Relationship between Arterial Stiffness and the Risk of Coronary Artery Disease in Subjects with and without Metabolic Syndrome

We examined the influence of metabolic syndrome (MetS) on the relationship between arterial stiffness and the risk of coronary artery disease (CAD). In 396 subjects (age, 63+/-11 years) who underwent coronary angiography, multiple linear regression analysis demonstrated that the brachial-ankle pulse...

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Published inHypertension research Vol. 30; no. 3; pp. 243 - 247
Main Authors Koji, Yutaka, Tomiyama, Hirofumi, Yamada, Jiko, Yambe, Minoru, Motobe, Kohki, Shiina, Kazuki, Yamashina, Akira
Format Journal Article
LanguageEnglish
Published England 01.03.2007
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Summary:We examined the influence of metabolic syndrome (MetS) on the relationship between arterial stiffness and the risk of coronary artery disease (CAD). In 396 subjects (age, 63+/-11 years) who underwent coronary angiography, multiple linear regression analysis demonstrated that the brachial-ankle pulse wave velocity (PWV), but not the presence of MetS, was a significant determinant of the number of diseased coronary arteries (beta=0.10, p<0.05), even though both the brachial-ankle PWV and the number of diseased coronary arteries were higher in subjects with MetS (n=100) than in those without MetS (n=296). However, in subjects with MetS, multiple linear regression analysis demonstrated that the brachial-ankle PWV was not a significant determinant of the number of diseased coronary arteries. The brachial-ankle PWV values were classified into tertile ranges in subjects with and without MetS. The number of diseased coronary arteries increased significantly with an increase in the tertile number of the brachial-ankle PWV in the subjects without MetS (tertile 1=1.00+/-0.86, tertile 2=1.29+/-1.01, and tertile 3=1.45+/-1.05), but not in those with MetS. In conclusion, the results of this study suggest that arterial stiffness is a marker of the risk of CAD in subjects without MetS, whereas in subjects with MetS, the syndrome may directly produce clinically significant atherosclerotic stenosis of the coronary arteries independent of its significant promotion of the development of coronary atherosclerosis via an increase of arterial stiffness.
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ISSN:0916-9636
1348-4214
DOI:10.1291/hypres.30.243