Arterial aging: pathophysiological principles

In the nineteenth century, prior to the introduction of the cuff sphygmomanometer, arteriosclerosis (stiffening of arteries) was recognized by clinicians and by life insurance companies as an indicator of vascular aging and cardiovascular risk, even in asymptomatic individuals. Through the twentieth century, views on aging came to focus on values of systolic and diastolic pressure and on obstructive atherosclerotic disease. Such focus deflected attention from the primary aging change which occurs in all societies, and is represented by stiffening and dilation of the proximal aorta. This review emphasizes the cushioning function of elastic arteries — principally the aorta — and how in youth this results in optimal interaction with the heart, and optimal steady flow through peripheral resistance vessels. Aortic stiffening with age is principally due to fatigue and fracture of elastin lamellae, with transfer of stress to stiffer collagenous components. Stiffening increases left ventricular load and myocardial blood requirement, but limits the capacity for blood supply during diastole. Consequences are cardiac failure and predisposition to ischaemia. The second, under-appreciated effect of aortic stiffening is transmission of flow pulsations downstream into vasodilated organs, principally brain and kidney, where pulsatile energy is dissipated and fragile microvessels are damaged. This accounts for micro infarcts and microhaemorrhages, with specialized cell damage, cognitive decline and renal failure. The aging process can be best monitored by change in the arterial pressure wave rather than by reliance on the cuff sphygmomanometer. This reintroduces the approaches by clinicians and life insurance examiners of the nineteenth century, endorses modern treatments for established disease, and holds the promise of detecting premature arterial degeneration, and better applying lifestyle measures and vasoactive medications to modify the aging process.