Diastolic heart function in hypertension-induced left ventricular hypertrophy

University dissertation from Stockholm : Karolinska Institutet, Department of Clinical Sciences

Abstract: Hypertensive left ventricular (LV) hypertrophy is an independent strong risk factor for cardiovascular morbidity and mortality. An abnormal diastolic relaxation in the absence of systolic impairment is often seen in patients with hypertension, whether LV hypertrophy is present or not. The aims of this thesis were to identify determinants of LV diastolic dysfunction, including myocardial fibrosis, in hypertensive patients, to evaluate different echocardiographic Doppler methods for the assessment of LV diastolic function, and to study the effects of antihypertensive treatment on diastolic function, and specifically the importance of the reninangiotensin-aldosterone system (RAAS). We examined 115 patients with hypertensive LV hypertrophy, who were treated for 48 weeks with an AT, receptor blocker (irbesartan), or a beta receptor blocker (atenolol). Furthermore, 38 patients with hypertension and with no LV hypertrophy, and 38 normotensive subjects, matched for age and sex, were examined on one occasion. Blood pressure, myocardial fibrosis, and LV wall thickness independently impair diastolic function. Compared to conventional mitral pulsed wave Doppler echocardiography, tissue velocity echocardiography is more sensitive and accurate to detect alterations in LV diastolic function. Circulating levels of the carboxyterminal propeptide of procollagen type I (PICP), a biomarker of the rate of tissue synthesis of collagen I and a marker of myocardial fibrosis, are higher in hypertensive patients than in norinotensive subjects. This increase in PICP is not dependent on the presence of LV hypertrophy, and might suggest that myocardial fibrosis precedes the development of LV hypertrophy in hypertensive heart disease. Both irbesartan and atenolol improve LV diastolic function, but through different mechanisms; irbesartan mainly by a reduction in blood pressure and LV mass, and atenolol mainly by a reduction in blood pressure and heart rate. Irbesartan and atenolol reduced PICP levels similarly. Changes in PICP related to changes in LV mass, blood pressure and diastolic function in patients treated with irbesartan, but not with atenolol, suggesting a role for angiotensin II in the control of LV mass and myocardial fibrosis. In conclusion, tissue velocity echocardiography is a valuable technique to evaluate LV diastolic function. RAAS plays a role for the control of blood pressure, myocardial fibrosis, and LV mass which are important determinants for LV diastolic function in hypertensive heart disease. Early identification and treatment of LV diastolic dysfunction might prevent the transition from hypertension to heart failure, and its complications.

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