Insulin resistance in nondiabetic patients with acute myocardial infarction.

BACKGROUND: Recent studies have shown that insulin resistance (IR) is an independent predictor of early restenosis after coronary stenting. The aim of this study was to examine the effects of IR and its linkage to late loss with bare metal stenting in nondiabetic patients with acute myocardial infarction (AMI). MATERIALS AND METHODS: We enrolled 61 nondiabetic patients with AMI who have undergone coronary stenting. Quantitative analyses of coronary angiographic data before and after the procedure and at 4 months were performed. Fasting plasma glucose (FPG) and insulin were measured every week until the subjects' hospital discharge. Stress hormones, endothelial nitric oxide synthase, tumor necrosis factor alpha, interleukin-6, leptin, and adiponectin were measured on admission and at 4 months after coronary stenting. RESULTS: Simple linear regression analyses showed a relationship between FPG and insulin [IR group: r=0.297, P=.0428; no insulin resistance (NIR) group: r=0.539, P=.0466] and that late loss was associated with the homeostasis model assessment of IR (HOMA-IR) at 4 months (r=0.435, P=.03). At multiple regression analyses, HOMA-IR on admission in the IR group significantly correlated with thyroid-stimulating hormone, glucagon, and cortisol. The HOMA-IR at 4 months correlated with leptin. CONCLUSIONS: Nondiabetic patients with AMI can be classified into two groups: the IR group and the NIR group. The IR consisted of the transient IR, which correlated with stress hormones, and the continuous IR, which correlated with leptin and contributed to restenosis after coronary stenting.

A randomized comparison of pioglitazone to inhibit restenosis after coronary stenting in patients with type 2 diabetes.

OBJECTIVE: Recent studies have demonstrated that the treatment with thiazolidinediones reduces in-stent restenosis. The aim of this study was to elucidate the mechanism of the efficacy of pioglitazone for preventing in-stent restenosis in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: We conducted a prospective, randomized trial involving 54 type 2 diabetic patients referred for coronary stenting who were randomly assigned to either the control or the pioglitazone group. Quantitative coronary angiography was performed at study entry and at 6 months follow-up. Endothelial nitric oxide synthase (eNOS), tumor necrosis factor alpha, interleukin-6, leptin, and adiponectin were measured at study entry and at 6 months follow-up. RESULTS: A total of 28 patients were randomly assigned to the control group, and 26 patients were assigned to the pioglitazone group. There were no significant differences in glycemic control levels or in lipid levels in the two groups at baseline or at follow-up. Insulin, homeostasis model assessment of insulin resistance, eNOS, and leptin at follow-up were significantly reduced in the pioglitazone group compared with the control group. The late luminal loss and in-stent restenosis were significantly less in the pioglitazone group than in the control group. Leptin independently correlated with late luminal loss at multiple regression analysis. CONCLUSIONS: The treatment with pioglitazone in type 2 diabetic patients significantly reduced leptin. This decreased leptin improved insulin resistance and endothelial function with the reduction of insulin. The improved endothelial function affected the reduction of in-stent restenosis.

Insulin resistance as a predictor for restenosis after coronary stenting.

PURPOSE: The rationale of this study was to determine whether insulin resistance is an independent risk factor for restenosis after coronary stenting. BACKGROUND: Previous studies suggested that hyperinsulinemia may be an important risk factor for ischemic heart disease. Restenosis after coronary stenting is neointimal tissue proliferation and de-novo stenosis is atherosclerosis from the point of view of histology. However, it has not been determined whether insulin resistance is independently related to restenosis after coronary stenting. METHODS: Clinical variables of unselected population of 110 patients were analyzed in multivariate logistic regression analyses for both restenosis and de-novo stenosis. Clinical, lesion-related, and procedural variables were analyzed by chi-square analysis, and relative risk. RESULTS: Multivariate logistic regression analysis showed that homeostasis model assessment insulin resistance (HOMA-IR) and HbA1c were associated with restenosis after coronary stenting (HOMA-IR; P=0.0447, HbA1c; P=0.0462), and HbA1c and low-density lipoprotein cholesterol (LDL-C) were associated with de-novo stenosis (HbA1c; P=0.0201, LDL-C; P=0.0204). Restenosis was influenced by insulin resistance [Relative Risk (RR) 2.06; 95 percent confidence interval (95%CI) 1.20 to 3.56], diabetes mellitus (DM: RR 1.92; 95%CI 1.25 to 2.95), and final minimal lumen diameter (RR 2.83; 95%CI 1.32 to 6.06). CONCLUSIONS: HOMA-IR and DM are the predictors of restenosis after coronary stenting, and HbA1c and LDL-C are the predictors of de-novo stenosis. These results may be reflected in histological differences between neointimal tissue proliferation as restenosis and atherosclerosis as de-novo stenosis.

Significance of low-dose dobutamine stress echocardiography for the prediction of the long-term prognosis for patients with acute myocardial infarction.

OBJECTIVES: Detection of stunned myocardium using low-dose dobutamine stress echocardiography is a good predictor of improvement of cardiac function in patients with acute myocardial infarction during short hospital stays. The present study evaluated the detection of stunned myocardium as a predictor of the long-term prognosis for patients with acute myocardial infarction. METHODS: One hundred and two patients (83 males, 19 females, mean age 61.5 years) with initial myocardial infarction underwent successful reperfusion therapy (direct percutaneous transluminal coronary angioplasty or stent) in the acute stage. Within 7 days, low-dose dobutamine was administered by intravenous drip and improvement of wall motion of the infarct area was evaluated by echocardiography. The patients were divided into two groups, the viable group that showed one grade or more improvement (61 patients), and the non-viable group that showed no improvement (41 patients). These groups were compared to determine the differences in clinical findings such as remodeling of the left ventricle measured by two-dimensional echocardiography, physical work capacity during serial multi-step exercise testing, and the prognosis. RESULTS: The viable group showed greater improvement in hemodynamics and wall motion of the infarct areas than the non-viable group. After discharge, the physical work capacity was significantly increased and there was no recognizable enlargement of the left ventricle in the viable group. No sudden cardiac death or heart failure occurred in the viable group, in contrast to incidences of 6% and 9%, respectively, in the non-viable group. Unstable angina and nonfatal re-infarction occurred more frequently in the viable group. CONCLUSIONS: The presence of stunned myocardium is a predictor of the prognosis for patients with acute myocardial infarction.