IMPAIRED GLUCOSE-TOLERANCE WITH LATE HYPERSECRETION OF INSULIN DURINGORAL GLUCOSE-TOLERANCE TEST IN PATIENTS WITH VASOSPASTIC ANGINA

Objectives. This study tested whether patients with vasospastic angina have impaired glucose tolerance or impaired insulin response. Backgro und. Hyperinsulinemia has been demonstrated in patients with coronary artery disease and syndrome X. Methods. We performed an oral glucose t olerance test (75 g) in 30 patients with vasospastic angina in whom se vere coronary vasospasm was induced by acetylcholine and in a matched group of 30 patients with atypical chest pain in whom no significant v asospasm was induced. The responses of insulin and glucose were compar ed between the two groups. No subjects had overt diabetes mellitus, hy pertension, dyslipidemia, obesity or angiographically detected signifi cant baseline coronary stenosis. Venous blood samples mere taken durin g fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasma glucose and immunoreactive insulin levels. Results. Impaired gl ucose tolerance was detected in the 19 (63%) of 30 patients with vasos pastic angina and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 min as well a s the interval to peak insulin level were significantly greater in pat ients with vasospastic angina (p < 0.001). Among patients with vasospa stic angina, those with acetylcholine-induced multivessel coronary vas ospasm shelved a significantly higher sum of insulin concentrations th an those with single vessel spasm (p < 0.01). During induction of coro nary spasm, 10 patients with vasospastic angina presented ventricular arrhythmias. The sum of insulin concentrations was significantly great er in patients with than in those without ventricular arrhythmias. Con clusions. Patients with vasospastic angina exhibited a high incidence of impaired glucose tolerance and delayed and significantly higher ins ulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesi s of severe coronary vasospasm.