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Brachial-ankle pulse wave velocity.

Pulse wave velocity (PWV) is a good marker of arterial distensibility and stiffness that reflect vascular damage (1). The PWV can be measured easily and noninvasively. The results of PWV are parallel with morphological changes of the artery (2). Arterial stiffening increases left ventricular afterload, and alters the coronary perfusion (3). Arterial stiffness is significantly and independently associated with both target organ damage and increased cardiovascular morbidity and mortality (4). Assessment of changes in gene expression associated with increased arterial stiffness and gene polymorphism suggests that components of the rennin-angiotensin system, matrix metalloproteinases, intracellular signaling, and extracellular matrix components may all be involved in arterial stiffening (4). Long-term treatment with angiotensin II inhibits the progression of arterial stiffness, independent of blood pressure reduction in the patients with essential hypertension (5), indicating a possible involvement of angiotensin II in the development of arterial stiffness. The brachial-ankle PWV (baPWV) is not only a simple marker of aortic stiffness (1), but it also increases with coronary artery disease severity and correlates with left ventricular systolic function independent of coronary artery disease severity (6). Blood pressure and heart rate are important determinants of the PWV in young, healthy males (7). In the evaluation of the PWV data, we have to take the existence of hypertension into the consideration. However, what factors determine the PWV other than systolic and diastolic blood pressure has not been fully understood in humans. In type 2 diabetic patients who frequently have accompanying insulin resistance, long-term glycemic control is correlated with the changes of baPWV for 12 months (8). However, change of anklobrachial blood pressure index (ABPI) does not reflect early-stage arteriosclerosis. In addition, hyperinsulinemia contributes to the development of arterial stiffness, assessed by the baPWV, in the early stage of type 2 diabetes mellitus (9). Glycemic control and hyperinsulinemic state are important factors that determine the PWV in diabetic patients. The baPWV was significantly higher in obese [body mass index (BMI) >30 kg/m] male subjects than in the overweight (25< BMI <30 kg/m) subjects of Japan university students, and in the male with nonalcoholic fatty liver disease (NAFLD) than in those without NAFLD (10). Recent data showed strong associations between weight gain and arterial stiffness progression, as well as weight loss and arterial stiffness regression among healthy young adults (11). Adipokines released from adipose tissues may affect vascular functions, and modify the PWV in obese subjects, but data from only a few clinical studies is available on the relation of adipokines to the baPWV. Multiple regression analysis revealed that adiponectin was a significant determinant for the PWV in subjects less than 70 years of age (12). Aortic PWV correlated with serum interleukin-6 and plasma basic fibroblast growth factor in the patients with end-stage renal disease (13). Therefore, the observation made by Shiotani et al (10) can, at least in part, be explained by the existence of hyperinsulinemia in young, obese subjects. An increase of the baPWV suggests the development of arteriosclerosis in diabetic and obese subjects by employing a non-invasive method. Measurement of the baPWV might be useful for the early evaluation of cardiovascular disease, in addition to the development of peripheral arterial disease.