [(3)H]-Leucine incorporation, cardiac myocyte area, and hypertrophic marker protein levels. Cardiac hypertrophy in vivo was produced by constriction of transverse aortic (TAC) in TG mice and their wild-type controls. The extent of cardiac hypertrophy was evaluated by echocardiography as well as by pathological and molecular analyses of heart samples. Traf2 overexpression in the heart remarkably enhanced cardiac hypertrophy, left ventricular dysfunction in mice in response to TAC. Further analysis of the signaling pathway in vitro and in vivo suggested that these adverse effects of Traf2 were associated with the activation of AKT/glycogen synthase kinase 3? (GSK3?). The present study demonstrates that Traf2 serves as a novel mediator that enhanced cardiac hypertrophy by activating AKT/GSK3? signaling. PMID:24378234

Huang, Yinqing; Wu, Dengyin; Zhang, Xin; Jiang, Minghua; Hu, Chaohui; Lin, Jiangfeng; Tang, Jifei; Wu, Lianpin

2014-02-25

345

Fast diastolic swinging motion of the mitral valve as a clinical marker of familial hypertrophic cardiomyopathy in genetically affected young children without left ventricular hypertrophy: a new role for noninvasive imaging?  

Science.gov (United States)

Structural mitral valve (MV) abnormalities are common in patients with hypertrophic cardiomyopathy (HCM). This is the first report demonstrating MV abnormalities in very young children as the sole overt clinical feature of a known HCM-causing sarcomere protein gene mutation. Due to MV leaflet elongation, we also noticed a typical fast diastolic swinging motion of the MV in our patients. This novel echocardiographic feature may be used as a clinical marker of HCM disease in the absence of left ventricular hypertrophy. PMID:23557229

Udink ten Cate, Floris E A; Junghaenel, Shino; Brockmeier, Konrad; Sreeram, Narayanswami

2013-08-01

346

Relación entre hiperinsulinemia, disfunción diastólica e hipertrofia del ventrículo izquierdo en pacientes con hipertensión arterial sistémica Association of hyperinsulinemia with left ventricular hypertrophy and diastolic dysfunction in patients with hypertension  

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Full Text Available Background: Hypertension is the main independent cardiovascular risk factor. However, there are additional factors that induce organic damage. Aim: To assess the association between hyperinsulinemia, ventricular hypertrophy and left ventricular diastolic function. Patients and Methods: Seventy-four patients aged 30 to 65 years, with mild or moderate systemic hypertension, with overweight or mild obesity and normal glucose tolerance curve (GTC, were studied. Serum insulin was measured during GTC. The maximum levels of insulin and glucose were observed 60 minutes after the oral glucose load and they were expressed as rG/1. Patients were stratified in three groups according to their glucose and insulin fasting levels (I0 and post-glucose challenge levels (rG/I: Group 1 (normoinsulinemic patients I0 2 (2.45+0.4. Group 2 (post-prandial hyperinsulinemic patients I0 17 mU/mL and <1 (0.7+0.3. Left ventricular mass and its diastolic function were measured by Doppler echocardiography. Results: No differences in blood pressure or age were observed between groups. There was a negative correlation between ventricular mass and rG/1 (r =-0.282, p =0.015. Left ventricular diastolic dysfunction was significantly more deteriorated in group 3, as compared with group 1 (p <0.001 ANOVA. There was a significant correlation between g/GI and diastolic dysfunction (r =0.232 p =0.047. Conclusions: Fasting, post challenge hyperinsulinemia and a rG/I <1 are associated with higher ventricular mass and left ventricular diastolic dysfunction, independent of blood pressure and age (Rev Méd Chile 2007; 135: 1125-31

Ernesto Germán Cardona-Muñoz

2007-09-01

347

Impact of alcohol habits and smoking on the risk of new-onset atrial fibrillation in hypertensive patients with ECG left ventricular hypertrophy: The LIFE Study  

DEFF Research Database (Denmark)

Abstract Background. The incidence of new-onset atrial fibrillation (AF) is increased by uncontrolled hypertension, and antihypertensive treatment reduces new-onset AF. However, it is unclear whether alcohol intake and smoking influence the risk of new-onset AF during antihypertensive treatment. Methods. In the Losartan Intervention For Endpoint reduction in Hypertension (LIFE) study, a double-blinded, randomized, parallel-group study, 9193 hypertensive patients with electrocardiogram (ECG)-documented left ventricular hypertrophy (LVH), randomized to once-daily losartan- or atenolol-based antihypertensive therapy were followed for a mean of 4.8 years. At baseline, 8831 patients (54% women, mean age 67 years, mean blood pressure 174/98 mmHg after placebo run-in) had neither a history of AF nor AF on ECG, and they were thus at risk of developing this condition during the study. Results. New-onset AF occurred in 353 (4%) patients. Univariate Cox analyses showed that intake of alcohol > 10 units/week compared with less or no alcohol intake predicted new-onset AF (Hazard ratio, HR = 1.60 [95% CI 1.02-2.51], p = 0.043). Multivariate Cox regression analysis showed that intake of alcohol > 10 units/week predicted new-onset AF (p = 0.010) independently of most other univariate predictors, except when also baseline serum cholesterol, serum potassium and urinary albumin/creatinine ratio were included in the model (HR = 1.60 [95% CI 0.94-2.72], p = 0.081). Impact of smoking was not significant in Cox univariate or multivariate analyses, and there were no significant interactions between high alcohol intake and either smoking or gender on the risk of getting AF. Conclusions. Up to 10 drinks of alcohol per week appears to be safe with respect to the risk for AF in hypertensive patients with LVH. Our data suggest that alcohol intake above this level may be marginally deleterious, while no effect of smoking on risk of AF was detected in hypertensive patients with LVH.

Ariansen, Inger; Reims, Henrik M

2012-01-01

348

New frontiers in heart hypertrophy during pregnancy  

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During Pregnancy, heart develops physiological left ventricular hypertrophy as a result of the natural volume overload. Previously we have characterized the molecular and functional signature of heart hypertrophy during pregnancy. Cardiac hypertrophy during pregnancy is a complex process that involves many changes including in the signalling pathways, composition of extracellular matrix as well as the levels of sex hormones. This review summarises the recent advances and the new frontiers in ...

Li, Jingyuan; Umar, Soban; Amjedi, Marjan; Iorga, Andrea; Sharma, Salil; Nadadur, Rangarajan D.; Regitz-zagrosek, Vera; Eghbali, Mansoureh

2012-01-01

349

Visualization of hypertrophied papillary muscle mimicking left ventricular mass on gated blood pool and T1-201 myocardial perfusion imaging  

International Nuclear Information System (INIS)

A sixty-year old man with acute myocardial infarction was incidentally found to have a hypertrophied anterolateral papillary muscle (ALPPM) of the left ventricle on gated blood pool (GBP) and T1-201 myocardial perfusion images. Hypertrophy of the ALPPM was visualized as a movable defect in the lateral basal area on GBP imaging throughout the cardiac cycle and on the TI-201 study as a radionuclide accumulating structure, consistent with the defect in the GBP. A combination of these findings may suggest the presence of a hypertrophied papillary muscle of the left ventricle

1981-01-01

350

Simvastatin Modulates Remodeling of Kv4.3 Expression in Rat Hypertrophied Cardiomyocytes  

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Full Text Available Objectives: Hypertrophy has been shown to be associated with arrhythmias which can be caused by abnormal remodeling of the Kv4-family of transient potassium channels. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins have recently been shown to exert pleiotropic protective effects in cardiovascular diseases, including anti-arrhythmias. It is hypothesized that remodeling of Kv4.3 occurs in rat hypertrophied cardiomyocytes and is regulated by simvastatin.Methods: Male Sprague-Dawley rats and neonatal rat ventricular myocytes (NRVMs underwent abdominal aortic banding (AAB for 7 weeks and angiotensin II (AngII treatment, respectively, to induce cardiac hypertrophy. Kv4.3 expression by NRVMs and myocardium (subepicardial and subendocardial in the left ventricle was measured. The transient outward potassium current (Ito of NRVMs was recorded using a whole-cell patch-clamp method.Results: Expression of the Kv4.3 transcript and protein was significantly reduced in myocardium (subepicardial and subendocardial in the left ventricle and in NRVMs. Simvastatin partially prevented the reduction of Kv4.3 expression in NRVMs and subepicardial myocardium but not in the subendocardial myocardium. Hypertrophied NRVMs exhibited a significant reduction in the Ito current and this effect was partially reversed by simvastatin.Conclusions: Simvastatin alleviated the reduction of Kv4.3 expression, Ito currents in hypertrophied NRVMs and alleviated the reduced Kv4.3 expression in subepicardial myocardium from the hypertrophied left ventricle. It can be speculated that among the pleiotropic effects of simvastatin, the anti-arrhythmia effect is partly mediated by its effect on Kv4.3.

Feifei Su, Miaoqian Shi, Zhiqiang Yan, Dongbo Ou, Juntang Li, Zifan Lu, Qiangsun Zheng

2012-01-01

351

Mechanisms of atrial and brain natriuretic peptide release from rat ventricular myocardium: effect of stretching.  

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Ventricular hypertrophy is characterized by augmentation of the synthesis and storage of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). To evaluate in vitro the cellular mechanisms of immunoreactive ANP (IR-ANP) and BNP (IR-BNP) release from ventricular cardiocytes, we measured the secretory response to graded passive myocardial stretch in isolated atrialectomized perfused hypertrophied hearts of 14- to 18-month-old spontaneously hypertensive rats. At this age, the ventricular levels of both IR-ANP and IR-BNP were markedly higher in spontaneously hypertensive (182 +/- 27 and 32 +/- 3 pmol/ventricle, respectively) than in age-matched normotensive Wistar-Kyoto rats (35 +/- 4 and 12 +/- 1 pmol/ventricle, respectively; P stretch was examined by increasing the volume of the intraventricular balloon for 10 min. Stretching of the hypertrophied ventricles produced a rapid transient (from 1-5 min) increase in both IR-ANP and IR-BNP secretion. As left ventricular pressure rose from 0 to 26 +/- 1 mm Hg, IR-ANP and IR-BNP release into the perfusion fluid increased 1.8 +/- 0.4- and 2.5 +/- 0.2-fold, respectively. Infusion of staurosporine, known to inhibit protein kinase-C activity in heart cells, blocked the stretch-induced increase in IR-ANP release (F = 3.10; P stretch-stimulated (F = 1.47; P = NS) IR-ANP release from hypertrophied rat myocardium.