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Association of Hypoadiponectinemia With Coronary Artery Disease in Men
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24
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2003
Year
Adiponectin, an adipocyte‑derived plasma protein, accumulates in injured arteries and may exert anti‑atherogenic effects. The study aimed to determine whether low plasma adiponectin levels are independently linked to coronary artery disease prevalence. The study enrolled 225 male coronary angiography patients and 225 age‑matched blood donors, categorizing participants into quartiles of plasma adiponectin (cutoffs 4.0, 5.5, 7.0 µg/mL). CAD patients had significantly lower adiponectin levels, and multivariate analysis showed hypoadiponectinemia was independently associated with CAD, with the lowest quartile (<4.0 µg/mL) conferring a two‑fold higher risk.
Adiponectin is an adipocyte-derived plasma protein that accumulates in the injured artery and has potential antiatherogenic properties. This study was designed to determine whether a decreased plasma adiponectin level (hypoadiponectinemia) can be independently associated with the prevalence of coronary artery disease (CAD). The consecutive 225 male patients were enrolled from inpatients who underwent coronary angiography. Voluntary blood donors (n=225) matched for age served as controls. Plasma adiponectin levels in the CAD patients were significantly lower than those in the control subjects. Multiple logistic regression analysis including plasma adiponectin level, diabetes mellitus, dyslipidemia, hypertension, smoking habits, and body mass index revealed that hypoadiponectinemia was significantly and independently correlated with CAD (P<0.0088). The entire study population was categorized in quartiles based on the distribution of plasma adiponectin levels. The interquartile cutoff points were 4.0, 5.5, and 7.0 microg/mL. The multivariate-adjusted odds ratios for CAD in the first, second, and third quartiles were 2.051 (95% confidence interval [CI], 1.288 to 4.951), 1.221 (95% CI, 0.684 to 2.186), and 0.749 (95%CI, 0.392 to 1.418), respectively. Male patients with hypoadiponectinemia (<4.0 microg/mL) had a significant 2-fold increase in CAD prevalence, independent of well-known CAD risk factors.
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