Cardiovascular Disease in the Elderly:Third Edition, Revised by Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich

By Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich

Absolute to develop into the main depended on resource in geriatric cardiology, this 3rd variation compiles the most recent experiences and services at the epidemiology, pathophysiology, and administration of heart problems within the aged patient-tracking the speedy velocity of innovation within the box with in-depth explorations of the newest medical trials and advances in vascular biology, cardiology, and cardiovascular surgical procedure for influential advancements in affliction prevention and administration.

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Extra info for Cardiovascular Disease in the Elderly:Third Edition, Revised and Expanded

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Although these age-associated changes in cardiovascular reserve, per se, are insufficient to produce clinical heart failure, they appear to lower the threshold for developing 20 Fleg and Lakatta Figure 9 Scatter plots of left ventricular volumes (A, B), ejection fraction (C), stroke volume (D), heart rate (E), and cardiac index (F) during maximal graded upright cycle exercise in healthy BLSA volunteers, carefully screened to exclude silent coronary artery disease. Note the similar age changes in men and women and the increasing heterogeneity with age in the end-systolic volume index, ejection fraction, and heart rate.

In healthy nonendurance-trained BLSA volunteers, normalization of peak VO2 to creatinine excretion, an index of muscle mass, rather than to body weight, reduced the magnitude of the apparent ‘‘age-associated’’ decline in VO2max from 39% to 18% in men and from 30% to 14% in women between ages 30 and 70 years (Fig. 8) [91]. Both cross-sectional [91] and longitudinal [92] analyses of aerobic capacity in this population indicate that the rate of peak VO2 decline varies among individuals and is influenced by physical activity habits.

01) but was not significantly age-related in men receiving propranolol. (From Ref. ) volunteers rigorously screened to exclude occult cardiac disease are due to a reduction in the efficacy of beta-adrenergic modulation of CV function. The major effects of age on CV performance during exhaustive upright exercise are summarized in Table 3. Aerobic capacity declines with advancing age in individuals without cardiac disease. , to an increase in body fat and a decrease in muscle mass with age). Although maximal heart rate is lower in healthy older versus younger individuals during exercise, maximal stroke volume is preserved across age via cardiac dilatation at end-diastole in older subjects.

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