Demonstration of Insulin Resistance in Coronary Artery Disease Documented With Angiography

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OBJECTIVETo evaluate the relation between insulin resistance and coronary atherosclerosis, insulin sensitivity in lean nondiabetic, normotensive subjects with and without obstructive coronary artery disease (CAD). The correlation between insulin resistance and degree of coronary stenosis was also investigated.RESEARCH DESIGN AND METHODSFour groups were studied: 1) nine subjects with normal glucose tolerance (NGT) without CAD, 2) 10 subjects with NGT with CAD, 3) nine subjects with impaired glucose tolerance (IGT) without CAD, and 4) 10 subjects with IGT with CAD. Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method using Sandostatin. Coronary angiography was performed in all study subjects, and the severity of coronary artery atherosclerosis was quantified in a modified Gensini score.RESULTSThe SSPG (millimoles per liter) levels were significantly higher in the patients with CAD compared with control subjects (control vs. patient group: 4.8 plus/minus 0.5 vs. 7.9 plus/minus 0.9 with NGT, P less than 0.05; 5.6 plus/minus 0.5 vs. 11.1 plus/minus 0.8 with IGT, P less than 0.001), indicating the presence of insulin resistance in patients with CAD. The coronary atherosclerosis score (CAS) was significantly and positively correlated with SSPG (r = 0.74, P less than 0.05) and 2-h insulin area (r = 0.78, P less than 0.01) in NGT subjects with CAD. On the other hand, the percentage fall of plasma free fatty acid (0-30 min) during an insulin sensitivity test was significantly decreased in the subjects with CAD and was inversely correlated with the CAS (r = -0.43, P less than 0.05), especially in NGT subjects with CAD.CONCLUSIONSThese data suggest that in patients with CAD, insulin-mediated glucose metabolism is significantly impaired, and a significant correlation was noted between insulin resistance and severity of CAD. Therefore, the hyperinsulinemia often observed in patients with CAD is attributable to the compensatory mechanism of the beta-cell to the inadequate action of insulin for glucose metabolism. Hyperinsulinemia in the presence of insulin resistance aggravates dyslipidemia and may stimulate the atheromatous process by an as-yet-unknown mechanism.

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