Arterial stiffness: a new surrogate end point for cardiovascular disease?

Abstract

Measurement of arterial stiffness is assuming an increasing role in the clinical assessment of patients. Indeed, arterial stiffness and wave reflections are now well accepted as the most important determinants of increasing systolic and pulse pressure in our aging community, and thus as the cause of cardiovascular (CV) complications and events, including stroke and myocardial infarction. Carotid-femoral pulse wave velocity (PWV), which is a direct measure of arterial stiffness, is the gold standard, since it requires little technical expertise and is supported by the greatest amount of epidemiological evidence. Indeed, aortic stiffness has independent predictive value for all-cause and CV mortality, CV disease, fatal and nonfatal coronary events and fatal strokes in patients with various levels of CV risk. Carotid pulse pressure and augmentation index are only indirect, surrogate measures of arterial stiffness. However, they provide additional information concerning wave reflections. They have demonstrated their predictive value in patients with end-stage renal disease (ESRD). Carotid stiffness was predictive of CV events in a small number of patients with ESRD or following renal transplantation, but had no independent predictive value in a larger number of patients with manifest arterial disease or in the healthy elderly patients of the Rotterdam study. To be not only an intermediate end point but also a surrogate end point, aortic stiffness has to demonstrate that its attenuation has an effect on CV mortality, coronary events and stroke. This remains to be established in populations at low to medium CV risk Eth i.e., with hypertension, dyslipidemia, diabetes and moderate chronic kidney disease.