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PubMed2005

Further evidence for low-dose combinations in patients with left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a powerful independent risk predictor for cardiovascular disease and reversal of LVH has become a primary goal of antihypertensive management. Recent evidence has confirmed that most hypertensive patients will benefit from a low-dose combination strategy to manage their hypertension, and two trials have recently examined the effect of this strategy on left ventricular mass. The REASON study (pREterax in regression of Arterial Stiffness in a contrOlled double-bliNd study) compared the low-dose combination of an angiotensin-converting enzyme (ACE) inhibitor and a diuretic with beta-blocker monotherapy in hypertensive patients with LVH, and the PICXEL study (Preterax In a double-blind Controlled study versus Enalapril in LVH) compared the same low-dose combination with ACE inhibitor monotherapy in hypertensive patients with echocardiographic LVH. The REASON study demonstrated that the low-dose combination produced a significantly greater change in left ventricular mass after 1 year than the beta-blocker, despite inducing a similar change in mean blood pressure. Additionally, perindopril/indapamide reduced central (carotid) and peripheral (brachial) systolic blood pressure (SBP) and pulse pressure (PP) to a significantly greater extent than beta-blocker, and these benefits were more pronounced for the central values; LVH is affected more by central rather than peripheral haemodynamic changes. Results of the analysis of the PICXEL study showed a significantly greater decrease in LVH parameters and blood pressure over 1 year in favour of the low-dose combination. This reduction cannot be entirely explained by the better efficacy of the low-dose combination on blood pressure reduction.

Antihypertensive Agents↗

PubMed1993

Ischaemia and left ventricular hypertrophy.

Left ventricular hypertrophy (LVH), diagnosed by ECG and echocardiography, is commonly associated with coronary heart disease. Hypertensive patients with LVH and myocardial ischaemia may be at particular risk. The prevalence of ischaemia in hypertensive LVH was addressed in THAMES (Tenormin in Hypertension and Myocardial Ischaemia Epidemiological Survey), which comprised 205 men with hypertension. Echocardiography revealed LVH (defined as a left ventricular mass index > or = 130 g m-2) in 140 patients (68%). Of these patients with LVH, myocardial ischaemia was diagnosed on exercise ECG testing in 24%, and by thallium scintigraphy in 14%. Although not proven, a logical approach would be to improve the prognosis by reversing LVH and reducing ischaemia. A recent meta-analysis has indicated that angiotensin-converting enzyme (ACE) inhibitors are the most effective drugs in reversing LVH. But beta-blockers may still be a logical first choice of drug, because of their valuable anti-ischaemic properties.

Adrenergic beta-Antagonists↗

PubMed2000

Therapeutic options in minimizing left ventricular hypertrophy.

Left ventricular hypertrophy (LVH), a target-organ response to chronic pressure or volume overload, is associated with its own independent risks of death in patients with hypertension. Numerous studies have shown that LVH increases the risk of coronary heart disease, congestive heart failure, stroke or transient ischemic attack, all-cause deaths, and sudden death. Although the mechanisms by which LVH develops are incompletely understood, the renin-angiotensin system may play an important role. All major classes of antihypertensive agents (calcium channel blockers, diuretics, beta-blockers, angiotensin-converting enzyme inhibitors) can cause LVH regression but not all to the same degree. Angiotensin-converting enzyme inhibitors may provide the most pronounced reduction in left ventricular mass per millimeter of mercury of blood pressure reduction. In addition, animal studies and human trials show promise for the regression of LVH with the use of angiotensin receptor blockers (ARBs). Because ARBs act specifically on the AT(1) receptor, angiotensin II can exert its favorable effects on cell growth inhibition through the AT(2) receptor. One small study that compared the ARB valsartan with atenolol found significant regression of LVH with the ARB by 8 months of treatment.

Angiotensin Receptor Antagonists↗

PubMed1994

Angiotensin-converting enzyme inhibitors and effects on left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a recognized complication of, rather than a physiological response to, hypertension, being a powerful independent indicator of cardiovascular disease risk. In addition, it is reasonable to assume that the reversal of LVH is a desirable therapeutic goal in the treatment of hypertension. Furthermore, the renin-angiotensin system plays an important role in LVH and, in particular, in the development of cardiac interstitial fibrosis. Therefore, the effect of angiotensin-converting enzyme (ACE) inhibition on LVH is of particular interest. In both experimental and human studies, ACE inhibitors appear to perform better than other antihypertensive agents in reversing cardiac structural changes. A recent meta-analysis showed ACE inhibitors to be more efficacious than other first-line antihypertensives in reducing left ventricular mass. A controlled long-term study of previously untreated men showed that enalapril reversed LVH significantly better than did hydrochlorothiazide and that the regression of LVH was independently related to blockade of the renin-angiotensin system. Indeed, there have been studies showing that ACE inhibitors can affect LVH without lowering blood pressure. Moreover, ACE inhibitors have shown cardioprotective and cardioreparative properties in experimental models of hypertensive LVH. In conclusion, ACE inhibitors are effective in reversing LVH as well as interstitial fibrosis. The prognostic implications of this remain to be seen. So far, the experience with spirapril on LVH is limited, but the accumulated data are promising.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2000

Low wall shear stress in carotid arteries in subjects with left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular complications including atherosclerosis. The close linkage between LVH and carotid atherosclerosis has been the focus of much research. However, the underlying mechanism linking the two conditions is not fully understood. Low wall shear stress contributes to intimal thickening and atherosclerosis development as a local mechanism. In the present study, we investigated the relationship between wall shear stress and LVH in subjects with risk factors for atherosclerosis. Eighty subjects with at least one risk factor for atherosclerosis; ie, hypertension, diabetes mellitus, hyperlipidemia, or smoking, were enrolled. Intimal-medial thickness (IMT), number of plaques, internal dimensions, and blood flow velocity in the common carotid artery were evaluated. Wall shear stress was calculated using a Poiseuillean parabolic model of velocity distribution: shear stress = 4 x blood viscosity x central flow velocity/internal dimension. Subjects were divided into two groups; LVH(-) (n = 36) and LVH(+) (n = 44), according to their left ventricular mass index (LVMI). Mean shear stress and systolic peak shear stress were significantly lower in subjects with LVH compared with subjects without LVH. Furthermore, mean shear stress (r = -0.42, P < .0001) and peak shear stress (r = -0.31, P < 0.01) were significantly inversely related to LVMI. Stepwise regression analysis revealed that wall shear stress independently correlated with LVMI as well as IMT. These results indicate that low shear stress could function as a local factor in the development of atherosclerosis in subjects with LVH.

Arteriosclerosis↗

PubMedDate not supplied

Transmural distribution of myocardial blood flow and of coronary reserve in canine left ventricular hypertrophy.

Left ventricular hypertrophy was induced by banding of the ascending aorta in pupies at the age of 6 weeks. At the age of one year left ventricular weight per body weight was increased by 87% compared to control litter mates. While myocardial perfusion and myocardial oxygen consumption per 100 g were identical in the hypertrophy and control group, there was a significantly diminshed ratio of subendocardial/subepicardial flow in the hypertrophy group during moderate exercise. With maximal coronary dilation subendocardial diastolic resistance (mm Hg/ml-min-1 per 100 g) was 0.16 +/- 0.03 in the control group and 0.26 +/- 0.03 in the hypertrophy group. This diminished coronary reserve indicates an insufficient growth of the vascular bed in these hypertrophied hearts.

Animals↗

PubMed1986

Nuclear magnetic resonance spectroscopy of rat ventricles following supravalvar aortic banding. A model of left ventricular hypertrophy.

Left ventricular hypertrophy produced by supravalvar aortic banding in infant rats was studied by proton magnetic resonance spectroscopy. Weight gain at 11 weeks of age in the 11 male Sprague-Dawley rats with aortic bands placed at three weeks was similar to that of the 14 controls. The left ventricle of banded rats hypertrophied, increasing the ratio of left ventricle plus septum to body weight (LV + S/BW) by more than 50% (P less than .00001). Right ventricular weight (RV/BW) increased slightly (P less than .03). T1 and T2 relaxation times of LV + S, RV, and thigh muscle (Th) from the banded and control rats were compared. The T2 value distinguished hypertrophied from control LV + S (P less than .003), but not between RV or Th from the two groups. For banded rats only, the T2 value distinguished each muscle type: LV + S from RV, LV + S from Th, and RV from Th (P less than .00001 for each). For control rats, cardiac muscle was distinguished from Th (P less than .00001), but LV + S and RV were similar. The T1 value did not distinguish either the banded from the control group or any of the muscle types. Percent water content was similar for all tissues. Any correlation between water content and T1 or T2 was inconsistent or weak.

Animals↗

PubMed1983

Physiologic considerations in left ventricular hypertrophy.

Left ventricular hypertrophy is both a target organ response to hypertensive vascular disease as well as a factor that might be responsible for other cardiovascular events. Recent work confirms that the increased cardiac mass associated with hypertension results as a structural adaptation to the increased afterload imposed on the heart. Initially there is a transient period of hyperfunction that is followed by the sustained structural adaptative period of stable hyperfunction. Even before left ventricular failure supervenes, the ventricular mass demonstrates impaired contraction. This article reviews the hemodynamic evidence in favor of this sequence of events but, in addition, points to the pathophysiological and clinical factors that may be responsible for the increased cardiac mass in addition to the pressure overload. These include: the pressor mechanisms per se; the age, sex, and race of the patient; and coexisting diseases. Some of these factors may account in part for the regression of cardiac mass with antihypertensive therapy. However, until we understand more clearly those factors that transduce the physical stimulus for hypertrophy into biochemical events, we shall neither understand completely the development of this structural adaptation of the heart nor its regression with treatment.

Adaptation, Physiological↗

PubMed1995

Which definition for echocardiographic left ventricular hypertrophy?

Left ventricular (LV) hypertrophy is diagnosed on the basis of LV mass measurement at echocardiography. However, various thresholds for defining LV hypertrophy have been published, ranging from 111 to 134 g/m2 and from 100 to 125 g/m2 in men and women, respectively. The aim of our study was to evaluate variations in the prevalence of LV hypertrophy induced by the application of different threshold values among hypertensive subjects. LV mass was calculated in 349 hypertensive patients from an M-mode LV tracing obtained by left parasternal view in 83% and by subcostal view in 17% of patients. The prevalence of LV hypertrophy ranged from 17% to 39%, according to the threshold value applied (from 10% to 47%, and from 19% to 39% in women and men, respectively). As expected, the prevalence of LV hypertrophy in obese patients of both sexes was higher when applying the usual height-indexed threshold (143 and 102 g/m for men and women, respectively) than when applying the usual body surface area-indexed threshold (134 and 110 g/m2 for men and women, respectively). The use of normalized thresholds when comparing different indexation methods (in this case, 145 g/m for men, 120 g/m for women) will minimize these variations in part due to the threshold choice. Considering the clinical and therapeutic implications associated with the presence of LV hypertrophy, better standardization of definitions is needed; this could be based either on better-designed cooperative normality studies or meta-analysis of risk stratification.

Adult↗

PubMed1990

Effects of indapamide on left ventricular mass and function in systemic hypertension with left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is frequently associated with hypertension and constitutes a major cardiovascular risk factor, the reduction of which should be considered when initiating antihypertensive therapy. To assess the effects of indapamide on LVH, 18 hypertensive patients were included in the study (11 men and 7 women, age 53.6 +/- 2.9 years, mean +/- standard deviation) whose supine diastolic blood pressure was greater than 95 mm Hg without (n = 11) or with (n = 7:6 beta blockers, 1 calcium antagonist) antihypertensive therapy. All presented with LVH, echocardiographically defined by a left ventricular mass index greater than 110 g/m2. After a 2-week preinclusion period, all patients received indapamide, 2.5 mg/day, for a period of 6 months. Physical examination including blood pressure measurement was performed on selection (M-1/2), before (M0), and after 1 (M1), 3 (M3) and 6 (M6) months of indapamide treatment, and echocardiography was performed at M0 and M6. Quality of life was evaluated by means of questionnaires completed by the patient and the physician, and a visual analog scale was completed by the patient at M-1/2, M0 and M6. All clinical parameters remained stable during the 2-week preinclusion period. Indapamide administration induced a highly significant reduction in both supine systolic and diastolic blood pressures from 173.9 +/- 2.9/100.5 +/- 1.2 mm Hg at M0 to 150.9 +/- 1.9/90.5 +/- 1.3 mm Hg at M1 (p less than 0.001), and 145.0 +/- 1.7/86.0 +/- 1.5 mm Hg at M6 (p less than 0.001). Similar favorable effects were observed in the upright position.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effects of calcium entry blockade on hypertension-induced left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart and is a response to increased hemodynamic and metabolic demands, which are most commonly caused by systemic hypertension. LVH induced by hypertension is associated with reduced myocardial compliance, structural alterations, and changes in coronary perfusion. Calcium entry blockers have caused LVH regression both in experimental studies and in clinical trials. Although their efficacy as antihypertensive agents is primarily due to their vasodilating properties, the mechanisms by which calcium entry blockers accomplish LVH regression are complex and include various hemodynamic and neurohumoral factors. Calcium entry blockade has decreased LVH with no apparent deterioration of left ventricular function. Because LVH is a major risk factor for sudden cardiac death and other cardiac morbidities, it is possible that the regression of LVH can improve the prognosis in hypertensive patients.

Animals↗

PubMed2000

Genetic contributions to left ventricular hypertrophy.

Left ventricular (LV) hypertrophy is a common condition that profoundly affects morbidity and mortality from cardiovascular diseases, including myocardial infarction, congestive heart failure, and stroke. Noninvasive imaging methods have greatly expanded our ability to evaluate cardiac structural and functional characteristics, and enhanced our understanding of the natural history of LV hypertrophy. The etiology of LV hypertrophy is likely due to the effects of multiple genes interacting with other genes and the environment. Although hypertension is recognized as a strong determinant of LV hypertrophy, blood pressure explains only a limited amount of the interindividual variation in LV mass. Moreover, LV hypertrophy occurs in the absence of hypertension, and in some cases precedes its development. Genes encoding proteins involved in the structure of the LV, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, and blood pressure, are likely candidates for the development of common forms of LV hypertrophy. An overview of the epidemiology and pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy.

Black People↗

PubMed2004

Genes for left ventricular hypertrophy.

Left ventricular (LV) hypertrophy is very common, particularly among hypertensives. The presence of LV hypertrophy profoundly affects morbidity and mortality from cardiovascular diseases and stroke, and is now recognized as the most important predictor of chronic heart failure. Hypertension, obesity, and diabetes are important determinants of LV hypertrophy, but they fail to identify many individuals with the condition, suggesting that other factors, likely genetic in origin, play a role. Although much research has been undertaken to understand the causes of hypertrophy and the medical treatments that can lead to its regression, much remains unknown about its genetic basis. LV hypertrophy is considered a complex genetic disease, likely representing an interaction of several genes with the environment. The heritability of LV mass, measured as a quantitative trait, falls between 0.3 and 0.7 in different populations, suggesting it has a familial component. Genes encoding proteins involved in LV structure, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, substrate metabolism, and blood pressure are likely candidates for the development of common forms of LV hypertrophy. An overview of the pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy in humans and animal models.

Genetic Predisposition to Disease↗

PubMed1991

Left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) may be physiological or pathological. Only pathological LVH has been shown to be a risk factor for cardiovascular events. LVH may not be homogeneous. It seems to progress from muscle hypertrophy to eventual cell death and myocardial fibrosis. Potential for reversal of LVH may therefore depend on the stage at which it has been attempted. An interaction between LVH and serum potassium levels could have important therapeutic implications, particularly with regard to the use of thiazide diuretics as long-term treatment for hypertension.

Animals↗

PubMed1990

[Dynamic left ventricular obstruction increased by nitroglycerin in elderly patients with hypertension and concentric left ventricular hypertrophy].

Left ventricular outflow tract (LVOT) obstruction has been observed in elderly patients with concentric hypertrophic hypertensive cardiomyopathy (HHCM) and no significant valvular disease or regional wall motion abnormalities. In order to determine whether nitroglycerin (NTG) can increase the intraventricular obstruction, we performed echocardiographic (echo) and doppler studies, before and during administration of sublingual NTG (0.8 mg). Twenty patients (n = 20) with long-standing hypertension (19 women and 1 man, mean age 78 +/- 8 yr, mean duration of hypertension 13 +/- 10 yrs were examined. The clinical findings in 17 patients were: angina 5 (29%), dyspnea 9 (53%), syncope or malaise 4 (23%). Electrocardiographic criteria of left ventricular hypertrophy was present in 4 patients and an increased cardio-thoracic ratio (greater than 0.5) in 9 cases. The following echo parameters were determined using M-mode echocardiograms: LV end-diastolic (LVID) and systolic diameter (LVIS), fractional shortening (FS), ventricular septum thickness (IVST), posterior wall thickness (PWT) and the ratio ISVT/PWT (less than 1.3 in all patients). LVM could be calculated in 15 patients and was corrected for body surface area (LVMI). Pulsed and continuous wave Doppler study showed a characteristic late-peaking velocity waveform. We localized the elevated velocities in the LVOT and determined before and during administration of NTG: LVOT peak velocities (V) and peak intraventricular gradients (G) using simplified Bernoulli equation. Results were as follows: [table: see text] Mild mitral regurgitation was observed in 14 patients (70%) and mitral annular calcifications in 11 (55%). Systolic function, as assessed by FS, was normal in all patients. NTG induced a significant acceleration of the LVOT velocities in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Influence of left ventricular hypertrophy on left ventricular function during dynamic exercise in the presence or absence of coronary artery disease.

OBJECTIVES: We investigated the influence of left ventricular hypertrophy in the presence or absence of coronary artery disease on hemodynamic characteristics during exercise in subjects without previous myocardial infarction. BACKGROUND: Left ventricular hypertrophy has been found to increase the vulnerability of the myocardium to the development of ischemia. However, the independent influences of left ventricular hypertrophy and coronary artery disease have not been assessed in humans. METHODS: Symptom-limited supine leg exercise tests were performed by 78 patients. They were classified into the following subgroups: no coronary artery disease or left ventricular hypertrophy (group I, n = 30), left ventricular hypertrophy only (group II, n = 12), coronary artery disease only (group III, n = 20) and both left ventricular hypertrophy and coronary artery disease (group IV, n = 16). Mean left ventricular mass index was 105, 158, 109 and 159 g/m2 in groups I to IV, respectively. RESULTS: Pulmonary artery wedge pressure increased from 6 +/- 3 (mean +/- SD) mm Hg at rest to 10 +/- 5 mm Hg at peak exercise in group I, from 8 +/- 2 to 18 +/- 8 mm Hg in group II (p < 0.05 vs. group I), from 6 +/- 3 to 23 +/- 6 mm Hg in group III (p < 0.01 vs. group I) and from 8 +/- 4 to 30 +/- 7 mm Hg in group IV (p < 0.01 vs. group I; p < 0.01 vs. group II; p < 0.05 vs. group III). Multiple regression analysis showed that the number of diseased coronary vessels and left ventricular mass index were independent predictors of peak pulmonary artery wedge pressure (F = 59.2 and 19.1, respectively; multiple correlation coefficient r = 0.74, p < 0.0001). CONCLUSIONS: Left ventricular hypertrophy and coronary artery disease independently increased left ventricular filling pressure during supine leg exercise. Severe left ventricular dysfunction was induced by exercise when both conditions were present.

Adult↗

PubMed1987

Population implications of electrocardiographic left ventricular hypertrophy.

Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.

Adult↗

PubMed1990

Regression of hypertensive left ventricular hypertrophy and left ventricular diastolic function.

The effect of antihypertensive therapy on regression of left ventricular hypertrophy and left ventricular diastolic function was investigated in 25 hypertensive patients for up to 18 months after initiation of treatment. Left ventricular mass index was calculated by two-dimensional echocardiography and left ventricular diastolic function assessed by transmitral pulsed doppler ultrasound. Significant reduction in left ventricular mass index was observed after 9 months of treatment. Only 13 patients had a reduction in mass greater than the intraobserver variability of the technique. There was no change in doppler indices of left ventricular diastolic function. In 7 patients who were studied for a further 9 months after regression had occurred there was still no appreciable difference in left ventricular diastolic function. These findings indicate that there is no direct relation between left ventricular mass and abnormal left ventricular diastolic function.

Adult↗