Abstract 9726: Prolonged Insulin Secretion After Oral Glucose Load is Associated With Severity of Coronary Artery Disease
Introduction: Hyperglycemia exerts its direct detrimental effects toward the progression of atherosclerosis. However, the role of hyperinsulinemia in the development of atherosclerosis remains to be determined. Little is known about the relationship between cardiovascular events and plasma insulin levels. Hypothesis: We hypothesize that hyperinsulinemia is associated with the severity of coronary atherosclerosis.
Methods: Three hundred and forty four consecutive patients (mean age 63±14 SD years; 272 male patients, 72 female patients) who underwent coronary angiography and 2-h 75-g oral glucose tolerance test (OGTT) from April 2006 to January 2012 were enrolled. We excluded the patients with left main trunk lesion, or prior diagnosed diabetes. Based on the number of stenotic vessels, the patients were classified into 4 groups; 0 vessel disease (VD) (n=35), 1VD (n=142), 2VD (n=92), and 3VD (n=36). We measured plasma glucose and insulin levels after 75-g oral glucose load.
Results: Baseline characteristics were similar among the 4 groups with respect to age, gender, medications, and each of major coronary risk factors. There were no differences glucose profiles in 75-g OGTT, homeostasis model assessment-insulin resistance (HOMA-IR), HOMA-β and HbA1c among these groups (Figure 1A). However, insulin secretion was higher in 2VD and 3VD groups at 120 min whereas no significant difference in insulin secretion at 0, 30 and 60 min (Figure 1B). Furthermore, insulinogenic index at 120 min was increased in 2VD (1.21±1.05[p<0.001]) and 3VD (1.14±0.5l[p=0.002]) compared with 0VD despite of no significant difference in common insulinogenic index.
Conclusions: Despite no significant difference in insulin resistance and postprandial hyperglycemia prolonged insulin secretion was associated with multivessel coronary artery disease. Prolonged postprandial hyperinsulinemia may promote progression of atherosclerosis.
- © 2012 by American Heart Association, Inc.