Abstract

See related article, pp 633–640 Afterload is an important determinant of myocardial contraction and relaxation. Afterload dependency of relaxation has been demonstrated in the intact left ventricle (LV).1–4 Experimental animal2,3 and human4 studies demonstrate that the effects of afterload depend on its timing, with late systolic load inducing more profound impairments in LV relaxation, compared with early systolic load. In this issue of Hypertension , Gu et al5 report on a study that provides novel insights into diastolic–systolic coupling and helps us integrate and reconcile several previous findings. Although the terms myocardial afterload and ventricular afterload are often used interchangeably, it is important to recognize that the relationship between LV and myocardial afterload is markedly influenced by the time-varying LV geometry during systole, which in turn affects the myocardial wall stress (MWS) for any given LV chamber pressure. LV afterload is the hydraulic load imposed by the entire systemic circulation (aortic input impedance), which depends on the pressure required to generate flow (ejection) into the proximal aorta. In contrast, myocardial afterload is determined by the MWS required to generate fiber shortening. In line with Laplace's law of the heart, for any given LV pressure, lower MWS occurs as the ratio of LV chamber volume/LV wall volume decreases. When the MWS and LV geometry are such that LV pressure exceeds diastolic aortic pressure, LV ejection starts. Throughout ejection, the time-varying MWS (and fiber shortening) is determined by complex interactions between myocardial contractile elements, the instantaneous LV geometry and the time-varying hydraulic load imposed by the arterial tree.6 All key correlates of MWS (LV wall thickness, cavity size, and pressure, which for any given flow ejected, depends on the aortic input impedance) exhibit marked variations during ejection. Therefore, time-resolving MWS during ejection (rather …

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