Abstract
Arterial aging is tightly regulated process at the cellular level that can be identified and modified by clinical means. In contrast to the atherosclerotic process, arterial aging does not cause arterial obstruction, but it changes composition of the artery wall, increases the ratio of collagen to elastin with fragmentation and hypertrophy of smooth muscle cells, calcification, and often leads to dilatation.
However, similarly as in the proces of atherosclerosis, it could damage myocardial, renal and cerebral vasculature. These changes are primarily related to age, partly genetic factors and accelerated by higher blood pressure, but also by other major risk factors as smoking, diabetes mellitus, dyslipidemia and renal failure.
Vascular age can be estimated by the presence of traditional cardiovascular risk factors, for example by SCORE algorithms. However, a more appropriate method could be direct assessment of the properties of the artery wall, showing also long-term effects of risk factors.
One of the most studied methods is the measurement of the pulse wave velocity and associated CAVI (cardio-ankle vascular index). Although measurements of vascular wall parameters have some drawbacks, they can appropriately modify treatment decisions on the individual level.
Regarding management of vascular aging also other future approaches are investigated including modification of the renin-angiotensin -aldosterone system or the adenosine monophosphate protein kinase pathway.