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Cardiovascular aging is a complex process of adaptive structural and functional changes over time. With advancing age, the arterial tree thickens and decreases in compliance, resulting in increased pulse wave velocity, systolic blood pressure, and left ventricular afterload. In response to these arterial changes, the myocardium remodels to maintain systolic function and diastolic filling. These adaptive mechanisms are not necessarily pathologic but increase the susceptibility for myocardial ischemia and heart failure in the presence of common age-associated comorbidities. This article reviews the pathophysiology of cardiovascular aging and discusses therapeutic interventions that may ameliorate these processes., (© 2019 The Authors. Clinical Cardiology published by Wiley Periodicals, Inc.)

Heart failure (HF) increases significantly in relation to advancing age, yet management for HF in very old adults remains ambiguous. With aging, not only do age-related, morphological and physiological cardiovascular changes predispose to HF, there is also increased prevalence of comorbid conditions that compound cardiac limitations (e.g., renal insufficiency and chronic obstructive lung disease) and others that tend to overwhelm limited cardiovascular reserves (e.g., infections and ischemia). Standard HF pharmacological and device therapies do little to moderate the wide spectrum of insidious age-related processes that are elemental to HF pathophysiology among older patients. Moreover, the utility of standard HF therapy is usually premised on its efficacy for life prolongation, whereas quality of life, increased physical and cognitive function, and preserved independence may be regarded as higher (or even highest) priority. In this review we study age-related susceptibility to HF, as well as the utility and limitations of standard HF strategies. Both HF with reduced ejection fraction and HF with preserved ejection fraction are considered.

Objectives: This study sought to determine the clinical predictors and prognostic significance of exercise-induced nonsustained ventricular tachycardia (NSVT) in a large population of asymptomatic volunteers., Background: Prior studies have reported variable risk associated with exercise-induced ventricular arrhythmia., Methods: Subjects in the BLSA (Baltimore Longitudinal Study of Aging) free of known cardiovascular disease who completed at least 1 symptom-limited exercise treadmill test between 1977 and 2001 were included. NSVT episodes were characterized by QRS morphology, duration, and rate. Subjects underwent follow-up clinical evaluation every 2 years., Results: The 2,099 subjects (mean age: 52 years; 52.2% male) underwent a mean of 2.7 exercise tests, in which 79 (3.7%) developed NSVT with exercise on at least 1 test. The median duration of NSVT was 3 beats (≤5 beats in 84%), and the median rate was 175 beats/min. Subjects with (vs. without) NSVT were older (67 ± 12 years vs. 51 ± 17 years, p < 0.0001) and more likely to be male (80% vs. 51%, p < 0.0001) and to have baseline electrocardiographic abnormalities (50% vs. 17%, p < 0.0001) or ischemic ST-segment changes with exercise (20% vs. 10%, p = 0.004). Over a mean follow-up of 13.5 ± 7.7 years, 518 deaths (24.6%) occurred. After multivariable adjustment for age, sex, and coronary risk factors, exercise-induced NSVT was not significantly associated with total mortality (hazard ratio: 1.30; 95% confidence interval: 0.89 to 1.90; p = 0.17)., Conclusions: Exercise-induced NSVT occurred in nearly 4% of this asymptomatic adult cohort. This finding increased with age and was more common in men. After adjustment for clinical variables, exercise-induced NSVT did not independently increase the risk of total mortality., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Normal aging is associated with a multitude of changes in the cardiovascular system, including decreased compliance of blood vessels, mild concentric left ventricular hypertrophy, an increased contribution of atrial contraction to left ventricular filling, and a higher incidence of many cardiac arrhythmias, both bradyarrhythmias and tachyarrhythmias. Conduction disorders also become more common with age, and may either be asymptomatic, or cause hemodynamic changes requiring treatment. The epidemiology of common arrhythmias and conduction disorders in the elderly is reviewed., (Published by Elsevier Inc.)

Important changes occur in the cardiovascular system with advancing age, even in apparently healthy individuals. Thickening and stiffening of the large arteries develop due to collagen and calcium deposition and loss of elastic fibers in the medial layer. These arterial changes cause systolic blood pressure to rise with age, while diastolic blood pressure generally declines after the sixth decade. In the left ventricle, modest concentric wall thickening occurs due to cellular hypertrophy, but cavity size does not change. Although left ventricular systolic function is preserved across the age span, early diastolic filling rate declines 30-50% between the third and ninth decades. Conversely, an age-associated increase in late diastolic filling due to atrial contraction preserves end-diastolic volume. Aerobic exercise capacity declines approximately 10% per decade in cross-sectional studies; in longitudinal studies, however, this decline is accelerated in the elderly. Reductions in peak heart rate and peripheral oxygen utilization but not stroke volume appear to mediate the age-associated decline in aerobic capacity. Deficits in both cardiac β-adrenergic receptor density and in the efficiency of postsynaptic β-adrenergic signaling contribute significantly to the reduced cardiovascular performance during exercise in older adults. Although these cardiovascular aging changes are considered "normative", they lower the threshold for the development of cardiovascular disease, which affects the majority of older adults.

A decline in maximal aerobic exercise capacity occurs across the adult age-span, accelerating in later years. This age-associated decline in aerobic capacity is accentuated by superimposed comorbidities common to the elderly such as cardiac, pulmonary, and peripheral artery disease. However, observational and training studies demonstrate significant improvement in peak oxygen consumption in both health and disease settings. In addition, exercise training exerts beneficial effects on blood pressure, lipids, glucose tolerance, bone density, depression, and quality of life. A major challenge to physicians and society is to increase the low participation rates of older adults in both home-based exercise and supervised exercise rehabilitation programs.

Increasing life expectancy in industrialized societies has resulted in a huge population of older adults with cardiovascular disease. Despite advances in device therapy and surgery, the mainstay of treatment for these disorders remains pharmacological. Hypertension affects two-thirds of older adults and remains a potent risk factor for coronary artery disease, chronic heart failure, atrial fibrillation, and stroke in this age group. Numerous trials have demonstrated reduction in these adverse outcomes with antihypertensive drugs. After acute myocardial infarction, β-adrenergic blockers reduce mortality regardless of patient age. Statins and antiplatelet drugs have proven beneficial in both primary and, especially, secondary prevention of coronary events in older adults. In elders with chronic heart failure, loop diuretics must be used cautiously, owing to their higher potential for adverse effects, whereas angiotensin-converting-enzyme inhibitors and β-blockers reduce symptoms and prolong survival. The high risk of stroke in elderly patients with atrial fibrillation is markedly reduced with warfarin, although bleeding risk is increased. The high prevalence of polypharmacy among older adults with cardiovascular disease, coupled with age-associated physiological changes and comorbidities, provides major challenges in adherence and avoidance of drug-related adverse events.

Objectives: This study sought to evaluate whether pulse wave velocity (PWV), a noninvasive index of arterial stiffness, is a predictor of the longitudinal changes in systolic blood pressure (SBP) and of incident hypertension., Background: Although arterial stiffness is believed to underlie, in part, the age-associated changes in SBP, particularly at older ages, few longitudinal studies in humans have examined the relationship between arterial stiffness and blood pressure., Methods: Pulse wave velocity was measured at baseline in 449 normotensive or untreated hypertensive volunteers (age 53 +/- 17 years). Repeated measurements of blood pressure were performed during an average follow-up of 4.9 +/- 2.5 years., Results: After adjusting for covariates including age, body mass index, and mean arterial pressure, linear mixed effects regression models showed that PWV was an independent determinant of the longitudinal increase in SBP (p = 0.003 for the interaction term with time). In a subset of 306 subjects who were normotensive at baseline, hypertension developed in 105 (34%) during a median follow-up of 4.3 years (range 2 to 12 years). By stepwise Cox proportional hazards models, PWV was an independent predictor of incident hypertension (hazard ratio 1.10 per 1 m/s increase in PWV, 95% confidence interval 1.00 to 1.30, p = 0.03) in individuals with a follow-up duration greater than the median., Conclusions: Pulse wave velocity is an independent predictor of the longitudinal increase in SBP and of incident hypertension. This suggests that PWV could help identify normotensive individuals who should be targeted for the implementation of interventions aimed at preventing or delaying the progression of subclinical arterial stiffening and the onset of hypertension.

Objectives: The purpose of this study was to characterize how aging impacts the left ventricular (LV) functional reserve., Background: Early diastolic LV filling slows markedly with advancing age, but the effects of beta-adrenergic stimulation on filling, and its major determinant, relaxation, have not been investigated in an aging population. Although the responses of contractility and heart rate to catecholamines reportedly diminish with age, the effect of age on the responses to steady-state dobutamine infusions is unclear., Methods: Groups of younger (40 +/- 10 years, n = 26) and older (68 +/- 11 years, n = 24) normal adult patients were studied at baseline and at three progressive dobutamine infusion dosages (5, 10, and 20 mug/kg/min). The LV function was evaluated by two-dimensional and Doppler echocardiography. Myocardial relaxation was evaluated from cardiovascular magnetic resonance (CMR)-based rho, a preload-independent surrogate for tau . Effective LV pump-function index (PFi), defined as systolic blood pressure/end-systolic LV diameter, was measured., Results: Both groups showed expected dose-dependent increases in heart rate and LV systolic function, diastolic function, and relaxation. Early LV filling reserve was much greater in younger than older patients (E-wave increase from baseline to highest dose, 24.0 vs. 9.5 cm/s, p < 0.004), although the dose responses of rho were indistinguishable (0.18% vs. 0.19%/ms, p = 0.22). Whereas dobutamine caused a significantly greater increase of PFi in younger than older patients (30.1 vs. 15.6 mm Hg/cm, p < 0.0001), there was no difference in heart rate augmentation (37 vs. 38 beats/min, p = 0.94)., Conclusions: Aging is accompanied by a blunted inotropic but preserved chronotropic response to steady-state dobutamine infusion. Although LV filling reserve declines with age, relaxation reserve does not.

Background: The ability of older persons to function independently is dependent largely on the maintenance of sufficient aerobic capacity and strength to perform daily activities. Although peak aerobic capacity is widely recognized to decline with age, its rate of decline has been estimated primarily from cross-sectional studies that may provide misleading, overly optimistic estimates of aging changes., Methods and Results: To determine longitudinal rate of change in aerobic capacity and the influence of age, gender, and physical activity on these changes, we performed serial measurements of peak treadmill oxygen consumption (peak VO2) in 375 women and 435 men ages 21 to 87 years from the Baltimore Longitudinal Study of Aging, a community-dwelling cohort free of clinical heart disease, over a median follow-up period of 7.9 years. A linear mixed-effects regression model was used to calculate the predicted longitudinal 10-year rate of change in peak VO2, expressed in milliliters per minute, for each age decade from the 20s through the 70s after adjustment for self-reported leisure-time physical activity. A longitudinal decline in peak VO2 was observed in each of the 6 age decades in both sexes; however, the rate of decline accelerated from 3% to 6% per 10 years in the 20s and 30s to >20% per 10 years in the 70s and beyond. The rate of decline for each decade was larger in men than in women from the 40s onward. Similar longitudinal rates of decline prevailed when peak VO2 was indexed per kilogram of body weight or per kilogram of fat-free mass and in all quartiles of self-reported leisure-time physical activity. When the components of peak VO2 were examined, the rate of longitudinal decline of the oxygen pulse (ie, the O2 utilization per heart beat) mirrored that of peak VO2, whereas the longitudinal rate of heart rate decline averaged only 4% to 6% per 10 years, and accelerated only minimally with age., Conclusions: The longitudinal rate of decline in peak VO2 in healthy adults is not constant across the age span in healthy persons, as assumed by cross-sectional studies, but accelerates markedly with each successive age decade, especially in men, regardless of physical activity habits. The accelerated rate of decline of peak aerobic capacity has substantial implications with regard to functional independence and quality of life, not only in healthy older persons, but particularly when disease-related deficits are superimposed.

Saturated fat (SF) intake contributes to the risk of coronary heart disease (CHD) mortality. Recently, the protective effects of fruit and vegetable (FV) intake on both CHD and all-cause mortality were documented. However, individuals consuming more FV may be displacing higher-fat foods. Therefore, we investigated the individual and combined effects of FV and SF consumption on total and CHD mortality among 501 initially healthy men in the Baltimore Longitudinal Study of Aging (BLSA). Over a mean 18 y of follow-up, 7-d diet records were taken at 1-7 visits. Cause of death was ascertained from death certificates, hospital records, and autopsy data. After adjustment for age, total energy intake, BMI, smoking, alcohol use, dietary supplements, and physical activity score, FV and SF intakes were individually associated with lower all-cause and CHD mortality (P < 0.05). When both FV and SF were included in the same model, associations of each were attenuated with CHD mortality, and no longer significant for all-cause mortality. Men consuming the combination of > or =5 servings of FV/d and < or =12% energy from SF were 31% less likely to die of any cause (P < 0.05), and 76% less likely to die from CHD (P < 0.001), relative to those consuming < 5 FV and >12% SF. Men consuming either low SF or high FV, but not both, did not have a significantly lower risk of total mortality; but did have 64-67% lower risk of CHD mortality (P < 0.05) relative to those doing neither. These results confirm the protective effects of low SF and high FV intake against CHD mortality. In addition, they extend these findings by demonstrating that the combination of both behaviors is more protective than either alone, suggesting that their beneficial effects are mediated by different mechanisms.

Objectives: The goal of this study was to examine the age-associated differences in ventricular-vascular coupling, defined by the ratio of arterial elastance (EaI) to left ventricular systolic elastance (E(LV)I), and its components, at rest and during exercise., Background: Ejection fraction (EF) increases during exercise, but the EF reserve decreases with aging. Ejection fraction is inversely related to EaI/E(LV)I, an index of the interaction between arterial and ventricular properties, which is an important determinant of cardiac performance. Thus, age differences in EaI/E(LV)I during exercise, due to age differences in EaI, E(LV)I, or both, may help to explain the age deficit in EF reserve., Methods: We noninvasively characterized EaI/E(LV)I = end-systolic volume index (ESVI)/stroke volume index (SVI) and its two determinants EaI = end-systolic pressure/SVI, and E(LV)I = end-systolic pressure/ESVI, at rest and during exercise in 239 healthy men and women (age range, 21 to 87 years). Blood pressures were assessed with cuff sphygomanometry, and cardiac volumes with gated blood pool scintingraphy., Results: Resting EaI/E(LV)I was not age related in men or women. In both sexes, EaI/E(LV)I decreased during exercise and declined to a lesser extent in older subjects. There were gender differences in the components of EaI/E(LV)I during exercise: EaI was greater in older versus young women (p = 0.01) but was unaffected by age in men. Left ventricular systolic elastance increased to a greater extent in young versus older subjects (p = 0.0001 for men, p = 0.07 for women)., Conclusions: Age-associated differences in EaI/E(LV)I occur in both genders during exercise. Sub-optimal ventricular-vascular coupling helps to explain the age-associated blunting of maximal exercise EF, and its underlying mechanisms appear to differ between men and women.

Purpose: The purpose of this study was to determine the effects of 6 months of whole-body resistive training (RT) on total and regional bone mineral density (BMD) and bone mineral content (BMC) by age and gender in young and older men and women., Methods: Younger men (n=10) and women (n=7) aged 20-29 years (25+/-1 years) and older men (n=10) and women (n=10) aged 65-74 years (69+/-1 years) participated in 6 months of progressive whole-body RT. Upper- and lower-body strength was assessed by the one repetition maximum (1RM) test, and total body fat, lean tissue mass, femoral neck BMD, Ward's triangle BMD, greater trochanter BMD, total-body BMD, and L2-L4 spine BMD were determined by dual-energy X-ray absorptiometry before and after 6 months of RT., Results: Percent body fat decreased only in the young men (P<0.05). Lean tissue mass increased after training in young men and women and older men (P<0.05) but did not change significantly in older women. Upper- and lower-body 1RM strength increased in all groups (P<0.01). Overall, there was a significant increase in BMD at the femoral neck, ward's triangle and greater trochanter BMD, as well as total body BMC and leg BMC (P<0.05). Total-body BMD and L2-L4 spine BMD did not change with RT. There were no gender differences in the training response between men and women for any of the BMD regions and no age differences in the training response, except for a trend between young and older subjects for femoral neck (P<0.08)., Conclusion: A 6-month RT program increases muscle mass and improves BMD of the femoral region in young and healthy older men and women as a group, with a trend for this to be greater in young subjects.

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(p)) 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/V(p)), and tissue Doppler (E/E(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(p) (P = 0.008) and increased pulmonary vein systolic fraction (P < 0.001), pulmonary vein DT (P = 0.0026), and E/E(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.

Echocardiographic left ventricular (LV) wall thickness increases with age, suggesting LV hypertrophy. However, autopsy studies have shown no change, or even a decrease, in LV mass with age. With many pathologies, LV remodeling results in changes in ventricular shape. Age-associated LV shape change might explain this discrepancy, although this has not been studied. Magnetic resonance imaging (MRI) was used in 336 healthy, normotensive adults (mean age 56 +/- 18 years; 200 women, 136 men) to measure LV mass, end-diastolic LV wall thickness, length, diameter, and shape. Echocardiographic LV mass was measured in a subset of 86 subjects by a standard algorithm. In women, LV wall thickness increased by 14% (r = 0.19, p <0.02), whereas LV length decreased by 9% (r = -0.26, p = 0.0006); LV diameter was unchanged. Thus, LV mass did not vary with age (r -0.04, p = 0.06) and the sphericity index decreased (r = -0.165, p <0.05). In men, LV wall thickness and diameter were unrelated to age, but there was an 11% decrease in LV length (r = -0.29, p = 0.003); therefore, there was an 11% decrease in LV mass (r = -0.20, p = 0.019) and a decrease in the sphericity index (r = -0.218, p <0.04). No change occurred in echocardiographic LV mass with age in either gender, although echocardiographic LV wall thickness increased in both. The left ventricle becomes more spherical with age in normal adults due to reduced LV length. In women, increased LV wall thickness offsets the decreasing LV length, whereas in men, LV wall thickness fails to compensate, resulting in decreased LV mass with age.

Objective: The goal of this study was to determine the effect of age on the hemodynamic response to prolonged submaximal aerobic exercise in healthy volunteers., Background: Reductions in peak work rate, heart rate (HR), and left ventricular (LV) emptying but higher blood pressure (BP) and systemic vascular resistance occur in healthy older versus younger humans during short bursts of graded maximal aerobic exercise. However, the effect of aging on the cardiovascular response to prolonged exercise at submaximal work rates typical of daily aerobic activities remains unknown., Methods: We evaluated cardiovascular performance throughout prolonged submaximal upright cycle ergometry in 40 carefully screened healthy untrained volunteers, 8 men and 12 women <50 years old, mean = 37 +/- 8 years (younger), and 10 men and 10 women >/=50 years old, mean = 66 +/- 9 years (older), during upright cycle exercise at 70% of peak cycle oxygen consumption (VO(2)) to exhaustion or a maximum of 120 min. Cardiac volumes were acquired by gated blood pool scans with (99m)Tc at rest and every 10 min throughout exercise., Results: Duration of exercise was similar in younger ([81 +/- 28 min] versus older [71+/- 29 min] subjects, p = NS). At 10 min of exercise in the steady state, older subjects demonstrated lower VO(2) (1.1 +/- 0.2 l/min vs. 1.3 +/- 0.3 l/min) and lower HR (118 +/- 17 vs. 135 +/- 11 beats/min, p < 0.001) but larger end-diastolic (80 +/- 11 ml/m(2) vs. 73 +/- 8 ml/m(2), p = 0.03) and end-systolic volume index (ESVI) 20 +/- 6 ml/m(2) vs. 17 +/- 4 ml/m(2), p < 0.05) than younger ones. Between 10 min and exercise termination, with VO(2) held constant in both groups, increases in HR (14.0 +/- 12.4 beats/min vs. 5.9 +/- 11.5 beats/min, p = 0.04), cardiac index (1.6 +/- 1.0 l/min/m(2) vs. 0.8 +/- 1.1 l/min/m(2), p = 0.03), and LV ejection fraction (7.1 +/- 4.0% vs. 2.9 +/- 4.4%, p = 0.003) were greater in younger than older subjects, respectively, as was the reduction in ESVI (-5.1 +/- 3.0 ml/m(2) vs. -1.8 +/- 3.3 ml/m(2), p = 0.002), despite similar declines in systolic BP (-12.3 +/- 6.3 mm Hg vs. -12.1 +/- 15.0 mm Hg, p = NS)., Conclusions: Thus, age-associated deficits in chronotropic and LV systolic reserve performance occur during prolonged submaximal upright cycle ergometry, analogous to those observed during graded maximal exercise.

BackgroundIn the main Digitalis Investigation Group (DIG) trial, digoxin reduced the risk of 30-day all-cause hospitalization in older systolic heart failure patients. However, this effect has not been studied in older diastolic heart failure patients.MethodsIn the ancillary DIG trial, of the 988 patients with chronic heart failure and preserved (> 45%) ejection fraction, 631 were age ≥ 65 years (mean age 73 years, 45% women, 12% non-whites), of whom 311 received digoxin.ResultsAll-cause hospitalization 30-day post randomization occurred in 4% of patients in the placebo group and 9% each among those in the digoxin group receiving 0.125 mg and ≥ 0.25 mg a day dosage (P = .026). Hazard ratios (HR) and 95% confidence intervals (CI) for digoxin use overall for 30-day, 3-month, and 12-month all-cause hospitalizations were 2.46 (1.25-4.83), 1.45 (0.96-2.20) and 1.14 (0.89-1.46), respectively. There was one 30-day death in the placebo group. Digoxin-associated HRs (95% CIs) for 30-day hospitalizations due to cardiovascular, heart failure, and unstable angina causes were 2.82 (1.18-6.69), 0.51 (0.09-2.79), and 6.21 (0.75-51.62), respectively. Digoxin had no significant association with 30-day all-cause hospitalization among younger patients (6% vs 7% for placebo; HR 0.80; 95% CI, 0.36-1.79).ConclusionsIn older patients with chronic diastolic heart failure, digoxin increased the risk of 30-day all-cause hospital admission, but not during longer follow-up. Although chance finding due to small sample size is possible, these data suggest that unlike in systolic heart failure, digoxin may not reduce 30-day all-cause hospitalization in older diastolic heart failure patients.

BackgroundHeart failure is the leading cause for hospital readmission, the reduction of which is a priority under the Affordable Care Act. Digoxin reduces 30-day all-cause hospital admission in chronic systolic heart failure. Whether digoxin is effective in reducing readmission after hospitalization for acute decompensation remains unknown.MethodsOf the 5153 Medicare beneficiaries hospitalized for acute heart failure and not receiving digoxin, 1054 (20%) received new discharge prescriptions for digoxin. Propensity scores for digoxin use, estimated for each of the 5153 patients, were used to assemble a matched cohort of 1842 (921 pairs) patients (mean age, 76 years; 56% women; 25% African American) receiving and not receiving digoxin, who were balanced on 55 baseline characteristics.ResultsThirty-day all-cause readmission occurred in 17% and 22% of matched patients receiving and not receiving digoxin, respectively (hazard ratio [HR] for digoxin, 0.77; 95% confidence interval [CI], 0.63-0.95). This beneficial association was observed only in those with ejection fraction

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]

Increased thickness and stiffness of large arteries may contribute to why aging is the most important risk for cardiovascular diseases. Arterial stiffness, intimal medial thickness, and alcohol intake were measured in 563 subjects. A U-shaped relation was found between alcohol intake and a stiffness index, with the lowest index in moderate drinkers, which may partially explain the relation between alcohol and cardiovascular disease. [Copyright &y& Elsevier]

OBJECTIVES: To compare the longitudinal changes in maximal aerobic capacity (VO2 max) in healthy middle aged and older athletes and sedentary men. DESIGN: A cohort study with mean follow-up of 8.7 years (range 4.0–12.8). SETTING: Outpatient research at a tertiary hospital. PARTICIPANTS: Forty-two healthy, middle aged, and older athletes (initial age 64 ± 1 year) and 47 healthy sedentary men of comparable age recruited for research studies. MEASUREMENTS: VO2 max during a maximal treadmill test. RESULTS: At baseline, the cross-sectional rates of decline in VO2 max with age (slope) were virtually identical in the athletes and sedentary men (-0.42 versus -0.43 mL·kg-1 · min-1 ·year-1 ). At follow-up, the VO2 max had declined by 11.9 ± 1.1 mL·kg-1 ·min-1 (22%) in the athletes, a crude average rate of -1.4 ± 0.14 mL·kg-1 ·min-1 ·year-1 . By comparison, the VO2 max declined by 4.4 ± 0.6 mL·kg-1 · min-1 (14%) in the sedentary men, a crude average rate of change of -0.48 ± 0.07 mL·kg-1 ·min-1 ·year-1 . Therefore, the observed absolute rate of longitudinal decline in VO2 max in the athletes was triple that of the sedentary men (P = .001) and significantly greater than the decline predicted by their baseline cross-sectional data (P = .001). Post hoc analyses of the longitudinal data in the athletes based on the training regimens over the follow-up period demonstrated that the seven individuals who continued to train vigorously (“high training”) had no significant decline in VO2 max (0.28% change in VO2 max per year). By contrast, the VO2 max declined by 2.6% per year in the “moderate training” group (N = 21),... [ABSTRACT FROM AUTHOR]

OBJECTIVES: To examine the possible influences of age and gender on muscle volume responses to strength training (ST). DESIGN: Prospective intervention study. SETTING: University of Maryland Exercise Science and Wellness Research Laboratories. PARTICIPANTS: Eight young men (age 20–30 years), six young women (age 20–30 years), nine older men (age 65–75 years), and ten older women (age 65–75 years). INTERVENTION: A 6-month whole-body ST program that exercised all major muscle groups of the upper and lower body 3 days/week. MEASUREMENTS: Thigh and quadriceps muscle volumes and mid-thigh muscle cross-sectional area (CSA) were assessed by magnetic resonance imaging before and after the ST program. RESULTS: Thigh and quadriceps muscle volume increased significantly in all age and gender groups as a result of ST (P < .001), with no significant differences between the groups. Modest correlations were observed between both the change in quadriceps versus the change in total thigh muscle volume (r = 0.65; P < .001) and the change in thigh muscle volume versus the change in mid-thigh CSA (r = 0.76, P < .001). CONCLUSIONS: The results indicate that neither age nor gender affects muscle volume response to whole-body ST. Muscle volume, rather than muscle CSA, is recommended for studying muscle mass responses to ST. [ABSTRACT FROM AUTHOR]

To determine the changes on chest x-ray attributable to the aging process, we evaluated cardiovascular and pulmonary structures on two standard postero-anterior chest x-rays taken at least 10 years apart ( = 16.9 years) in 67 carefully screened healthy men initially aged 23 to 76 years. The aortic knob diameter increased in 79% of subjects. Although mean cardiothoracic ratio increased overall, only 3% of men developed a cardiothoracic ratio greater than .50, and none exceeded .51. Pulmonary abnormalities on initial chest x-ray consisted mainly of hyperinflation (27%) and increased markings (19%), both of which doubled in prevalence during follow-up. Kerley B lines and enlarged pulmonary arteries were rare initially but increased three-to five-fold. The prevalence of these findings did not differ between smokers and nonsmokers. Based on commonly accepted x-ray criteria, chronic obstructive lung disease was suggested in 15% of the initial films and 21% of the final films despite the absence of clinical or spirometric abnormalities. [ABSTRACT FROM PUBLISHER]

Abstract: Background : Higher levels of leisure time physical activity (LTPA) are associated with reduced mortality. However it is unclear how changes in LTPA over time impact all-cause mortality in men and women. Methods : From 1958 to 1996 for men (n =1316) and 1978 to 1996 for women (n =776), participants aged 19–90+ years from the Baltimore Longitudinal Study of Aging (Baltimore, MD) were assessed for LTPA at baseline and at ∼2-year intervals over a mean follow-up of 21.2±9.4 years for men and 10.2±5.6 years for women. Death occurred in 538 men and 90 women. LTPA was derived from self-reports of time spent in 97 activities converted into MET-min per 24 h and was further grouped into high-, moderate- and low-intensity LTPA. The longitudinal data was analyzed using mixed effects models to determine the rate of change in LTPA at each assessment. Proportional hazard models were used to assess the associations between LTPA at baseline and rate of change in LTPA with all-cause mortality. Results : In younger (<70 years) men, those who reported increases or negligible declines in total and high-intensity LTPA had lower all-cause mortality compared to those with greater declines in LTPA. In older (≥70 years) men, the association between rate of change in high-intensity LTPA and mortality was similar to that seen in younger men. For women, longitudinal analyses showed neither rates of change in total, high-, moderate- nor low-intensity LTPA were predictive of mortality. Conclusions : In this health-conscious population, greater longitudinal declines in total and high-intensity LTPA are independent predictors of all-cause mortality in men. [Copyright &y& Elsevier]

Studies the effect of normative aging on midwall left ventricular systolic performance. Key issues of interest; Analysis of pertinent topics and relevant issues; Implications on cardiology.