Role of arterial stiffness in cardiovascular disease

Abstract

Propagation of the pressure wave along the arterial tree (pulse wave velocity [PWV]) is related to the intrinsic elasticity of the arterial wall. PWV is increased in stiffer arteries and, when measured over the aorta, is an independent predictor of cardiovascular morbidity and mortality. Given the predictive power of PWV, identifying strategies that prevent or reduce stiffening may be important in prevention of cardiovascular events. One view is that aortic stiffness occurs as a result of atherosclerosis along the aorta. However, there is little or no association between PWV and classical risk factors for atherosclerosis, other than age and blood pressure. Furthermore, PWV does not increase during early stages of atherosclerosis, as measured by intima-media thickness and non-calcified atheroma, but it does increase in the presence of aortic calcification that occurs within advanced atherosclerotic plaque. Age-related widening of pulse pressure is the major cause of age-related increase in prevalence of hypertension and has been attributed to arterial stiffening. This review summarizes the methods of measuring aortic stiffness in humans, the pathophysiological mechanisms leading to aortic stiffness, including its association with atherosclerosis, and the haemodynamic consequences of increased aortic stiffness.

Figure 1

PWV measurement. Carotid-to-femoral PWV is calculated by dividing the distance (d) between the two arterial sites by the difference in time of pressure wave arrival between the carotid (t1) and femoral artery (t2) referenced to the R wave of the electrocardiogram

Figure 2

Results of the systematic review. The number of studies in which classical risk factors and heart rate were included (bars) and the proportion of these (solid line) in which the risk factor was significantly independently associated with pulse wave velocity. Reprinted from Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension : a systematic review. Hypertension 2009; 54:1328–36

Figure 3

Mean values of carotid-femoral PWV as a function of plaque type (adjusted for age, mean arterial pressure, heart rate and fasting glucose)

Figure 4

Contours of peripheral and aortic pressure waveforms. Peripheral and aortic pressure waveforms showing peripheral PP (pPP), peripheral SBP (pSBP), cPP, central SBP (cSBP) and DBP. Reprinted from Cecelja M, Jiang B, Spector TD, Chowienczyk P. Progression of central pulse pressure over 1 decade of aging and its reversal by nitroglycerin: a twin study. J Am Coll Cardiol 2012; 59:475–83, with permission from the American College of Cardiology Foundation

Figure 5

Aortic pressure waveform. The systolic pressure rise can be separated by a first systolic peak (P1) resulting from the ejection of blood from the left ventricle into the aorta; T1 is time to first peak and AP is the difference between central SBP (cSBP) and P1. P1 and AP sum to give cPP