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At least 37 records · Page 2Linked to original sources
PubMed1994

Myocyte cellular hypertrophy is responsible for ventricular remodelling in the hypertrophied heart of middle aged individuals in the absence of cardiac failure.

OBJECTIVE: The aim was to measure changes in the numbers and size of ventricular myocytes in human hearts with marked ventricular hypertrophy and no clear signs of cardiac failure, to determine whether myocyte cellular hypertrophy is the only factor involved in the increase in cardiac mass. METHODS: Morphometric techniques were applied to estimate the number of myocyte nuclei per unit volume of myocardium which, in combination with the determination of the volume percent of myocytes, allowed the computation of the average myocyte cell volume per nucleus and total number of myocyte nuclei in the ventricles. Subsequently, the volume fraction of replacement fibrosis in the tissue was assessed and absolute component volumes in the ventricles obtained. RESULTS: Eight hypertrophied human hearts, weight 561(SD 68) g, were collected at necropsy from hypertensive patients who died from non-cardiac causes and were compared with eight normal hearts, weight 387(37) g, obtained from healthy individuals who also died from non-cardiac causes. With cardiac hypertrophy, left and right ventricular weight increased by 53% and 57%, whereas myocyte cell volume increased by 112% and 84%, respectively. The disproportion between the increase in ventricular weight and the increase in myocyte volume was due to a 30% and 16% loss in left and right ventricular myocytes following hypertensive hypertrophy. Myocyte loss also provoked a 319% and a 188% increase in the amount of replacement fibrosis in the left and right ventricular myocardium. These tissue and cellular processes resulted in an expansion in ventricular mass which exceeded the thickening of the wall so that an increase in cavitary volume occurred in both ventricles. CONCLUSIONS: Myocyte cellular hypertrophy is responsible for ventricular hypertrophy in hypertensive cardiomyopathy in its compensated stage. Myocyte loss precedes the impairment in ventricular pump function and may be implicated in the initiation of ventricular maladaptation.

Cardiomegaly↗
PubMed1993

Transition from compensated hypertrophy to intrinsic myocardial dysfunction during development of left ventricular pressure-overload hypertrophy in conscious sheep. Systolic dysfunction precedes diastolic dysfunction.

BACKGROUND: Patients with aortic stenosis have a period of compensated left ventricular hypertrophy but may eventually develop congestive heart failure. Previous experimental studies showed either normal myocardial contractility in mild short-term pressure overload or myocardial dysfunction with severe pressure overload. Transition from compensated left ventricular hypertrophy to myocardial dysfunction has not been experimentally demonstrated in an adult large animal. Controversial issues in pressure-overload hypertrophy include whether the left ventricular dysfunction is due to insufficient hypertrophy (afterload mismatch) or to intrinsic myocardial dysfunction and whether diastolic dysfunction precedes systolic dysfunction. METHODS AND RESULTS: We induced left ventricular hypertrophy (41% increase in left ventricular to body weight ratio) by gradually tightening a hydraulic constrictor around the ascending aorta in 9 chronically instrumented conscious sheep. Afterload (end-systolic stress) elevation remained constant (approximately 33% greater than baseline) by adjustment of the aortic constrictor over 6 weeks, gradually increasing left ventricular pressure (from 117 +/- 6 to 163 +/- 5 mm Hg) as hypertrophy developed. Four sets (baseline, 2 weeks, 4 weeks, and 6 weeks) of serial hemodynamic studies were performed in each animal with beta-blockade, first with and then without aortic constriction to mechanically match loading conditions. Stepwise methoxamine infusion was performed to obtain load-independent assessment of myocardial contractility. Midwall shortening (P < .05) and shortening rate (P < .05) at mechanically matched loading conditions showed that myocardial dysfunction developed between the fourth and the sixth week. Shortening-preload-afterload (P < .05) and shortening rate-preload-afterload (P < .05) relations, load-independent contractility indices based on the systolic myocardial stiffness concept, also revealed depressed myocardial contractility at the sixth week. Time constant of left ventricular isovolumic relaxation and diastolic myocardial stiffness constant did not change over the 6 weeks. CONCLUSIONS: Transition from normal myocardial contractility to myocardial dysfunction was demonstrated. This transition occurred even when the elevation of afterload remained constant as hypertrophy incompletely adapted to increasing left ventricular pressure. Systolic dysfunction preceded diastolic dysfunction in this model.

Adaptation, Physiological↗
PubMed1985

[Biventriculographic and clinicopathologic evaluation of apical hypertrophy: with reference to asymmetrical septal hypertrophy with hypertension].

To clarify the pathogenesis of apical hypertrophy with asymmetrical septal hypertrophy (ASH), left ventriculography in the right anterior oblique projection (LVG), biventriculography (BVG), and endomyocardial biopsy of the right ventricle were performed for patients with ASH. The patients were categorized in four groups according to ECG, LVG and BVG. Patients with hypertrophic cardiomyopathy (HCM) were divided into two subsets; (A) Apical hypertrophy group (AH: nine patients), with ECG showing left ventricular hypertrophy (LVH) and giant negative T waves (GNT), and with LV configurations showing the S or SR form at end-diastole on LVG. (B) Non-apical hypertrophy group (non-AH: 12 patients), with ECG showing LVH without GNT and LV configuration showing R form at end-diastole on LVG (cf: Fig. 1). Patients with ASH and hypertension (ASH-HT) were also divided into two subsets; (A) AH: seven patients. (B) non-AH: nine patients. Analysis of LVG and BVG: In HCM, the septal configuration showed the TS X S form in both two subset groups. The septal configuration in ASH-HT was divided into the NH form, which was clearly distinguishable from the septal configuration in HCM, and the TS X S form as in cases with HCM. In both HCM and ASH-HT, the diastolic thickness of the anterior apical wall was significantly thicker in all patients with AH than that in non AH. In HCM, the diastolic thickness of the septum and the percent systolic thickening did not significantly differ between AH and non-AH groups. In ASH-HT, the NH form showed similar diastolic thickness of the septum and % systolic thickening in AH and non-AH groups. On the other hand, the TS X S form in non-AH group showed greater thickness and lower % systolic thickening similar to those of HCM. Histological analysis of endomyocardial biopsy; In HCM, the transverse diameters of the myocytes and the biopsy scores did not differ significantly between AH and non-AH groups. In ASH-HT, the TS X S form in non-AH group had longer diameters and higher biopsy scores similar to those of HCM compared to the NH form in AH group. In conclusion, both HCM and ASH-HT may have apical hypertrophy manifested by giant negative T waves in the EKG and spade like form of left ventriculogram. In addition, apical hypertrophy in ASH-HT with the NH form of septal configuration seemed to be caused by hypertension.

Adult↗
PubMed1995

[A case of hypertensive hypertrophy in which both regression of hypertrophy and improvement of the abnormalities in iodine-123-metaiodobenzylguanidine (MIBG) myocardial imagings were observed after antihypertensive therapy].

A case of hypertensive hypertrophy is described in which both regression of hypertrophy and improvement of the abnormalities in iodine-123-metaiodobenzylguanidine (MIBG) myocardial imagings were seen after 7 months of antihypertensive therapy. A 58-year-old man was diagnosed as having essential hypertension and hypertensive hypertrophy. The patient was treated with antihypertensive drugs and showed regression of left ventricular hypertrophy on electrocardiograms and echocardiograms. MIBG observations made before and after antihypertensive therapy showed increased heart-to-mediastinum activity ratio and decreased cardiac washout ratio. Despite the many theories addressing the mechanisms of regression of left ventricular hypertrophy, the process is still unclear. In the present case, the improvement of cardiac sympathetic nervous dysfunction might have been related to the regression of left ventricular hypertrophy because the abnormality in MIBG images improved. MIBG, therefore, may be helpful in clarifying the mechanisms of the regression of hypertensive hypertrophy.

3-Iodobenzylguanidine↗
PubMed2003

Molecular determinants of myocardial hypertrophy and failure: alternative pathways for beneficial and maladaptive hypertrophy.

The implementation of molecular biological approaches has led to the discovery of single genetic variations that contribute to the development of cardiac failure. In the present review, the characteristics that are invariably associated with the development of failure in experimental animals and clinical studies are discussed, which may provide attractive biological targets in the treatment of human heart failure. Findings from the Framingham studies have provided evidence that the presence of left ventricular hypertrophy is the main risk factor for subsequent development of heart failure in man. Conventional views identify myocardial hypertrophy as a compensatory response to increased workload, prone to evoke disease. Recent findings in genetic models of myocardial hypertrophy and human studies have provided the molecular basis for a novel concept, which favours the existence of either compensatory or maladaptive forms of hypertrophy, of which only the latter leads the way to cardiac failure. Furthermore, the concept that hypertrophy compensates for augmented wall stress is probably outdated. In this article, we provide the molecular pathways that can distinguish beneficial from maladaptive hypertrophy.

Apoptosis↗
PubMed1996

Heparin and heparan sulfate block angiotensin II-induced hypertrophy in cultured neonatal rat cardiomyocytes. A possible role of intrinsic heparin-like molecules in regulation of cardiomyocyte hypertrophy.

BACKGROUND: Heparan sulfate, one of the primary components of extracellular matrix, is a potent antigrowth factor in certain types of cells. To elucidate a possible role of endogenous heparin-like molecules in regulating cardiomyocyte hypertrophy, we investigated the effects of heparin and heparan sulfate on angiotensin (Ang) II-induced hypertrophy in cultured neonatal rat cardiomyocytes. METHODS AND RESULTS: Competitive [3H]heparin binding assay showed that cardiomyocytes had specific binding sites for heparin. In situ [3H]heparin binding assay demonstrated that heparin, which rapidly bound to the cardiomyocyte surface, was subsequently accumulated around the nuclei, suggesting that heparin might work in the nucleus. Cotreatment with heparin (20 micrograms/mL) completely inhibited increased cell surface area by Ang II (10(-6) mol/L). Increased [3H]leucine incorporation by Ang II was reduced by heparin dose-dependently. The inhibitory effect of heparin on Ang II-induced cardiomyocyte hypertrophy also was confirmed by Northern blot analysis: heparin dose-dependently inhibited skeletal alpha-actin and atrial natriuretic peptide gene expression, genetic markers for cardiomyocyte hypertrophy. Heparan sulfate showed similar inhibitory effects on cell surface area, [3H]leucine incorporation, and skeletal alpha-actin gene expression. Treatment with heparinase I or III, which specifically digests the disaccharide chains of endogenous heparin-like molecules, upregulated protein synthesis and skeletal alpha-actin and atrial natriuretic peptide gene expression in cardiomyocytes. CONCLUSIONS: Our findings in this study strongly suggest that heparin and heparan sulfate are potent inhibitors of cardiomyocyte hypertrophy and that endogenous heparin-like substances negatively regulate cardiomyocyte hypertrophy.

Angiotensin II↗
PubMed2006

Endogenous inhibitors of hypertrophy in concentric versus eccentric hypertrophy.

Left ventricular (LV) hypertrophy (LVH) is an adaptive response to hemodynamic overload, but also contributes to the pathogenesis of heart failure. LVH can be concentric (cLVH) but subsequent dilatation and progression to eccentric hypertrophy (eLVH) may lead to global pump failure. Recently, several endogenous molecular inhibitors of hypertrophy have been identified. Using real-time PCR, we compared the myocardial mRNA expression of these inhibitors in pressure-overload induced cLVH (severe aortic stenosis) and in volume overload-induced eLVH (severe mitral regurgitation) in patients, and during the progression from cLVH to eLVH in pressure overload in rat. Each of these genes showed a unique temporal expression profile. Strikingly, except for SOCS-3, changes in gene expression of these negative regulators in rat cLVH and eLVH vs sham were recapitulated in human cLVH and eLVH. In particular, VDUP-1 and MCIP-1 were high in cLVH but expression levels were normal in eLVH, both in rat and human. These data indicate that during the progression of LVH, both in pressure and volume overload, expression levels of endogenous inhibitors of hypertrophy are modified and that these changes may have pathophysiological significance. In particular, MCIP-1 (the endogenous calcineurin inhibitor) and VDUP-1 (the endogenous inhibitor of thioredoxin) are potential molecular switches in the progression of LV hypertrophy.

Animals↗
PubMed2003

[Left ventricular hypertrophy in hypertension. Part II. Prognostic value of left ventricular hypertrophy].

This part of review is based on results of prospective studies of prognostic value of left ventricular hypertrophy defined by electro- or echocardiographical criteria. Increased risk of cardiovascular complications has been found to be associated with left ventricular hypertrophy detected not only by voltage ECG criteria but also by ST-segment and T-wave changes in left precordial leads. Left ventricular myocardial mass is an independent factor of prognosis too. Prognostic significance of left ventricular hypertrophy depends on echocardiographical criteria used and on age, sex, race of patients and presence of coronary heart disease. Unfavorable prognostic significance of left ventricular hypertrophy becomes evident after several years of follow-up. Concentric left ventricular remodeling is also associated with increased risk of cardiovascular complications, however its value for prognosis is inferior to that of left ventricular hypertrophy.

Echocardiography↗
PubMed2005

Hypertrophic cardiomyopathy with progression from apical hypertrophy to asymmetrical septal hypertrophy: a case report.

A 41-year-old man was referred to our hospital for further examination because of abnormal electrocardiography findings at a health-check examination. Transthoracic echocardiography showed left ventricular hypertrophy confined to the most distal portion of the left ventricle, which is a typical feature of apical hypertrophic cardiomyopathy. Ten years later, he was again admitted for the evaluation of chest pain. Echocardiography showed asymmetrical septal hypertrophy in addition to apical hypertrophy. These findings demonstrate morphologic evolution in hypertrophic cardiomyopathy from apical hypertrophy to asymmetrical septal hypertrophy.

Adult↗
PubMed1997

Rapamycin inhibits alpha 1-adrenergic receptor-stimulated cardiac myocyte hypertrophy but not activation of hypertrophy-associated genes. Evidence for involvement of p70 S6 kinase.

The 70-kD S6 kinase (p70S6K) has been implicated in the regulation of protein synthesis in many cell types and in the angiotensin II-stimulated hypertrophy of cardiac myocytes. Our purpose was to determine whether p70S6K plays a role in cardiomyocyte hypertrophy induced by the alpha 1-adrenergic receptor (alpha 1-AR) agonist phenylephrine (PE). PE stimulated the activity of p70S6K > 3-fold, and this increase was blocked by rapamycin, an immunosuppressant macrolide that selectively inhibits p70S6K. When administered for 3 days, PE stimulated a 30% increase in total protein content, a 2-fold increase in the incorporation of [14C]phenylalanine (14C-Phe) into protein, and a 50% increase in two-dimensional myocyte area. Rapamycin pretreatment (> or = 500 pg/mL) significantly inhibited each of these PE-stimulated changes. Two days of PE treatment resulted in a 1.6-fold increase in total RNA yield per dish, a 2-fold increase in incorporation of [14C]uridine into myocyte RNA, and increases in relative mRNA levels of the hypertrophy-associated atrial natriuretic factor (ANF, 2.1-fold) and skeletal alpha-actin (SK, 2.2-fold) genes. Although rapamycin abolished the PE-stimulated increases in total RNA and incorporation of [14C]uridine, it had no effect on the induction of the ANF and SK genes. LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3-K) activity, inhibited PE-stimulated increases in p70S6K activity and the incorporation of labeled precursors into myocyte protein and RNA. These results demonstrate that p70S6K is activated by the hypertrophic agent PE and that a PI3-K or PI3-K-like activity is required for p70S6K activation and myocyte hypertrophy. The data suggest that p70S6K activation may be required for PE-stimulated hypertrophy of cardiac myocytes. Our results demonstrate that intracellular signaling pathways responsible for transcriptional and translational responses diverge early after alpha 1-AR stimulation in cardiac myocytes.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2005

Delineation of sequences essential for specific promoter activation during pressure overloaded hypertrophy or factor-induced hypertrophy.

Earlier studies from our laboratory have demonstrated the appearance of a high Mr (182-kDa) phosphoprotein during early stages of development of cardiac hypertrophy in the sera of animals subjected to aortic constriction. Furthermore, it has been reported that the injection of purified 182-kDa protein into normal animals led to the development of hypertrophy, and the injection of polyclonal antibodies into the aorta constricted animals completely, abolished the development of hypertrophy, and downregulated the expression of the beta-Myosin heavy chain (MHC) gene. To identify the cis-acting regulatory element(s), which controls induction of the beta-MHC gene in acute pressure-overloaded cardiac hypertrophy induced by the 182-kDa protein, the beta-MHC promoter fragments of various lengths linked to the chloramphenicol acetyl transferase (CAT) reporter were injected into the left ventricular apex of adult rats, which underwent aortic constriction/182-kDa protein injection or were sham-operated. Activation of the beta-MHC gene by the 182-kDa protein was studied by a chimeric gene constructed by fusion of the 5' regulatory regions of the beta-MHC gene to bacterial CAT, demonstrating that at least 431 bp of the beta-MHC promoter (+103 to -328) with one E-box motif, along with upstream regulatory sequences such as the TATA box, N-Fe, C-rich, and M-CAT elements are required for beta-MHC gene expression in vivo during cardiac hypertrophy induced by the 182-kDa protein.

Animals↗
PubMed1983

[ECG features of hypertrophy in hypertrophic cardiomyopathy, with special reference to asymmetric septal hypertrophy].

Thirty-eight cases of hypertrophic cardiomyopathy associated with asymmetric septal hypertrophy (ASH) were analyzed in order to correlate the electrocardiographic findings with the distribution of hypertrophic portions identified by two-dimensional echocardiograms. The electrocardiographic features which characterize the selected cases with ASH in this study were abnormal Q waves or regression of R waves in the left precordial leads (six obstructive type and six non-obstructive type) and a pattern of left ventricular hypertrophy (LVH) (31 cases including five cases with abnormal Q waves) (Table 1). There was no significant relation between the voltage of a R wave in V1 and the degree of septal thickness. From the electrocardiographic features mentioned above, the patients were divided into two groups, i.e., 1) the patients with abnormal Q waves (12 cases) and 2) those with LVH without abnormal Q waves (26 cases). The difference in the pattern of distribution of hypertrophy was evaluated based on the presence or absence of the abnormal Q waves. The results were as follows: Although there were no differences in the degree of septal thickness in both groups, the posterior wall in the group with LVH was significantly thicker. The group with LVH showed diffuse hypertrophy in the left ventricular free wall as well as the septum. Moreover, the short-axis view of two-dimensional echocardiograms revealed that hypertrophy in the septum was diffuse in both anterior and posterior portions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Biatrial appendage hypertrophy but not ventricular hypertrophy: a unique feature of canine pacing-induced heart failure.

BACKGROUND: The canine model of pacing-induced heart failure is characterized by an absence of ventricular hypertrophy despite severe hemodynamic stress and neurohormonal activation. Given the mode of ventricular pacing, hypertrophy might occur in the atrial appendage. METHODS AND RESULTS: Seventeen dogs underwent continuous right ventricular pacing for 3 weeks to severe heart failure. Twelve normal dogs served as control subjects. Pacing produced marked increases in both pulmonary capillary wedge pressure (7.6 +/- 1.8 mmHg at baseline to 32.6 +/- 7.5 mmHg at 3 weeks, P < .001) and right atrial pressure (6.5 +/- 1.8 to 15.1 +/- 2.4 mmHg, P < .001), marked increases in normalized left ventricular volume (3.0 +/- 0.5 to 4.6 +/- 0.5 mL/kg, P < .001) and left atrial volume (1.0 +/- 0.2 to 2.6 +/- 0.5 mL/kg, P < .001), but no change in left ventricular mass (2.3 +/- 0.4 to 2.6 +/- 0.5 g/kg, differences not significant), indicating no ventricular hypertrophy. Compared to the control dogs, total heart weight in the test animals was similar, but both the left appendage (0.18 +/- 0.04 vs 0.10 +/- 0.03 g/kg, P < .001) and right atrial appendage (0.15 +/- 0.03 vs 0.12 +/- 0.02 g/kg, P = .004) were much heavier than those of the control dogs. CONCLUSIONS: Rapid right ventricular pacing in the dog induces severe heart failure associated with a dichotomous response in the atrial appendage versus the ventricle. Aside from being a useful heart failure model that simulates the human condition, this unique feature may have physiologic implications in terms of atrial mechanical and endocrine functions and have applications for future studies into the mechanisms of cardiac remodeling and hypertrophy.

Animals↗
PubMed1976

Quantitative analysis of muscle cell changes in compensatory hypertrophy and work-induced hypertrophy.

The cytological characteristics of two modes of muscle hypertrophy were studied in the extensor digitorum longus muscle of the rat. Comprensatory hypertrophy (CH) was produced by tenotomy of the tibialis anterior muscle and work-induced hypertrophy (WIH) was produced by forced swimming of the animal. While both methods produced an increase in muscle weight and cell size, these two parameters did not correlate. Morphometric analyses of the hypertrophied muscle cells demonstrated that in CH-muscle there was an increase in mitochondrial volume density, a decrease in myofibrillar volume density and no change in sarcotubular or nuclear volume density. WIH-muscle demonstrated an increase in sarcotubular volume density but no change in mitochondrial, myofibrillar or nuclear volume density. It is concluded that in CH-muscle, the cell volume increase is attributable to mitochondrial volume increase and that there is no increase in the contratile myofibrillar component of the cell. WIH-muscle, on the other hand, has a cell volume increase which is attributable to a proportional increase in these organelles.

Animals↗
PubMed1992

Effect of captopril on the prevention and regression of myocardial cell hypertrophy and interstitial fibrosis in pressure overload cardiac hypertrophy.

This article reports on the effects of captopril on both the prevention and the regression of myocardial cell hypertrophy and interstitial fibrosis in experimental animals (rats) with pressure overloaded hearts. Constriction of the abdominal aorta just below the diaphragm during periods of 20 days (prevention experiment) and 40 days (regression experiment) resulted in hypertension and cardiac hypertrophy. In the prevention experiment, captopril was able to inhibit the development of high blood pressure levels and cardiac hypertrophy in aortic-constricted rats. Similarly, the treatment of sham-operated rats with captopril led to a reduction in the weight of the heart and in the myocyte diameter compared with controls. The myocyte volume fraction of the left ventricles of both aortic-constricted and sham-operated animals that were treated with captopril was significantly diminished compared with that of the control group. The interstitial collagen volume fraction of all experimental groups was elevated as compared with the control group. As a consequence, the ratios of myocytes to interstitial collagen in groups of aortic-constricted rats, aortic-constricted rats that were treated with captopril, and sham-operated rats that were treated with captopril were reduced compared with the control group; that is, although captopril was able to prevent myocardial cell hypertrophy after aortic constriction, it could not prevent the maintenance of a normal ratio of myocytes to interstitial collagen, which was due to increased collagen volume fraction. In the regression experiment, captopril lowered high blood pressure levels and augmented heart weights to control values. The mean myocyte transverse diameter in aortic-constricted rats that were treated with captopril was significantly smaller than that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Comparison of actions of irbesartan versus atenolol on cardiac repolarization in hypertensive left ventricular hypertrophy: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA).

Left ventricular (LV) hypertrophy is associated with a substantial risk for malignant arrhythmias and sudden death. The effects of antihypertensive therapy on QT dispersion, which reflects cardiac repolarization heterogeneity, in relation to changes in LV mass has not been well studied. Repeat echocardiography and QT measurements (standard 12-lead electrocardiograms) were performed in hypertensive patients with LV hypertrophy, who were randomized double-blind to receive the angiotensin II type 1-receptor blocker irbesartan (n = 44) or the beta(1)-receptor blocker atenolol (n = 48) for 48 weeks, and in 37 matched hypertensive control subjects without LV hypertrophy. LV mass index was related to QT dispersion (r = 0.34, p <0.001). The reduction in LV mass was greater using irbesartan than using atenolol (-27 +/- 28 vs -15 +/- 21 g/m(2) at 48 weeks, p = 0.021), with similar reductions in blood pressure. Irbesartan decreased QT dispersion (from 56 +/- 24 ms to 45 +/- 20 ms at 48 weeks; p <0.001) and QTc dispersion (from 57 +/- 24 to 44 +/- 19 ms at 48 weeks; p <0.001). In contrast, atenolol had minor effects. The decreases in QT and QTc dispersions were greater using irbesartan than using atenolol (p = 0.001 and p = 0.011, respectively); the same results were found when changes in LV mass, blood pressure, and heart rate were also included in multivariate analyses. Thus, heterogeneity of ventricular repolarization is related to the degree of LV hypertrophy. Irbesartan, but not atenolol, reduces QT and QTc dispersions independent of changes in LV mass, blood pressure, or heart rate, and thus seems to induce structural and electrical remodeling in a direction that could decrease the risk of fatal events in hypertensive patients.

Adrenergic beta-Antagonists↗