Structural changes in the heart and carotid arteries in hypertensive patients associated with cardiovascular risk factors.

OBJECTIVE: To estimate the relationship between structural changes in the heart and in the carotid arteries in hypertensives and to analyze the correlations between these structural changes and cardiovascular risk factors. METHODS: We studied 76 subjects (39 men and 27 women, mean age 45+/-7 years) with mild-to-moderate untreated and uncomplicated hypertension. All of the subjects underwent ambulatory blood pressure monitoring, M-mode echocardiography for evaluation of their left ventricular mass and B-mode high-resolution ultrasonography to determine their carotid arterial wall thickness. RESULTS: The mean intimal plus medial thickness of the common carotid artery was found to be related significantly and independently to the left ventricular mass indexed by the body surface area. In multivariate analysis, age and the high-density lipoprotein cholesterol level were related strongly to the intimal plus medial thickness, whereas the clinic systolic blood pressure, average night-time systolic blood pressure and glycemia were the most important determinants of the left ventricular mass index. Logistic regression analysis suggested that the thickness of the posterior left ventricular wall was a stronger predictor of the carotid intima-medial thickness than were age and the high-density lipoprotein cholesterol level. CONCLUSION: The carotid wall thickness and left ventricular mass of hypertensives are related independently; nevertheless the main determinants of structural cardiac and vascular changes are probably different.

Determinants of left ventricular function before and after regression of myocardial hypertrophy in hypertension.

Using digitized M-mode echocardiograms, we evaluated the determinants of left ventricular (LV) systolic and diastolic function in 30 hypertensives with LV hypertrophy (LV mass > 230 g and normal LV diastolic diameter), before (LV mass 319 +/- 26 g) and after normalization of LV mass (196 +/- 21 g) by antihypertensive treatment with angiotensin converting enzyme inhibitors. As a control group we selected 50 normal subjects. Using multiple regression analysis we studied the relative role of preload (LV end-diastolic diameter), afterload (end-systolic wall stress), inotropic state (systolic pressure/end-systolic LV diameter ratio), and LV mass on LV systolic (peak shortening rate of LV diameter) and diastolic function (peak lengthening rate of LV diameter). The major determinant of systolic function was the end-systolic stress in hypertensives before treatment and the systolic pressure/end-systolic LV diameter ratio in normals and in hypertensives after treatment. The major determinant of diastolic function was LV mass in hypertensives before treatment and end-systolic stress in normals and in hypertensives after normalization of LV mass by treatment. Preload seems not to influence LV function in normals and in hypertensives with normal LV diameter. The inotropic state is the major determinant of systolic function in normals and in hypertensives after treatment, whereas this role is played by afterload in hypertensives before treatment. The diastolic function is primarily influenced by after-load in normals and in hypertensives after regression of myocardial hypertrophy, whereas in hypertensives with myocardial hypertrophy LV mass is the major determinant of diastolic function.