Impaired glucose tolerance with late hypersecretion of insulin during oral glucose tolerance test in patients with vasospastic angin

Objectives. This study tested whether patients with vasospastic angin have impaired glucose tolerance or impaired insulin response. Background. Hyperinsulinemi has been demonstrated in patients with coronary artery disease and syndrome X. Methods. We performed an oral glucose tolerance test (75 g) in 30 patients with vasospastic angin in whom severe coronary vasospasm was induced by acetylcholine and in matched group of 30 patients with atypical chest pain in whom no significant vasospasm was induced. The responses of insulin and glucose were compared between the two groups. No subjects had overt diabetes mellitus, hypertension, dyslipidemia, obesity or angiographically detected significant baseline coronary stenosis. Venous blood samples were taken during fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasm glucose and immunoreactive insulin levels. Results. Impaired glucose tolerance was detected in the 19 (63%) of 30 patients with vasospastic angin and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 mins as well as the interval to peak insulin level were significantly greater in patients with vasospastic angin (p < 0.001). Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). During induction of coronary spasm, 10 patients with vasospastic angin presented ventricular arrhythmias. The sum of insulin concentrations was significantly greater in patients with than in those without ventricular arrhythmias. Conclusions. Patients with vasospastic angin exhibited high incidence of impaired glucose tolerance and delayed and significantly higher insulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesis of severe coronary vasospasm.