Glucose metabolism and coronary heart disease in patients with normal glucose tolerance

Context Several investigations as well as prospective studies have shown a significant correlation between glucose metabolism and atherosclerosis in patients without diabetes, but differences in parameters of glucose metabolism among the various degrees of coronary disease in such patients have not been specifically evaluated. Objective To investigate glucose metabolism in patients with normal glucose tolerance (NGT) and coronary heart disease (CHD). Design, Setting, and Participants Cross-sectional study of 234 men (mean [SDI age, 56.2 [6.1] years) with NGT and suspected CHD who were admitted from January 1 through June 30, 2001, to an academic medical center in Italy for coronary angiography. Main Outcome Measures Correlation of glucose metabolic factors and extent of atherosclerosis determined by coronary angiography. Factors included levels of fasting and postload glucose and insulin, glycosylated hemoglobin (HbA(1c)), and lipids, as well as insulin resistance measured by homeostasis model assessment (HOMA-IR). Results Patients were divided into 4 groups based on coronary angiography: no significant stenosis (n=42), 1-vessel disease (n=72), 2-vessel disease (n=64), and 3-vessel disease (n =56). Simple correlation analysis showed that the factors correlated with the extent of atherosclerosis were levels of postload glucose (r=0.667), HbA(1c) (r=0.561), postload insulin (r=0.221), and fasting insulin (r=0.297), as well as HOMA-IR (r=0.278) (P<.001 for all). Multiple stepwise regression analysis suggested that the factors independently associated with the number of stenosed coronary arteries were levels of postload plasma glucose (r=0.572), HbA(1c) (r=0.413), postload insulin (r=0.267), and fasting insulin (r=0.174), as well as HOMA-IR (r=0.250) (P<.001 for all). Similar results were obtained after grouping patients by Duke Myocardial Jeopardy Score. Conclusions For patients with NGT and different extents of atherosclerotic disease, postload glycemia and HbA(1c) level are not equally distributed but are significantly higher in those with more severe disease. This suggests that the glycemic milieu correlates with the cardiovascular risk according to a linear model.