Review article: implications of vascular aging

Abstract

Chronological age is a well-established risk factor for the development of cardiovascular diseases. The changes that accumulate in the vasculature with age, however, are highly variable. It is now increasingly recognized that indices of vascular health are more reliable than age per se in predicting adverse cardiovascular outcomes. The variation in the accrual of these age-related vascular changes is a function of multiple genetic and environmental factors. In this review, we highlight some of the pathophysiological mechanisms that characterize the vascular aging phenotype. Furthermore, we provide an overview of the key outcome studies that address the value of these vascular health indices in general and discuss potential effects on perioperative cardiovascular outcomes.

Conflict of interest statement

The authors declare no conflicts of interest.

© 2011 International Anesthesia Research Society

Figures

Figure 1

Summary of the multiple causes and locations of arterial stiffness. AGEs, advanced glycation end-products; I-CAM, Inter-Cellular Adhesion Molecule; MMP, matrix metalloproteinase; VSMC, vascular smooth muscle cells. (Arterioscler Thromb Vasc Biol 2005;25:932, reprinted with permission from the publisher, Wolters Kluwer Health).

Figure 2

Illustration of the influence of increased vascular stiffness on peripheral (radial) and central (aortic) derived pressures. Note the similarity of peripheral radial pressures in individuals with normal (lower left panel) and increased (upper left panel) vascular stiffness. In young individuals with normal vascular stiffness, central aortic pressures are lower than radial pressures (lower panels). In contrast, in older individuals with increased vascular stiffness, central aortic pressures are increased and can approach or equal peripheral pressures as a result of wave reflection and central wave augmentation during systole (top panels).

Figure 3

Example of pulse wave velocity measurements in two individuals, one with profoundly increased vascular stiffness (top panel) and the other with high normal vascular stiffness (lower panel). Pulse wave velocity is calculated as the distance (femoral—carotid) divided by time (derived from the electrocardiogram).

Figure 4

A, Example pressure-volume loops with ventricular systolic (Ees) and effective arterial elastance (Ea) relations from a young and old patient. Ees defines chamber systolic stiffness, and the intersection point of the Ea and Ees lines is the ventricular-arterial equilibrium set point. The ratio of Ea/Ees is used to index relative coupling between the heart and vascular systems. In both instances, the Ea and Ees values are similar to each other, coupling with a relative ratio near 1.0. However, in the elderly subject, both variables are increased, consistent with both vascular stiffening and ventricular systolic stiffening. Note the relatively small changes in left ventricular (LV) pressure with changes in LV volume in the young patient. In contrast, the elderly patient exhibits increases in LV diastolic pressure with similar increases in LV volume. This indication of diastolic dysfunction portends marked fluctuations in blood pressure with changes in LV preload as may occur with drug-induced venodilation. B, Group data from 57 patients. There is a significant relation between an increase in effective arterial stiffness reflected by Ea and ventricular systolic stiffness as reflected by Ees. Tandem increases in both characterize aging (Heart Failure Reviews 7:51-62, 2002, reprinted with permission by the publisher, Springer).

Figure 5

Top: Changes in brachial (solid symbols) and derived central aortic (open symbols) pulse pressure (PP) over time (mean, 95% CI) for patients randomized to receive atenolol±thiazide- or amlodipine±perinodopril-based therapy. Bottom, Changes in PP difference (brachial – derived central aortic; mean, 95% CI) over time. For calculation of area under the curve (AUC), see the data supplement numbers below the abscissa, which represent the number of patients seen at each time point. Time represents the period from randomization to patient follow-up visit at which tonometry measurement was made in the CAFE study (Circulation 2006;113:1213, reprinted with permission from the publisher, Wolters Kluwer Health).