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Determinants of left ventricular function before and after regression of myocardial hypertrophy in hypertension
1Department of Internal Medicine and Medical Therapy--University of Pavia, I.R.C.C.S. Policlinico San Matteo, Pavia, Italy.
Insights
Antihypertensive treatment with ACE inhibitors improves cardiac function in hypertensive patients with left ventricular hypertrophy. Key determinants of systolic and diastolic function shift after LV mass normalization.
Area of Science:
- Cardiology
- Hypertension Research
- Echocardiography
Background:
- Hypertension often leads to left ventricular hypertrophy (LVH), impacting cardiac function.
- Understanding the factors influencing systolic and diastolic function in LVH is crucial for effective treatment.
Purpose of the Study:
- To evaluate the determinants of left ventricular (LV) systolic and diastolic function in hypertensive patients with LVH.
- To assess how these determinants change after antihypertensive treatment that normalizes LV mass.
Main Methods:
- Digitized M-mode echocardiograms were used to assess LV function in 30 hypertensive patients and 50 controls.
- Multiple regression analysis examined the roles of preload, afterload, inotropic state, and LV mass before and after treatment.
Main Results:
- Before treatment, LV mass was the main determinant of diastolic function, and end-systolic stress determined systolic function in hypertensives.
- After treatment with ACE inhibitors normalized LV mass, the inotropic state became the main determinant of systolic function, and end-systolic stress influenced diastolic function.
Conclusions:
- Antihypertensive therapy effectively reduces LV mass and alters the determinants of LV systolic and diastolic function.
- Treatment shifts the primary drivers of cardiac function from structural (LV mass) to dynamic factors (inotropic state, afterload).
Abstract:
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.