Several age-associated cardiovascular changes directly impact the development and progression of atherosclerosis and CAD.¹Over a century ago, it was recognized that arterial walls stiffen with age in both animals and man. Major aging changes in the arterial wall include increased calcium and collagen content and loss of elastin fibers. An increase in collagen cross-linking also occurs. Greater wall thickness is observed in both central and peripheral arteries and can be detected by ultrasound as increased intima-medial thickness. The loss in arterial resiliency results in increases in the systolic blood pressure and pulse pressure, both of which are potent cardiovascular and coronary risk factors in older patients. Pulse wave velocity, a more direct measure of arterial stiffness, also increases with age. The central arterial pressure wave contour is also altered with age, typically demonstrating late systolic augmentation, thought to represent the effects of early wave reflection returning from the periphery. Stiffer arteries with higher systolic and pulse pressures coupled with late systolic pressure augmentation combine to increase the left ventricular (LV) pulsatile load with age.

Thus, the older adult heart requires greater LV stroke work, wall tension and myocardial oxygen consumption during systole than does the younger heart, thereby increasing the risk of ischemia, even in the absence of CAD. In addition, vascular wall stress is increased, predisposing to vascular injury, an important stimulus to the development and progression of atherosclerosis.

[1] Lakatta EG, et al. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises – part I: aging arteries: a “set up” for vascular disease. Circulation. 2003; 107:139–146

[2] Lakatta EG, et al. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises – part II: the aging heart in health: links to heart disease. Circulation. 2003; 107:346–354