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PubMed2000

Optimal antihypertensive therapy for prevention and treatment of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is considered an adaptation to a pressure load on the left ventricle and is common in hypertensive patients. The condition is a profound risk factor for cardiovascular events, greater than and independent of blood pressure. It is now recognized in hypertension management guidelines as an indication for more stringent blood pressure control. All of the first-line antihypertensive agents have been shown to variably regress LVH, but no definitive evidence yet shows that one agent is superior to others in decreasing risk independent of blood pressure control. Although some evidence suggests that reduction of LVH is associated with improved prognosis independent of blood pressure control, relative efficacy of drug classes in this regard has yet to be demonstrated. At present, recommendations for optimal therapy in hypertensive patients with LVH must rest on the presence of underlying cardiac and noncardiac conditions, with the understanding that the major classes of antihypertensive agents will probably decrease LVH.

Antihypertensive Agents↗

PubMed1992

Reversibility of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a powerful independent risk factor for coronary artery disease. This overview of 104 studies examines the ability of various types of antihypertensive therapies to reverse LVH as assessed by echocardiography. Combination therapy, angiotensin converting enzyme (ACE) inhibitors, and methyldopa were the most effective in reversing LV mass; vasodilators such as minoxidil and hydralazine had no effect on LVH. These differences were independent of the degree of fall in blood pressure and duration of therapy. beta-blockers were as effective as ACE inhibitors in decreasing LV wall thickness. Possible reasons for drug differences in reversing LVH are discussed. Preliminary evidence suggests that reversing LVH by antihypertensive drug therapy is associated with a reduction in cardiovascular complications.

Antihypertensive Agents↗

PubMed2000

The influence of antihypertensive drug treatment on the prevention and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) has been recognized as an important cardiovascular risk factor. Hypertensive disease is the most frequent background of LVH and it is generally felt that anti-hypertensive treatment should not only lower blood pressure but also cause regression of LVH. In the present survey the patho-physiology of LVH, its measurements and animal models used to study LVH are briefly discussed. Subsequently, the effects of various drugs in animal models and in human hypertensives are reviewed. It has been shown repeatedly that various types of antihypertensive drugs show differential activities on the prevention or regression of LVH. It is not only the lowering of blood pressure which determines the anti-LVH activity, but also the interaction of drugs with neuro-endocrine mechanisms such as the renin-angiotensin-aldosterone system and the sympathetic nervous system.

Animals↗

PubMed1992

Effect of diuretic therapy on hypertensive left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) has been identified as a major independent risk factor for cardiovascular morbidity in patients with essential hypertension. It is also established that antihypertensive drug therapy is associated with regression of LVH in many patients. However, it is unclear whether all antihypertensive agents are equally effective in regressing LVH and whether this process is drug-specific or primarily related to blood pressure control. There is no universal agreement on the influence of diuretics on LVH in hypertension. Several major trials have shown consistent reversal of electrocardiographic manifestations of LVH during diuretic-based therapy. The results of studies employing echocardiographic measurements have been more variable; however, most echocardiographic studies have been flawed by lack of controls or blinding, short duration of follow-up, small sample size, inclusion of patients without LVH, and lack of consideration of previous or concomitant therapy. This review provides a critical examination of the available data on both sides of the question.

Diuretics↗

PubMed2002

Are all antihypertensive drug classes equal in reducing left ventricular hypertrophy?

Left ventricular hypertrophy (LVH) is a major cardiovascular risk factor for morbidity and mortality. It is caused by arterial hypertension, although various hemodynamic and nonhemodynamic factors contribute to its development. Especially, the renin-angiotensin-aldosterone system is involved in the pathophysiology of LVH. The Treatment of Mild Hypertension study demonstrated that in mild essential hypertension, nonpharmacologic treatment is an effective tool for treating LVH. There are at least three major meta-analyses with several thousand patients examining the ability of antihypertensive drugs on the reversal of LVH. The results of these meta-analyses are very consistent. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers achieve significantly better results than b-blockers. The most recently published Losartan Intervention For Endpoint reduction in hypertension study confirmed the superiority of angiotensin receptor blockers against b-blockers in a large-scale prospective trial. It also proves for the first time that regression of LVH is associated with better cardiovascular outcome.

Angiotensin II↗

PubMed1996

Increased guanylate cyclase activity is associated with an increase in cyclic guanosine 3',5'-monophosphate in left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) produced by aortic valve plication leads to increased myocardial cyclic GMP. We tested whether this was a result of increased soluble guanylate cyclase activity or nitric oxide (NO) synthase and its functional consequences. We used the nitric oxide donor 3-morpholino-sydnonimine (SIN-1) or the NO synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME) in 12 control and 12 LVH anesthetized open-chest mongrel dogs. L-NAME (6 mg/kg) or SIN-1 (1 microgram/kg per min) was infused into the left anterior descending coronary artery and regional segment work and cyclic GMP levels were determined. In vitro myocardial guanylate cyclase sensitivity (0.43 +/- 0.04 to 0.28 +/- 0.04 mM [EC50]) and maximal activity (10.1 +/- 2.9 to 25.5 +/- 6.5 pmol/mg protein per min) were significantly increased in LVH as compared with control animals in response to nitroprusside stimulation, but cyclic GMP-phosphodiesterase activity was similar. In LVH dogs, basal cyclic GMP was significantly elevated in vivo when compared with controls. Treatment of dogs with SIN-1 resulted in a significant increase in cyclic GMP in control (1.09 +/- 0.12 to 1.48 +/- 0.19 pmol/gram) and a greater increase in the LVH group (1.78 +/- 0.16 to 3.58 +/- 0.71 pmol/g). L-NAME had no effect on myocardial cyclic GMP levels in control or LVH dogs. Segment work decreased in the control group after SIN-1 (1,573 +/- 290 to 855 +/- 211 grams x mm/min). LVH dogs showed no decrement in work as a result of treatment with SIN-1. L-NAME did not cause significant changes in myocardial cyclic GMP, O2 consumption, or work in either control or LVH dogs, but vascular effects were evident. SIN-1 increased cyclic GMP, and with greater effect on LVH; however, this resulted in a decrement in function only in the control group. The greater increased cyclic GMP in LVH dogs is not related to increased NO production, but is related to significantly higher sensitivity and maximal activity of soluble myocardial guanylate cyclase.

Animals↗

PubMed1992

ACE inhibitors and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a common condition and a powerful independent risk factor for coronary heart disease, congestive heart failure, and other cardiac morbidity. It is associated with the male sex and advancing age. Its most common cause is hypertension, and many antihypertensive agents induce regression of LVH. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reverse LVH by a mechanism as yet unknown. Reduction in afterload and other hemodynamic abnormalities by reduction of blood pressure is clearly a factor, but ACE inhibitors also block adrenergic action and other sympathetic nervous system influences, and the reduction in angiotensin II produces many effects. By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Angiotensin II promotes protein synthesis in myocardial myocytes, and blocking this action may arrest the hypertrophic process. To determine the effect of angiotensin II on LVH and normalization of LV function, a study is now underway evaluating the effects of lisinopril, a new lysine analog of enalapril, and a diuretic agent in the treatment of hypertension LVH.

Adult↗

PubMed1993

The ionic mechanism of reperfusion-induced early afterdepolarizations in feline left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) potentiates reperfusion-associated ventricular fibrillation. To study the mechanism responsible, patch-clamp techniques were used to evaluate transmembrane ionic currents during "reperfusion" after a CN(-)-induced metabolic surrogate for ischemia in isolated myocytes from a feline model of experimental LVH. Reperfusion caused the generation of early afterdepolarizations (EADs) from an average take-off potential of -33 mV in LVH cells but not in cells from normal hearts. 10 min after initiating reperfusion of normal cells, action potential duration (APD) at 50% repolarization (APD50) lengthened from 198 +/- 41 to 233 +/- 57 ms whereas in LVH cells APD50 lengthened from 262 +/- 84 to 349 +/- 131 ms (P < 0.05). Among the LVH cells, APD50 lengthening was significantly greater in the cells that had developed EADs. During reperfusion, steady state outward current in the voltage range of the action potential plateau (between -20 and +20 mV) was reduced from the control values in LVH cells but not in normal cells. Reperfusion-related reduction of steady state outward current in LVH cells was abolished under experimental conditions in which L-type Ca2+ current was isolated from other classes of currents whereas it was still observed under the condition in which pure K+ currents could be recorded. Thus, reduction of steady state outward current due to the reduction of outward K+ current over the action potential plateau voltage range appears to be responsible for an excessive prolongation of APD, leading to the development of EADs.

Action Potentials↗

PubMed1997

Effects of angiotensin-converting enzyme inhibition and angiotensin II AT1 receptor antagonism on cardiac parameters in left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is considered to be an independent risk factor giving rise to ischemia, arrhythmia, and left ventricular dysfunction. In this article, we summarize recent studies performed in our laboratory to investigate (1) the contribution of the renin-angiotensin system to the cardiac remodeling process, which is triggered by myocardial infarction (MI) or hypertension-induced cardiac hypertrophy; (2) the effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin AT1 receptor antagonism on cardiac parameters, such as myocardial infarct size, cardiac hypertrophy, heart function, and myocardial metabolism; (3) the mechanism of an ACE inhibitor-induced increase in cardiac capillary density in spontaneously hypertensive rats (SHR) and stroke prone SHR (SHR-SP). We observed that AT1 receptor gene expression in rat vascular smooth muscle cells (but not in rat coronary endothelial cells) was markedly enhanced after an ischemic insult in vitro. In a rat model in which MI was induced by coronary artery ligation, the AT1 receptor mRNA levels were transiently increased after MI and reached a peak level 24 hours post-MI. The AT2 receptor gene expression increased in a pattern similar to that of the AT1 receptor. ACE expression at the protein level in the repairing scar, which was demonstrated by monoclonal antibody staining, started to increase 2 weeks after MI and reached a peak level 3 weeks post-MI. Furthermore, long-term treatment with an ACE inhibitor limited infarct size, prevented cardiac hypertrophy, and improved heart function in the rat MI model. In SHR-SP, long-term treatment with either an ACE inhibitor or an AT1 receptor antagonist improved cardiac function and metabolism. Cardiac metabolism was even improved after low-dose ACE inhibitor treatment, which did not prevent hypertension and cardiac hypertrophy. In both SHR and SHR-SP, we found that the ACE inhibitor ramipril significantly increased capillary length density independently of its antihypertensive and antihypertrophic actions. Most of the cardiac effects of the ACE inhibitor could be abolished by a bradykinin B2 receptor antagonist. Thus, these cardiac effects of ACE inhibitors can be ascribed, at least under our experimental conditions, to ACE inhibitor-induced bradykinin potentiation.

Angiotensin Receptor Antagonists↗

PubMed1999

Angiotensin II antagonism and the heart: valsartan in left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study, the angiotensin II (AT1-receptor) antagonist valsartan (Diovan ; 80-160 mg q.d.) was compared with the beta-blocker atenolol (50-100 mg q.d.) over 8 months in previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated by echocardiography. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001). In the valsartan group (n = 9 with HCTZ), blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m2 in the atenolol group and from 127 to 106 g/m2 in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.

Angiotensin II↗

PubMed1999

Angiotensin II antagonism and the heart: valsartan in left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study the angiotensin II (AT(1) receptor) antagonist valsartan (Diovan((R)); 80 mg/160 mg q.d.) was compared with the beta-blocker atenolol (50 mg/100 mg q.d.) over 8 months in predominantly previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated with echocardiographic data. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001), and in the valsartan group (n = 9 with additional HCTZ) blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m(2) in the atenolol group and from 127 to 106 g/m(2) in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.

Aged↗

PubMed1997

Effect of chronotropic and inotropic stimulation on the coronary pressure-flow relation in left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during increased cardiac work. The present study was performed to study the effects of chronotropic and inotropic stimulation on the coronary pressure-flow relation of the hypertrophied left ventricle of dogs and to determine the individual contributions of increases in heart rate and contractility to the exaggerated exercise-induced increases in effective back pressure (pressure at zero flow; Pzf). Ascending aortic banding in seven dogs increased the LV to body weight ratio to 7.7 +/- 0.3 g/kg compared to 4.8 +/- 0.2 g/kg in 10 normal dogs (p < or = 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. During resting conditions maximum coronary blood flow in the pressure overloaded hypertrophied left ventricle was impaired by both an increase in Pzf (25.1 +/- 2.6 vs 13.8 +/- 1.2 mmHg in hypertrophied vs normal ventricles, respectively, p < or = 0.01) and a decrease in maximum coronary conductance (slope of the linear part of the pressure-flow relation, slopep > or = linear) (8.6 +/- 1.1 vs 12.7 +/- 0.9 ml/min/mmHg, p < or = 0.01). Right atrial pacing at 200 and 250 beats/min resulted in similar rightward shifts of the pressure-flow relation in hypertrophied and normal hearts with 3.1 +/- 0.8 and 4.7 +/- 0.8 mmHg increases in Pzf in LVH and normal dogs, respectively; stepwise multivariate regression analysis indicated that the exaggerated decrease in filling pressure (10 +/- 2 vs 6 +/-2 mmHg) and decrease in left ventricular systolic pressure (45 +/- 5 vs 3 +/- 3 mmHg, p < or = 0.01) may have blunted a greater rightward shift of the pressure-flow relation produced by atrial pacing in the hypertrophied hearts. Inotropic stimulation with dobutamine (10-20 micrograms/kg/min, i.v.) resulted in minimal flow changes in normal hearts but produced a 4.4 +/- 1.5 mmHg (p < or = 0.05) rightward shift of the pressure-flow relation in hypertrophied hearts. which correlated with a greater increase in left ventricular systolic pressure (83 +/- 16 vs 18 +/- 4 mmHg. p < or = 0.05). Exercise resulted in a rightward shift in both normal and hypertrophied left ventricles, but the increase in Pzf was significantly greater in the hypertrophied hearts (15.2 +/- 0.9 vs 10.3 +/- 0.9 mmHg. p < or = 0.05). Stepwise multivariate regression analysis indicated that not only increases in left ventricular filling pressure, but also increases in heart rate and LV systolic pressure contributed to the abnormally great increase in effective coronary back pressure which results in limitation of myocardial perfusion during exercise in the pressure overloaded hypertrophied left ventricle.

Adenosine↗

PubMed2004

Contractile and electrical functions of rat heart during left ventricular hypertrophy.

Left ventricular hypertrophy of the hearts in Wistar rats caused by renovascular hypertension prolongs depolarization of epicardial surface of the ventricles and increases the duration of excitation phase in the left ventricular epicardium. Sex-related differences in changes of myocardial contractility were revealed during hypertrophy of the left ventricle caused by renovascular hypertension.

Animals↗

PubMed1999

[Left ventricular performance, ventriculo-arterial coupling and mechanical output in hypertensive patients with and without left ventricular hypertrophy].

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p < 0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.

Biomechanical Phenomena↗

PubMed2006

Cardiac response to pressure overload in 129S1/SvImJ and C57BL/6J mice: temporal- and background-dependent development of concentric left ventricular hypertrophy.

Left ventricular hypertrophy (LVH), a risk factor for cardiovascular morbidity and mortality, is commonly caused by essential hypertension. Three geometric patterns of LVH can be induced by hypertension: concentric remodeling, concentric hypertrophy, and eccentric hypertrophy. Clinical studies suggest that different underlying etiologies, genetic modifiers, and risk of mortality are associated with LVH geometric patterns. Since pressure overload-induced LVH can be modeled experimentally using transverse aortic constriction (TAC) and since C57BL/6J (B6) and 129S1/SvImJ (129S1) strains, which have different baseline cardiovascular phenotypes, are commonly used, we conducted serial echocardiographic studies to assess cardiac function up to 8 wk of post-TAC in male B6, 129S1, and B6129F1 (F1) mice. B6 mice had an earlier onset and more pronounced impairment in contractile function, with corresponding left and right ventricular dilatation, fibrosis, change in expression of hypertrophy marker, and increased liver weights at 5 wk of post-TAC. These observations suggest that B6 mice had eccentric hypertrophy with systolic dysfunction and right-sided heart failure. In contrast, we found that 129S1 and F1 mice delayed transition to decompensated heart failure, with 129S1 mice exhibiting preserved systolic function until 8 wk of post-TAC and relatively mild alterations in histology and markers of hypertrophy at 5 wk post-TAC. Consistent with concentric hypertrophy, our results show that these strains manifest different cardiac responses to pressure overload in a time-dependent manner and that genetic susceptibility to initial concentric hypertrophy is dominant to eccentric hypertrophy. These results also imply that genetic background differences can complicate interpretation of TAC studies when using mixed genetic backgrounds.

Animals↗

PubMed1990

Improvement in left ventricular hypertrophy and left ventricular diastolic function following verapamil therapy in mild to moderate hypertension.

We evaluated the effect of verapamil therapy on left ventricular hypertrophy and left ventricular diastolic function in 13 patients with mild to moderate hypertension. Left ventricular hypertrophy was determined by M-mode echocardiographic measurements of interventricular septal thickness (IVST), posterior wall thickness (PWT) and left ventricular mass index (LVMI) both before (T0) and after 3 months (T3) of verapamil therapy. Left ventricular diastolic transmitral flow was measured by pulsed Doppler indices of early (E) and atrial (A) velocity, E/A ratio, total area (Ta), A area (Aa), Aa/Ta ratio, E-pressure half-time (E-PHT). A-pressure half-time (A-PHT) and E-PHT/A-PHT ratio both before and after 3 months of verapamil therapy. No significant changes occurred in mean heart rate, systolic function or body weight. We conclude that 3 months' therapy with verapamil resulted in an improvement in left ventricular hypertrophy and left ventricular diastolic function and a normalization of blood pressure, without a corresponding deterioration in left ventricular systolic function.

Adult↗

PubMed1995

[Physiopathology of left ventricular hypertrophy].

Left ventricular hypertrophy (LVH) is an early complication of hypertension. To a certain degree, this process counteracts the parietal stress induced by high blood pressure. Genetic factors, obesity, high salt diet and different growth factors, notably angiotensin II and noradrenaline, can also predispose to hypertrophic cardiomyopathy. Left ventricular mass is increased on echocardiography in about 20% of hypertensive subjects. LVH is initially associated with a change in myocardial diastolic function and later with abnormal systolic function. It is a major risk factor, a cause of cardiac failure, reduction in coronary reserve and of ventricular arrhythmias. Treatment of hypertension is associated with regression of LVH and preservation or improvement in myocardial diastolic and systolic functions. The decrease in left ventricular mass could reduce the incidence of cardiovascular complications in hypertension.

Electrocardiography↗

PubMed1993

Structural basis for pathologic left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a major risk factor associated with the emergence of symptomatic congestive heart failure. Cardiac myocyte excitation-contraction coupling has been the biochemical focus in the search for insights into the impaired contractility, relaxation, and stiffness of the hypertrophied myocardium. Although hypertrophied myocytes are the hallmark of LVH, other aspects of myocardial structure may be altered to impair pump function--specifically an abnormal accumulation of connective tissue (interstitial fibrosis). Cardiac fibroblasts, which are nonmyocyte cells of the cardiac interstitium, synthesize and degrade collagen and, therefore, represent an important determinant of pathologic LVH. Significantly, this reactive fibrosis has been found not only in the pressure-overloaded hypertrophied left ventricle but also in the normotensive, nonhypertrophied right ventricle of animals with experimental hypertension. These findings suggest the involvement of a circulating substance that has access to the coronary circulation common to both ventricles. Based on in vivo studies that examined this hypothesis, it can be concluded that chronic elevation of circulating aldosterone, relative to sodium intake, is associated with myocardial fibrosis, which initially adversely alters diastolic function and ultimately systolic ventricular function. The mechanisms by which fibroblast collagen metabolism is invoked in this setting are under investigation. Elucidation of these mechanisms may prepare the way to the prevention as well as the reversal of myocardial fibrosis and, in turn, of pathologic LVH.

Animals↗