Arterial Blood Pressure and Stiffness in Hypertension

Abstract

Increasingly, in recent years, the stiffness of large elastic arteries has been recognized as a major determinant of vascular function and cardiovascular risk.1,2 The distally propagating arterial pressure pulse is reflected at arterial branch points (sites of impedance mismatch), and the velocity and magnitude of these reflections is determined by arterial stiffness. Whereas peripheral vascular resistance largely determines diastolic BP, central systolic BP and pulse pressure are influenced by the augmentation of aortic pressure because of wave reflections, as well as by the character of ventricular ejection. Increased stiffness leads to greater pulsatile stress and strain and may influence endothelial shear stress, contributing to remodeling and structural abnormalities of the blood vessel wall and to atherogenesis. An increase in aortic stiffness also results in an increase in left ventricular afterload and, consequently, myocardial oxygen consumption3 and compromise of myocardial perfusion during diastole, particularly in the subendocardial region.4 That central arterial stiffness is clinically relevant is evident from the studies showing a positive predictive value of aortic stiffness for cardiovascular risk in hypertension,5,6 although the precise mechanism of this association remains unclear. Arterial stiffness is largely determined by 2 influences: first, those related to the arteries themselves (wall structure and function and lumen size); and, second, the mean distending arterial BP. The main load-bearing components of the arterial wall are elastin fibers, stiffer collagen fibers, and vascular smooth muscle. Smooth muscle contraction results in increased arterial stiffness because of a decrease in lumen size and shifting of load onto stiffer collagen fibers. Increasing mean distending pressure causes a small increase in lumen size. However, transfer of stress …