Abstract
Nearly one in three or four adults in the world (over 50 million people in the US alone) has systemic hypertension, many of whom are unaware and untreated. Hypertension is listed among the three leading risk factors for death from cardiovascular diseases by the World Health organization and thus, has been called “the silent killer”. It is also a leading cause of heart failure with preserved ejection fraction. Although the mechanisms by which hypertension leads to heart failure are not well elucidated, studies over the past three decades have identified changes in vascular stiffness, structural remodeling of the left ventricle and development of diastolic dysfunction (impaired relaxation and decreased compliance) as important components. (1) The term, “diastolic heart failure” has been used for years and preceded the more recently proposed term, “heart failure with preserved ejection fraction”. Regardless how these factors interact with each other, the fact is that by the time clinical manifestations of heart failure occur, patients show clear evidence of diastolic dysfunction and the majority have enlargement of the left atrium (LA). (2) Subtle abnormalities of myocardial contraction and relaxation have been documented in asymptomatic hypertensive patients with normal left ventricular (LV) ejection fraction. In 1992, Habib et al reported abnormalities of diastolic filling consistent with impaired relaxation in both ventricles of asymptomatic hypertensive patients using pulsed- wave Doppler. (3) The magnitude of changes in the right ventricle paralleled those observed in the left. Since then a multiple of publications have described diastolic abnormalities in hypertensive patients, and although they tend to worsen with concentric hypertrophy, they can occur in the absence of hypertrophy and improve with sustained blood pressure reduction.(4) Likewise, there are several reports of reduced systolic mid-wall circumferential strain, longitudinal systolic strain and mitral annular descent in asymptomatic hypertensive patients with normal EF. (5-7) Furthermore, contraction abnormalities have been shown to relate closely with diastolic abnormalities, implying a functional and/or structural effect of the disease on the contractile apparatus of the myocardium. (6) In this issue of Revista Argentina de Cardiologia, Deschle et al report finding subtle contractile abnor
Published Version
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