Arterial Stiffness and Vascular Aging: From Pathophysiology to Treatment, with a Look at the Future

Excerpt

In the last decade, a growing literature raised arterial stiffness as a “hot topic” in terms of pathophysiology of cardiovascular (CV) system and clinical relevance [1, 2]. In order to comprehend the main aspects of such interest, a brief explanation of the “Windkessel” model is required. The arterial tree can be assimilated to a distensible tube terminating at the peripheral resistances, in order to explain the two main functions of the arteries: the conduit function (to deliver an adequate supply of blood to peripheral tissues) and the cushioning function (to buffer pressure oscillations due to intermittent ventricular ejection). The viscoelastic properties of large arteries guarantee that the pulsatile pressure and flow resulting from intermittent ventricular ejection are smoothed out, leading to the peripheral microcirculation to delivery oxygen and nutrients to the tissues. The velocity of pulse wave propagation is inversely related to the distensibility of the tube. At its end, the pulse wave is reflected and retrograde waves are generated, that, summated with the forward wave generated by ventricular ejection, constitute the effective blood pressure (BP) curve, contributing to the amplitude of pulse pressure and systolic BP. When the arterial stiffness increases, the pulse wave is transmitted more rapidly and, once reflected from the peripheral vasculature, returns to the heart during left ventricular contraction, resulting in a greater augmentation of the central aortic systolic BP [3]. …