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Effective arterial elastance(EA) is a measure of the net arterial load imposed on the heart that integrates the effects of heart rate(HR), peripheral vascular resistance( PVR), and total arterial compliance(TAC) and is a modulator of cardiac performance. To what extent the change in EA during exercise impacts on cardiac performance and aerobic capacity is unknown. We examined EA and its relationship with cardiovascular performance in 352 healthy subjects. Subjects underwent rest and exercise gated scans to measure cardiac volumes and to derive EA[end-systolic pressure/stroke volume index(SV)], PVR[MAP/(SV*HR)], and TAC(SV/pulse pressure). EA varied with exercise intensity: the ΔEA between rest and peak exercise along with its determinants, differed among individuals and ranged from -44% to +149%, and was independent of age and sex. Individuals were separated into 3 groups based on their ΔEAI. Individuals with the largest increase in ΔEA(group 3;ΔEA⩾0.98 mmHg.m²/ml) had the smallest reduction in PVR, the greatest reduction in TAC and a similar increase in HR vs. group 1(ΔEA<0.22 mmHg.m²/ml). Furthermore, group 3 had a reduction in end-diastolic volume, and a blunted increase in SV(80%), and cardiac output(27%), during exercise vs. group 1. Despite limitations in the Frank-Starling mechanism and cardiac function, peak aerobic capacity did not differ by group because arterial-venous oxygen difference was greater in group 3 vs. 1. Thus the change in arterial load during exercise has important effects on the Frank-Starling mechanism and cardiac performance but not on exercise capacity. These findings provide interesting insights into the dynamic cardiovascular alterations during exercise. [ABSTRACT FROM AUTHOR]

The coupling between arterial elastance (EA; net afterload) and left ventricular elastance (ELV; pump performance), known as EA/ELV, is a key determinant of cardiovascular performance and shifts during exercise due to a grEAter incrEAse in ELV versus EA. This normal exercise-induced reduction in EA/ELV decrEAses with advancing age. We hypothesized that sodium nitroprusside (SNP) can acutely ameliorate the age-associated deficits in EA/ELV. At rest and during graded exercise to exhaustion, EA was characterized as end-systolic pressure/stroke volume and ELV as end-systolic pressure/end-systolic volume. Resting EA/ELV did not differ between old (70 ± 8 yr, n = 15) and young (30 ± 5 yr, n = 17) subjects because of a tandem incrEAse in EA and ELV in older subjects. During pEAk exercise, a blunted incrEAse in ELV in old (7.8 ± 3.1 mmHg/ml) versus young (11.4 ± 6.5 mmHg/ml) subjects blunted the normal exercise-induced decline in EA/ELV in old (0.25 ± 0.11) versus young (0.16 ± 0.05) subjects. SNP administration to older subjects lowered resting EA/ELV by 31% via a reduction in EA (10%) and an incrEAse in ELV (47%) and lowered pEAk exercise EA/ELV (36%) via an incrEAse in ELV (68%) without a change in EA. Importantly, SNP attenuated the age-associated deficits in EA/ELV and ELV during exercise, and at pEAk exercise EA/ELV in older subjects on drug administration did not differ from young subjects without drug administration. In conclusion, some age-associated deficiencies in EA/ELV, EA, and ELV, in older subjects can be acutely abolished by SNP infusion. This is relevant to common conditions in older subjects associated with a significant impairment of exercise performance such as frailty or hEArt failure with preserved ejection fraction. [ABSTRACT FROM AUTHOR]

In healthy subjects the arterial system and the left ventricle (LV) are tightly coupled at rest to optimize cardiac performance. Systolic hypertension (SH) is a major risk factor for heart failure and is associated with structural and functional alterations in the arteries and the LV. The effects of SH and resting systolic blood pressure (SBP) on arterial-ventricular coupling (EaI/ELVI) at rest, at peak exercise, and during recovery are not well described. We noninvasively characterized EaI/ELVI as end-systolic volume index/stroke volume index in subjects who were normotensive (NT, n = 203) or had SH (brachial SBP ≥140 mmHg, n = 79). Cardiac volumes were measured at rest and throughout exhaustive upright cycle exercise with gated blood pool scans. EaI/ELVI reserve was calculated by subtracting peak from resting EaI/ELVI. At rest, EaI/ELVI did not differ between SH and NT men but was 23% (P < 0.001) lower in SH vs. NT women. EaI/ELVI did not differ between SH and NT men or women at peak exercise or during recovery. Nevertheless, EaI/ELVI reserve was 61% (P < 0.001) lower in SH vs. NT women. Similarly, resting SBP (as a continuous variable) was not associated with EaI/ELVI in men (β = -0.12, P = 0.17) but was inversely associated with EaI/ELVI in women (β = -0.47, P < 0.001). SH and a higher resting brachial SBP are associated with a lower EaI/ELVI at rest in women but not in men, and SH women have an attenuated EaI/ELVI reserve. Whether a smaller EaI/ELVI reserve leads to functional limitations warrants further examination. [ABSTRACT FROM AUTHOR]

MRI and echocardiographic assessment of the diastolic dysfunction of normal aging: altered LV pressure decline or load? Am J Physiol Heart Circ Physiol 286: H782–H788, 2004. First published October 9, 2003; 10.1152/ajpheart.01092.2002.—Changes in diastolic indexes during normal aging, including reduced early filling velocity (E), lengthened E deceleration time (DT), augmented late filling (A), and prolonged isovolumic relaxation time (IVRT), have been attributed to slower left ventricular (LV) pressure (LVP) decay. Indeed, this constellation of findings is often referred to as the ‘abnormal relaxation’ pattern. However, LV filling is determined by the atrioventricular pressure gradient, which depends on both LVP decline and left atrial (LA) pressure (LAP). To assess the relative influence of LVP decline and LAP, we studied 122 normal subjects aged 21–92 yr by Doppler echocardiography and MRI. LVP decline was assessed by color M-mode (Vp) and the LV untwisting rate. Early diastolic LAP was evaluated using pulmonary vein flow systolic fraction, pulmonary vein flow diastolic DT, color M-mode (E/Vp), and tissue Doppler (E/Em). Linear regression showed the expected reduction of E, increase in A, and prolongation of IVRT and DT with advancing age. There was no relation of age to parameters reflecting the rate of LVP decline. However, older age was associated with reduced E/Vp (P = 0.008) and increased pulmonary vein systolic fraction (P < 0.001), pulmonary vein DT (P = 0.0026), and E/Em (P < 0.0001), all suggesting reduced early LAP. Therefore, reduced early filling in older adults may be more closely related to a reduced early diastolic LAP than to slower LVP decline. This effect also explains the prolonged IVRT. We postulate that changes in LA active or passive properties may contribute to development of the abnormal relaxation pattern during the aging process. [ABSTRACT FROM AUTHOR]