Influence of Vascular Function and Pulsatile Hemodynamics on Cardiac Function

Abstract

Interactions between cardiac and vascular structure and function normally are optimized to ensure delivery of cardiac output with modest pulsatile hemodynamic overhead. Aortic stiffening with age or disease impairs optimal ventricular-vascular coupling, increases pulsatile load, and contributes to left ventricular (LV) hypertrophy, reduced systolic function, and impaired diastolic relaxation. Aortic pulse pressure and timing of peak systolic pressure are well-known measures of hemodynamic ventricular-vascular interaction. Recent work has elucidated the importance of direct, mechanical coupling between the aorta and the heart. LV systolic contraction results in displacement of aortic and mitral annuli, thereby producing longitudinal stretch in the ascending aorta and left atrium, respectively. Force associated with longitudinal stretch increases systolic load on the LV. However, the resulting energy stored in the elastic elements of the proximal aorta during systole facilitates early diastolic LV recoil and rapid filling. This review discusses current views on hemodynamics and mechanics of ventricular-vascular coupling.

Aortic stiffness, pressure and flow pulsatility, and target organ damage

“…During diastole (right), recoil of the aortic spring pulls the base of the heart upward (green arrow), which translocates a volume of blood from the left atrium into the LV (pink disk), because of motion of the atrioventricular plane alone, but also stretches and thins the walls of the LV, creating suction that facilitates early diastolic filling (thick, black arrow). [Reprinted by permission from Springer Nature Current Hypertension Reports (c) 2015 Bell and Mitchell (9).] the hypothesis that disproportionate stiffening of the aorta leads to impedance matching, which reduces wave reflection and increases transmission of harmful pulsatility into the microcirculation, where it causes small vessel damage that is quantifiable by imaging and associated with reduced function, as was evident in cognitive testing.…”

Global left atrial failure in heart failure

“…Another factor adversely affecting LA size and mechanical function, which is frequently observed in patients with HF and preserved ejection fraction (HFpEF), is stiffening of the aorta; this impairs optimal ventricular–vascular coupling, increases pulsatile load, and contributes to LV hypertrophy, reduced systolic function, and impaired diastolic relaxation …”

Female Heart Health: Is GPER the Missing Link?

“…During systole, the long axis of the left ventricle normally shortens by pulling the aortic annulus toward the relatively fixed LV apex (162,163). Displacement of the aortic annulus and sinotubular junction without concomitant movement of the aortic arch during systole promotes longitudinal stretch of the proximal aorta (162,164,165). While the aortic stretch that occurs during systole imposes a systolic load on the heart, it actually enhances early diastolic filling by serving as a reservoir for elastic energy (165).…”

“…Displacement of the aortic annulus and sinotubular junction without concomitant movement of the aortic arch during systole promotes longitudinal stretch of the proximal aorta (162,164,165). While the aortic stretch that occurs during systole imposes a systolic load on the heart, it actually enhances early diastolic filling by serving as a reservoir for elastic energy (165). With loss of aortic distensibility due to advancing age, and presumably estrogen deficiency (163), or HFpEF (166) the displacement of the aortic annulus is reduced, as is the longitudinal long axis force or shortening of the left ventricle, leading to less stored elastic energy and impaired LV filling (167).…”