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The weak relation of systolic blood pressure to left ventricular mass in hypertensive patients is often interpreted as evidence of nonhemodynamic stimuli to muscle growth. To test the hypothesis that left ventricular chamber size, reflecting hemodynamic volume load and myocardial contractility, influences the development of left ventricular hypertrophy in hypertension, we studied actual and theoretic relations of left ventricular mass to left ventricular diastolic chamber volume, pressure and volume load, and an index of contractility. Data were obtained from independently measured M-mode and two-dimensional echocardiograms in 50 normal subjects and 50 untreated patients with essential hypertension. Two indices of overall left ventricular load were assessed: total load (systolic blood pressure x left ventricular endocardial surface area) and peak meridional force (systolic blood pressure x left ventricular cross sectional area). A theoretically optimal left ventricular mass, allowing each subject to achieve mean normal peak stress, was calculated as a function of systolic blood pressure and M-mode left ventricular end-diastolic diameter. Left ventricular mass measured by M-mode echo correlated better with two-dimensional echocardiogram derived left ventricular end-diastolic volume (r = 0.56, p less than 0.001) than with systolic blood pressure (r = 0.45, p less than 0.001) and best with total load or peak meridional force (r = 0.68 and 0.70, p less than 0.001). In multivariate analysis both end-diastolic volume and blood pressure were independent predictors of systolic mass (p less than 0.001) and explained most of its variability (R = 0.75, p less than 0.001). Theoretically optimal left ventricular mass was more closely related to end-diastolic volume (r = 0.72, p less than 0.001) than to systolic blood pressure (r = 0.46, p less than 0.001); thus, the relatively weak correlation between blood pressure and optimal mass reflected the influence of left ventricular cavity size, rather than a lack of proportionality between load and hypertrophy. Actual and theoretically optimal left ventricular mass were closely related (r = 0.76, p less than 0.001), indicating that left ventricular hypertrophy in most cases paralleled hemodynamic load. Left ventricular mass was positively related to stroke index and inversely to contractility (as estimated by the end-systolic stress/volume index ratio), the main determinants of left ventricular chamber volume. In multivariate analysis, systolic blood pressure, stroke index, and the end-systolic stress/volume index ratio were each independently related to left ventricular mass index (all p less than 0.001, multiple R = 0.81) and accounted for 66% of its overall variability.(ABSTRACT TRUNCATED AT 400 WORDS)

BACKGROUND Although vascular damage in the noncoronary circulation is a major cause of complications in hypertension, relatively little is known of the in vivo geometry and function of the arterial circulation in patients with uncomplicated hypertension or of their relation to left ventricular hypertrophy, a marker of enhanced risk of cardiovascular complications. METHODS AND RESULTS Wall thickness and internal diameter of the common carotid artery and the presence of atherosclerosis within the extracranial carotid arteries were determined by ultrasound in 43 asymptomatic hypertensive patients and 43 normotensive subjects matched for sex, age, and body size. Vascular stiffness was estimated from simultaneous superimposed carotid pressure waveforms obtained with an external solid-state transducer. Left ventricular size and function were determined echocardiographically. Compared with normal subjects, hypertensive patients had greater left ventricular absolute and relative wall thicknesses, left ventricular mass, and carotid absolute and relative wall thicknesses (p < 0.005). Carotid intimal-medial thickness exceeded the 95th percentile of normal values in 28% of hypertensive patients (p < 0.01). Carotid atherosclerosis was equally prevalent within the two blood pressure groups and was associated with older age, larger left ventricular and carotid wall thicknesses, and carotid diameter. Despite similar carotid pulse pressures, vascular stiffness was significantly increased in the hypertensive patients. Among the population as a whole, significant relations existed between cardiac and vascular wall thicknesses and internal dimensions. In multivariate analyses, these relations were statistically independent of age and blood pressure. CONCLUSIONS The present study documents the presence of geometric and functional changes within the common carotid artery in uncomplicated hypertension that parallel findings within the left ventricle. The potential contribution of these changes to the cardiovascular complications of hypertension, particularly in the setting of left ventricular hypertrophy, is unknown.

Mitral valve prolapse, the most common inherited cardiovascular condition, has been associated with a variety of signs, symptoms and electrocardiographic abnormalities, but the true spectrum of the mitral prolapse syndrome remains in doubt because clinical findings often contribute to patient identification and their prevalence in patient groups may be overstated because of ascertainment bias. Accordingly, clinical findings in 88 patients with echocardiographic mitral prolapse were compared with those in 81 of their adult first degree relatives with mitral prolapse (a group free of ascertainment bias) and in two control groups without mitral prolapse: 172 first degree relatives and 60 spouses. Comparison of relatives with and without mitral prolapse demonstrated true associations between mitral prolapse and clicks or murmurs, or both (67 versus 9%, p less than 0.001), thoracic bony abnormalities (41 versus 16%, p less than 0.001), systolic blood pressure less than 120 mm Hg (53 versus 31%, p less than 0.001), body weight 90% or less of ideal (31 versus 14%, p less than 0.005) and palpitation (40 versus 24%, p less than 0.01). In contrast, relatives with mitral prolapse showed no significant increase over normal relatives or spouses without mitral prolapse in prevalence of chest pain, dyspnea, panic attacks, high anxiety or repolarization abnormalities, but these features were all more common in women than in men (p less than 0.01 to less than 0.001). Thus, the true spectrum of the mitral prolapse syndrome encompasses a midsystolic click and late systolic murmur, thoracic bony abnormalities, low body weight and blood pressure and palpitation. Other suggested clinical features, including nonanginal chest pain, dyspnea, panic attacks and electrocardiographic abnormalities, have appeared to be associated with mitral valve prolapse because of ascertainment bias and an erroneous classification of differences between men and women as being due to mitral valve prolapse.

The association of primary mitral valve prolapse (MVP) with thoracic bony abnormalities has led to the suggestion that MVP may be a forme fruste of the Marfan syndrome. Echocardiographic, skeletal and anthropometric findings in 59 subjects with primary MVP and 59 age- and sex-matched patients with Marfan syndrome were compared with those in 59 control subjects. Subjects with mitral prolapse were similar to control subjects and differed (p less than 0.025 to p less than 0.001) from the patients with Marfan syndrome in aortic root dimensions, height, arm span, upper/lower segment ratio and prevalences of arachnodactyly, scoliosis and pectus carinatum. Subjects with mitral prolapse and patients with Marfan syndrome had similar body mass indexes and prevalences of pectus excavatum and straight back. All 3 groups were similar in arm span/height ratio. The 5 subjects with MVP and arachnodactyly had lower weights, smaller body surface areas and smaller aortic root dimensions, and were more likely to have scoliosis than subjects with MVP without arachnodactyly. Thus, primary MVP differs from the Marfan syndrome in all major skeletal and cardiovascular features.

To determine the prevalence and correlates of echocardiographic left ventricular hypertrophy among subjects in a general population, we studied 621 employed subjects. Patients with uncomplicated essential hypertension in a worksite-based treatment program included 145 with borderline hypertension and 316 with sustained hypertension by World Health Organization criteria. Normotensive subjects were randomly selected from members of the same unions. M-mode echocardiographic left ventricular dimensions were used to calculate left ventricular mass and other indexes of left ventricular anatomy. The specificity of 13 echocardiographic criteria of left ventricular hypertrophy was determined in normotensive individuals, and the prevalence of left ventricular hypertrophy by each criterion was assessed in patients with borderline or sustained essential hypertension. The results suggest that the most suitable reference standard for detection of left ventricular hypertrophy in a heterogeneous urban population utilizes sex-specific cutoff values for left ventricular mass index of 110 g/m2or greater for women and 134 g/m2or greater for men. With 97% specificity, the prevalence of left ventricular hypertrophy by these criteria is approximately 12 % among patients with borderline hypertension and 20% among patients with relatively mild, uncomplicated sustained essential hypertension. Wall thickness measurements performed slightly less well. At similar levels of blood pressure, black patients were more likely than white patients to exhibit concentric left ventricular hypertrophy, especially among borderline hypertensive patients. Left ventricular hypertrophy occurred in patients with sustained hypertension who also exhibited increased cardiac output, strongly associated with low plasma renin activity.

To evaluate the relation of aortic root dilatation to aortic regurgitation, we examined clinical, echocardiographic, and radionuclide cineangiographic findings in 102 patients with severe aortic regurgitation. Aortic root dilatation was the only apparent cause in 31 patients (30%), exceeding in prevalence any valvular cause, and was independently associated only with older age (p less than 0.001). Echocardiography showed dilatation to be either localized to the sinuses of Valsalva or to be generalized. At initial evaluation, patients with generalized dilatation had severer abnormalities of left ventricular size and function than those with localized or no dilatation. Aortic valves were subsequently replaced in more patients with generalized than localized dilatation during 28 +/- 17 month follow-up (9 of 15 patients compared with 2 of 15, p less than 0.03). Thus, idiopathic aortic root dilatation is the commonest definable cause of severe aortic regurgitation; aortic root dilatation is associated independently with age but not blood pressure; and generalized aortic root dilatation is associated with marked ventricular dilatation, hypertrophy, and dysfunction.