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Cardiovascular System:
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
With high blood pressure (hypertension), the afterload effect is increased. The left ventricle must reach a higher pressure before it can push open the aortic valve against the higher aortic pressure. Thus, the isovolumic contraction period may be elongated, and there would be a shorter ejection period. This would result in a decrease in stroke volume that would have to be compensated for by a higher heart rate. Over time, this can lead to heart failure. In response to hypertension, the ventricular muscle may sometimes thicken in an attempt to achieve higher pressures. Usually, this thickening comes at the expense of the lumen size (concentric hypertrophy), and stroke volumes may again be decreased. Heart failure can also develop with an aortic valve stenosis (decreased ejection) or after a myocardial infarction (weakened muscles and decreased ejection).
Approaches to improving exercise capacity in patients with left ventricular assist devices: an area requiring further investigation
Published in Expert Review of Medical Devices, 2019
Richard Severin, Ahmad Sabbahi, Cemal Ozemek, Shane Phillips, Ross Arena
Afterload during exercise is mainly dependent on peripheral vascular function and the ability of the blood vessels to vasodilate in response to increased metabolic demand. Witman et al. demonstrated that flow-mediated dilation (FMD), a surrogate of endothelial-dependent vasodilation, was found to be reduced in patients with LVAD support compared to healthy controls and patients with HF with reduced ejection fraction (HFrEF) classified as NYHA stage II [31]. When % FMD was normalized to shear rate, patients with CF-LVAD support had reduced vascular function when compared to patients with HFrEF stages III/IV as well. When comparing nitroglycerin-induced dilation, a surrogate of endothelial-independent vasodilation, there were no significant differences between both groups [31], suggesting reduced endothelial function in patients with CF-LVAD support. This attenuation in endothelial function may be the result of a near lack of pulsatility in CF-LVAD devices and is supported by reduced FMD in patients with CF-LVAD compared to those with pf-LVAD support [30]. Interestingly, total vasodilatory capacity (reactive hyperemia – representing both endothelial-dependent and -independent vasodilation) was not found to be different between patients with LVAD support, patients with HFrEF, and healthy controls and would indicate the absence of microvascular dysfunction [31,49]. Further studies on the effect of vascular function on TCO and exercise tolerance in patients with CF-LVAD support are needed.