The hypertensive heart in groups of African ancestry in South Africa

Abstract

Hypertensive heart failure is a major cause of death and disability in Africa and the world today. Although much is known about the transition to heart failure in hypertension, there is uncertainty as to the dominant haemodynamic determinant of cardiac dysfunction across the adult lifespan. Furthermore, whether in volume-dependent hypertension, the foremost cause of hypertension in Africa, these effects can be adequately detected by the presence of left ventricular (LV) structural changes, is uncertain. In 605 to 709 participants from a community-based study in SOWETO, using central arterial pressure assessments and aortic velocity and diameter measured in the outflow tract (echocardiography); contemporary approaches to central arterial waveform construction and the assessment of LV cardiac systolic and diastolic function (tissue Doppler indexes), we therefore assessed the haemodynamic determinants and LV structural changes that account for LV dysfunction across the adult age range. We show that LV diastolic function linearly declines with age across the full adult lifespan starting from late teenage years and the principle factor accounting for these effects is a linear age-related increase in aortic reflected (backward) wave pressures. In contrast, neither systemic vascular resistance (SVR), that component of forward wave pressures determined by the product of aortic flow and characteristic impedance to flow (Zc)(PQxZc), or total arterial compliance determined age-related decreases in LV diastolic function independent of backward wave pressures. However, after 50 years of age, age-related increases in backward wave pressure were determined by PQxZc. Importantly, backward wave pressure effects were not adequately detected by brachial blood pressure (BP) measurements and hence alternative approaches to recognising the adverse effects are therefore required. As the detection of LV structural remodelling is a well-recognised method of identifying the adverse cardiac effects of hypertension, we then assessed whether LV hypertrophy (LVH) or geometric remodelling accounted for the impact of backward wave pressures and BP on LV diastolic function. However, because LVH depends as much on increases in stroke work (SW) as on afterload, the dominant volume-dependence of hypertension in this community sample (which increases stroke volume as hence SW), rendered LVH a poor index of the adverse effects of backward wave pressures and BP on LV diastolic function. This was explained by the lack of impact of SW on LV diastolic function. In addition, concentric LVH was as dependent on volume-dependent increases in stroke volume as eccentric LVH, and LV geometric remodelling was not associated with backward wave pressures or BP. Thus, concentric as opposed to eccentric LVH failed to better identify the presence of LV diastolic dysfunction.

The results of these studies either published, or in-press in the high impact journals, Hypertension, Journal of Hypertension and the American Journal of Hypertension, therefore provide insights into how best to prevent the development of hypertensive heart failure in Africa. In this regard, from 50 years of age, when brachial pulse pressure begins to increase, intense BP reduction is required in those with hypertension. This, is the only approach that will eliminate increases in backward wave pressures and hence prevent further deterioration of LV diastolic function. This is an essential approach as the impact of backward wave pressures is poorly detected at the brachial pulse; is not adequately indexed by the presence of concentric LV hypertrophy; and only a half of LV diastolic functional reserve remains at 50 years of age.