BACKGROUND: Impaired glucose tolerance is a preliminary stage in the development of type 2 diabetes mellitus and has been shown to increase the risk of cardiovascular morbidity and mortality in addition to causing endothelial dysfunction. In this study, we sought to determine if impaired glucose tolerance is related to slow coronary flow, an angiographic phenomenon caused by coronary micro and macrovascular endothelial dysfunction. METHODS: The population of this prospective study consisted of 28 patients with documented slow coronary flow, defined according to TIMI frame count method, [20 (71.4%) males; 51+/-9 years] and 30 patients with normal coronary flow [17 (56.6%) males; 47+/-6 years]. All study patients underwent an oral glucose tolerance test after 12 h of fasting. Lipid profile, hemoglobin A1c and systemic blood pressure were measured in all patients. RESULTS: There was no difference between two groups with respect to age, fasting plasma glucose, triglyceride, total cholesterol, high density lipoprotein, low density lipoprotein, hemoglobin A1c, systolic-diastolic blood pressure levels, history of smoking and alcohol consumption. Plasma glucose at 2 h of oral glucose tolerance test was significantly higher in slow coronary flow patients compared to control group (145+/-44 vs. 112+/-38 mg/dl, P = 0.001, respectively). In addition, the number of patients who met the criteria of impaired glucose tolerance was significantly higher in slow coronary flow patient group [16 (57%) vs. 7 (23%), P = 0.002, respectively). CONCLUSIONS: Our results suggest that impaired glucose tolerance may be an independent etiological factor for slow coronary flow phenomenon.
BACKGROUND:Impaired glucose tolerance is a preliminary stage in the development of type 2 diabetes mellitus and has been shown to increase the risk of cardiovascular morbidity and mortality in addition to causing endothelial dysfunction. In this study, we sought to determine if impaired glucose tolerance is related to slow coronary flow, an angiographic phenomenon caused by coronary micro and macrovascular endothelial dysfunction. METHODS: The population of this prospective study consisted of 28 patients with documented slow coronary flow, defined according to TIMI frame count method, [20 (71.4%) males; 51+/-9 years] and 30 patients with normal coronary flow [17 (56.6%) males; 47+/-6 years]. All study patients underwent an oral glucose tolerance test after 12 h of fasting. Lipid profile, hemoglobin A1c and systemic blood pressure were measured in all patients. RESULTS: There was no difference between two groups with respect to age, fasting plasma glucose, triglyceride, total cholesterol, high density lipoprotein, low density lipoprotein, hemoglobin A1c, systolic-diastolic blood pressure levels, history of smoking and alcohol consumption. Plasma glucose at 2 h of oral glucose tolerance test was significantly higher in slow coronary flow patients compared to control group (145+/-44 vs. 112+/-38 mg/dl, P = 0.001, respectively). In addition, the number of patients who met the criteria of impaired glucose tolerance was significantly higher in slow coronary flow patient group [16 (57%) vs. 7 (23%), P = 0.002, respectively). CONCLUSIONS: Our results suggest that impaired glucose tolerance may be an independent etiological factor for slow coronary flow phenomenon.