Search

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.

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.