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Objectives. The purpose of this was to examine the relation of the arterial pressure waveform to left ventricular and carotid structure. Background. The pressure waveform in the central arteries is affected by reflection of the pressure wave from the periphery. When reflected waves merge with the incident wave during systole, a late systolic peak and increment in systolic blood pressure are observed. The consequent increase in hemodynamic load may stimulate left ventricular and vascular adaptive changes. Methods. Sixty-seven normotensive adults were studied by noninvasive techniques. Anatomy and function of the left ventricle and carotid artery were investigated by ultrasonography. Pressure waveforms were recorded by an external tonometer applied to the carotid artery, and waveform shape was expressed by the augmentation index, calculated from the difference between the maximal systolic pressure and that at the infection between early and late systolic pressure peaks divided by the pulse pressure. Subjects were assigned to groups with a dominant early (group 1, augmentation index ≤0) or dominant late systolic peak(group 2, augmentation index >0). Results.Left ventricular mass index was significantly higher in group 2 than in group1, a difference that persisted after controlling for the confounding effects of gender, age and blood pressure. Carotid wall thickness and regional arterial stiffness were significantly increased in group 2, but differences disappeared in the analysis of covariance for age. Conclusions. Left ventricular and carotid artery structure are related to the shape of the central waveform. Although the increase in left ventricular mass seen in subjects with a dominant late systolic peak pressure appears to be directly to the shape of the pressure waveform, changes in the structural and physical properties of the carotid artery to be more closely related to the aging process.

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)

Mild instances of mitral valve prolapse (MVP) have been suggested to represent variants of normal, whereas individuals with complicated forms of MVP have a distinct medical condition. This hypothesis would predict different phenotypic features and patterns of inheritance in relatives of index cases with complicated or uncomplicated MVP. Accordingly, we performed clinical and echocardiographic assessment of 16 MVP patients with and 76 without moderate to severe mitral regurgitation (MR+and MR– probands) and 60 and 256, respectively, first-degree relatives (MR+ and MR– relatives). MR+ probands were older (p = 0.01), more likely to be male (p = 0.002), were more overweight (p = 0.004) and had higher systolic blood pressures (p = 0.05) and larger aortic roots (p = 0.034) after the effects of age and body size were taken into account. MR+ and MR– relatives had similar prevalences (27 and 32%) and age distribution of MVP, but affected MR+ relatives were younger (expected because more children and fewer parents of MR+ probands could be evaluated). and more likely to be male. MR+ and MR- relatives were virtually identical in regard to body habitus, blood pressure, the prevalence of auscultatory findings, thoracic bony abnormalities and palpitations and all echo measurements including anterior mitral leaflet thickness. Four instances of significant MR and two MVP-related complications (infective endocarditis and transient ischemic attack) occurred in the 82 relatives of MR– probands as opposed to none among relatives of MR+ probands. In 20 families, one proband or relative with MVP had severe MR and at least one other with MVP (presumably due to the same gene) was free of MR or complications. Thus, MVP with severe MR does not represent a heritable phenotype and commonly coexists with mild forms of MVP in the same family, making their classification as separate conditions illogical and potentially misleading.

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.

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.