Search

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 ([E.sub.a]I/[E.sub.LV]I) at rest, at peak exercise, and during recovery are not well described. We noninvasively characterized [E.sub.a]I/[E.sub.LV]I as end-systolic volume index/stroke volume index in subjects who were normotensive (NT, n = 203) or had SH (brachial SBP [greater than or equal to] 140 mmHg, n = 79). Cardiac volumes were measured at rest and throughout exhaustive upright cycle exercise with gated blood pool scans. [E.sub.a]I/[E.sub.LV]I reserve was calculated by subtracting peak from resting [E.sub.a]I/[E.sub.LV]I. At rest, [E.sub.a]I/[E.sub.LV]I did not differ between SH and NT men but was 23% (P = 0.001) lower in SH vs. NT women. [E.sub.a]I/[E.sub.LV]I did not differ between SH and NT men or women at peak exercise or during recovery. Nevertheless, [E.sub.a]I/[E.sub.LV]I reserve was 61% (P < 0.001) lower in SH vs. NT women. Similarly, resting SBP (as a continuous variable) was not associated with [E.sub.a]I/[E.sub.LV]I in men ([beta] = -0.12, P = 0.17) but was inversely associated with [E.sub.a]I/[E.sub.LV]I in women ([beta] = -0.47, P < 0.001). SH and a higher resting brachial SBP are associated with a lower [E.sub.a]I/[E.sub.LV]I at rest in women but not in men, and SH women have an attenuated [E.sub.a]I/[E.sub.LV]I reserve. Whether a smaller [E.sub.a]I/[E.sub.LV]I reserve leads to functional limitations warrants further examination. arterial elastance; left ventricular end-systolic elastance; systolic hypertension; exercise; sex

Circulating testosterone levels (T) decrease with age in men. Low T has been associated with coronary disease and with risk factors for atherosclerosis. This study examines the relationship in men between androgenic hormones and arterial stiffness, a major risk factor for cardiovascular events. T, sex hormone-binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEAS) were measured longitudinally over 33 yr (follow-up 11.8 [+ or -] 8.3 yr) in 901 men from the Baltimore Longitudinal Study of Aging, of whom 206 (68.1 [+ or -] 13.7 yr) underwent carotid duplex ultrasonography. The 901 men were used to characterize age-associated hormone levels by means of mixed-effects models. Hormone values were estimated for the 206 men at the time of ultrasonography. Free T index (FTI) was calculated by dividing T by SHBG. The arterial stiffness index was calculated from peak systolic and end diastolic diameters of the common carotid artery and simultaneous brachial artery blood pressure. T, FTI, and DHEAS were correlated negatively with age, pulse pressure (PP), and stiffness index (each P < 0.01), whereas SHBG was correlated positively with age and stiffness index (P < 0.01). However, T was the only hormone that predicted the stiffness index after adjustment for age, PP, fasting plasma glucose, body mass index, and total cholesterol. T values 5-10 yr before the carotid study also predicted the stiffness index (P < 0.05). Thus the adverse influence of low T on the cardiovascular system in men may be mediated in part via the effects of T on vascular structure and function. testosterone; dehydroepiandrosterone; carotid ultrasonography; intimal medial thickness; coronary heart disease

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 ([V.sub.p]) and the LV untwisting rate. Early diastolic LAP was evaluated using pulmonary vein flow systolic fraction, pulmonary veto flow diastolic DT, color M-mode (E/[V.sub.p]), and tissue Doppler (E/[E.sub.m]). 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/[V.sub.p] (P = 0.008) and increased pulmonary vein systolic fraction (P < 0.001), pulmonary vein DT (P = 0.0026), and E/[E.sub.m] (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. left ventricular deformation; torsion; untwist; noninvasive imaging. left atrial pressure

Aging is associated with a significant decline in exercise fitness assessed by maximal exercise oxygen consumption (VO2-max). The specific VO2-max components driving this decline, namely cardiac output (CO) and arteriovenous oxygen difference (A-V) O2, remain unclear. We examined this issue by analyzing data from 99 community-dwelling participants (baseline age 21-96 years; average follow-up 12.6 years) from the Baltimore Longitudinal Study of Aging, free of clinical cardiovascular disease. VO2-peak, a surrogate of VO2-max, was used to assess aerobic capacity during upright cycle exercise. Peak exercise left ventricular (LV) volumes, heart rate, and cardiac output were estimated using repeated gated cardiac blood pool scans. The Fick equation was used to calculate (A-V) O2-peak from CO-peak and VO2-peak. In unadjusted models, VO2-peak, (A-V) O2-peak, and CO-peakdeclined longitudinally over time at steady rates with advancing age. In multiple linear regression models adjusting for baseline values and peak workload, however, steeper declines in VO2-peak and (A-V) O2 peak were observed with advanced entry age but not in CO-peak. The association between the declines in VO2-peak and (A-V) O2-peakwas stronger among those >=50 years compared to their younger counterparts but the difference between the two age groups did not reach statistical significance. These findings suggest that age-associated impairment of peripheral oxygen utilization during maximal exercise poses a stronger limitation on peak VO2 than that of CO. Future studies examining interventions targeting the structure and function of peripheral muscles and their vasculature to mitigate age-associated declines in (A-V) O2 are warranted.

Effective arterial elastance(E(A)) 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 E(A) during exercise impacts on cardiac performance and aerobic capacity is unknown. We examined E(A) and its relationship with cardiovascular performance in 352 healthy subjects. Subjects underwent rest and exercise gated scans to measure cardiac volumes and to derive E(A)[end-systolic pressure/stroke volume index(SV)], PVR[MAP/(SV*HR)], and TAC(SV/pulse pressure). E(A) varied with exercise intensity: the ΔE(A) 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 ΔE(A)I. Individuals with the largest increase in ΔE(A)(group 3;ΔE(A)≥0.98 mmHg.m(2)/ml) had the smallest reduction in PVR, the greatest reduction in TAC and a similar increase in HR vs. group 1(ΔE(A)<0.22 mmHg.m(2)/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.

The coupling between arterial elastance (E(A); net afterload) and left ventricular elastance (E(LV); pump performance), known as E(A)/E(LV), is a key determinant of cardiovascular performance and shifts during exercise due to a greater increase in E(LV) versus E(A). This normal exercise-induced reduction in E(A)/E(LV) decreases with advancing age. We hypothesized that sodium nitroprusside (SNP) can acutely ameliorate the age-associated deficits in E(A)/E(LV). At rest and during graded exercise to exhaustion, E(A) was characterized as end-systolic pressure/stroke volume and E(LV) as end-systolic pressure/end-systolic volume. Resting E(A)/E(LV) did not differ between old (70 ± 8 yr, n = 15) and young (30 ± 5 yr, n = 17) subjects because of a tandem increase in E(A) and E(LV) in older subjects. During peak exercise, a blunted increase in E(LV) in old (7.8 ± 3.1 mmHg/ml) versus young (11.4 ± 6.5 mmHg/ml) subjects blunted the normal exercise-induced decline in E(A)/E(LV) in old (0.25 ± 0.11) versus young (0.16 ± 0.05) subjects. SNP administration to older subjects lowered resting E(A)/E(LV) by 31% via a reduction in E(A) (10%) and an increase in E(LV) (47%) and lowered peak exercise E(A)/E(LV) (36%) via an increase in E(LV) (68%) without a change in E(A). Importantly, SNP attenuated the age-associated deficits in E(A)/E(LV) and E(LV) during exercise, and at peak exercise E(A)/E(LV) in older subjects on drug administration did not differ from young subjects without drug administration. In conclusion, some age-associated deficiencies in E(A)/E(LV), E(A), and E(LV), 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.