Ventricular Arterial Stiffening

Abstract

Abstract-Vascular stiffening of the large arteries is a common feature of aging and is exacerbated by many common disorders such as hypertension, diabetes, and renal disease. This change influences the phasic mechanical stresses imposed on the blood vessels that in turn is important to regulating smooth muscle tone, endothelial function, and vascular health. In addition, the heart typically adapts to confront higher and later systolic loads by both hypertrophy and ventricular systolic stiffening. This creates altered coupling between heart and vessel that importantly affects cardiovascular reserve function. In this overview, I discuss the notion of a coupling disease in which stiffness of both heart and arteries interact to limit performance and generate clinical symptoms. This involves changes in the mechanical interaction of both systems, changes in signaling within the arteries themselves, and alterations in coronary flow regulation. Lastly, I briefly review recent development in de-stiffening strategies that may pave the way to treat this syndrome and its clinical manifestations.

Ventricular–Arterial Coupling in Chronic Heart Failure

“…For example, in patients with heart failure with severely reduced LVEF these ratios may rise to as high as 4.0 due to the relative pressure-volume analyses can help us understand some aspects of the pathophysiology of HFpEF, including the limited stroke volume reserve, increased blood pressure lability and pre-load sensitivity in this population. 1,12,21,22 In particular, subjects with HFpEF have been shown to exhibit a reduced contractile and vasodilatory reserve during exercise, which reduces the "coupling" reserve, as manifested by a less pronounced reduction in the Ea/Ees ratio and a less pronounced increase in EF and cardiac index during exercise. 23 …”

The Effects of Aging and Physical Activity on Doppler Measures of Diastolic Function

“…17 Higher afterload decreases the ability of the ventricle to contract below the equilibrium volume during end-systole, thus preventing the development of diastolic suction during the next cardiac cycle. In the present study, the highly screened healthy, but sedentary, seniors had normal 24-hour ambulatory blood pressures, although as previously detailed, arterial elastance increased in sedentary seniors compared with fit seniors.…”

Ventricular-Arterial Coupling in Breast Cancer Patients After Treatment With Anthracycline-Containing Adjuvant Chemotherapy

“…Understanding not only how the heart and systemic vasculature function independently, but also how they interact (termed ventricular-arterial coupling) is important when evaluating global cardiovascular function [7]. Ventricular-arterial coupling combines a measure of net arterial load or arterial elastance (Ea) and end-systolic elastance (Ees), a loadindependent measure indicating LV contractility, specifically under stress [8].…”

“…Although ventricular-arterial coupling (Ea/ Ees) is inversely related to LVEF [9], it provides information beyond systolic function by also evaluating alterations in arterial function or ventricular function, or both. Under stress, Ea/Ees is a surrogate measure of cardiovascular reserve capacity (CVRC), because it permits integrative assessment of the heart and vasculature's ability to respond to an increased workload [7,10]. During exercise, the cardiovascular system favors Ees to supply appropriate cardiac output, resulting in a reduction in Ea/Ees [10].…”