Metabolic syndrome shown to produce clinically significant coronary atherosclerosis stenosis by a mechanism independent of an increase in arterial stiffness
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Arterial stiffness, a risk marker for cardiovascular events, may accelerate atherosclerotic vascular damage, increase cardiac workload, and exert direct atherogenic effects. Increase in arterial stiffness was reported in subjects with metabolic syndrome. To examine the influence of metabolic syndrome, an atherogenic state, on the relationship between arterial stiffness and the risk of coronary artery disease (CAD), 396 subjects underwent both coronary angiography and brachial-ankle pulse wave velocity (PWV) measure. Multiple regression analysis revealed that brachial-ankle PWV was a significant determinant of the number of diseased coronary arteries (P<0.05) whereas metabolic syndrome was not. However, brachial-ankle PWV was not a significant determinant of the number of diseased coronary arteries in subjects with metabolic syndrome. Brachial-ankle PWV values were classified into tertile ranges for subjects with or without metabolic syndrome. In subjects without metabolic syndrome, the number of diseased coronary arteries increased significantly with an increase in the tertile values of brachial-ankle PWV; this was not the case in subjects with metabolic syndrome. The authors conclude that arterial stiffness is a marker of the risk of CAD in subjects without metabolic syndrome. By contrast, metabolic syndrome directly produces significant atherosclerosis stenosis independently of an increase in arterial stiffness.
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