Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise

Abstract

Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (E(A)/E(LV)), is a central determinant of cardiovascular performance and cardiac energetics. E(A)/E(LV) can be indexed by the ratio of effective arterial elastance (E(A); a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (E(LV); a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, E(A)/E(LV) is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in E(LV) (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg.ml(-1).m(-2) in men and women, respectively) vs. E(A) (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg.ml(-1).m(-2) in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result E(A)/E(LV) decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of E(A)/E(LV), and examine the effects of age, hypertension, and heart failure on E(A)/E(LV) and its components (E(A) and E(LV)) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying E(A)/E(LV).

Figures

Fig. 1.

Ventricular pressure-volume diagram from which effective arterial elastance (EA) and left ventricular (LV) end-systolic elastance (ELV) are derived. EA represents the negative slope of the line joining the end-diastolic volume (EDV) and the end-systolic pressure (ESP) points. ELV represents the slope of the end-systolic pressure-volume relationship passing through the volume intercept (V0). The shaded area represents the cardiac stroke work (SW), and the hatched area represents the potential energy (PE). LV ESP is the LV pressure at the end of systole. EDV is the LV volume at the end of diastole. End-systolic volume (ESV) is the LV volume at the end of systole. Stroke volume (SV) is the volume of blood ejected by the LV with each beat and is obtained from subtracting ESV from EDV. BP, blood pressure; EF, ejection fraction; PVA, pressure-volume area.

Fig. 2.

The association between age and EA indexed to body surface area (EAI) (A) and ELV (Ees = ELV) (B) in men (solid line) and women (dashed line) at rest. Pearson correlation coefficients, and probability values for each association are shown. With advancing age, both EaI and Ees increase. However, the increase in Ees with age is significantly greater in women than men. Furthermore, EaI and Ees are higher in women vs. men at all ages. [Modified from Redfield et al. (61).]

Fig. 3.

Arterial ventricular coupling (EaI/ELVI) (A), EaI (B), and ELV indexed to body surface area (ELVI) (C) in men (dashed lines) and women (solid lines) <40 yr of age (triangles) and >60 yr of age (squares) in the supine and seated positions, at 50% of maximal workload, and at peak exercise. EaI/ELVI decreases during exercise in both young and older men and women (P < 0.0001). However, older men and women have a blunted decline in EaI/ELVI (P < 0.001). EAI increases during exercise in both young and older men and women (P < 0.0001). At maximal exercise, EAI is greater in older vs. younger women (P < 0.002). In contrast, EAI does not differ between young and older men. ELVI increases during exercise in both young and older men and women (P < 0.0001). At maximal exercise, ELVI is greater in younger vs. older men (P < 0.001) and tended to be greater in younger than older women (P = 0.07). [From Najjar et al. (50).]

Fig. 4.

EAI/ELVI (A), ELVI (B), and EAI (C), measured at rest in normotensive (NT) and systolic hypertensive (SH) men and women. EAI/ELVI does not differ at rest between NT and SH men due to tandem increases in EAI and ELVI in SH vs. NT men. In contrast, resting EAI/ELVI is lower in SH women vs. NT women, due to a disproportionate increase in ELVI vs. EAI. *P < 0.05, **P < 0.01, ***P < 0.001, comparing NT to SH after adjusting for age. [From Chantler et al. (15).]

Fig. 5.

The change in EAI/ELVI (A), EAI (B), and ELVI (C) in NT (solid symbols) and SH (open symbols) men (solid lines) and women (dashed lines). At rest, EAI/ELVI is similar between NT and SH men and is lower in SH vs. NT women (P < 0.01). EaI/ELVI decreases during exercise in both NT and SH men and women (P < 0.01). There are no differences between NT and SH men and women at 50% maximal workload (MWL) or at peak exercise. At rest, EAI is higher in SH vs. NT men and women (P < 0.001). EAI increases during exercise in both NT and SH men and women (P < 0.05). However, only SH men have a higher EAI at 50% MWL and at peak exercise vs. NT men (P < 0.001), as no differences are found between NT and SH women at 50% MWL or peak exercise. At rest, ELVI is higher in SH vs. NT men (P < 0.05). ELVI increases during exercise in both NT and SH men and women. However, only SH men have a higher ELVI at 50% MWL or at peak exercise vs. NT men (P < 0.001), as no differences are found between NT and SH women at 50% MWL or at peak exercise. [Modified from Chantler et al. (15).]

Fig. 6.

Pressure-volume relationships comparing the slope of the end-systolic pressure-volume relationship (ELV) and the slope of the line joining the ESP and EDV points (EA) between healthy controls (left) and systolic heart failure (HF) patients (right). Systolic HF patients have a downward and rightward shift of the end-systolic pressure-volume relationship, reflecting a reduced LV contractility. In addition, systolic HF patients have a higher EA than healthy controls. Thus, systolic HF patients have a higher resting arterial-ventricular coupling ratio than healthy controls.