Arterial stiffness has been known to be a surrogate marker of arteriosclerosis, and also of vascular function.
Pulse wave velocity (PWV) had been the most popular index and was known to be a predictor of cardiovascular events.
But, it depends on blood pressure at measuring time. To overcome this problem, cardio-ankle vascular index (CAVI) is
developed. CAVI is derived from stiffness parameter β by Hayashi, and the equation of Bramwell-Hill, and is
independent from blood pressure at a measuring time. Then, CAVI might reflect the proper change of arterial wall by
CAVI shows high value with aging and in many arteriosclerotic diseases and is also high in persons with main coronary
risk factors. Furthermore, CAVI is decreased by an administration of α1 blocker, doxazosin for 2-4 hours, Those results
suggested that CAVI reflected the arterial stiffness composed of organic components and of smooth muscle cell
contracture. Angiotensin II receptor blocker, olmesartan decreased CAVI much more than that of calcium channel
antagonist, amlodipine, even though the rates of decreased blood pressure were almost same. CAVI might differentiate the
blood pressure-lowering agents from the point of the effects on proper arterial stiffness.
This paper reviewed the principle and rationale of CAVI, and the possibilities of clinical applications, especially in the
studies of hypertension.