Abstract
Current methodology for the in vitro determination of aortic and large artery stiffness is reviewed and involves three approaches: (1) the estimation of distensibility by pulse wave velocity measurement; (2) the estimation of distensibility from the fractional diameter change of a given arterial segment by imaging techniques (e. g., angiography, Doppler ultrasound) against pressure change; (3) the estimation of compliance by determining volume change against pressure change in the arterial system during diastolic runoff from the Windkessel model of the circulation. Clinical correlations may be summarized as follows: (1) age: a progressive stiffening on aging due to structural changes up to the seventh decade; (2) sex: a lower degree of stiffness in women until menopause, after which they show an accelerated stiffening, catching up with men by the seventh decade; (3) atherosclerosis: a dissociation between degree of stiffness and extent of atherosclerosis, with a suggestion that in advanced atherosclerosis the extensive calcification may lead to increased stiffness; (4) coronary disease: an inconsistent correlation by pulse wave velocity studies, but a strongly positive correlation by angiographic study of the aortic root; (5) diabetes mellitus: a significant correlation by pulse wave velocity study, particularly in the presence of advanced peripheral vascular disease; (6) hypertension (both essential and elderly patients with systolic): positive correlation but only referable to the stiffening effect of a higher mean arterial pressure (i. e., unrelated to structural changes), although an experimental study did show a loss of compliance unrelated to the mean arterial pressure level in baboons with chronic renovascular hypertension.