Insulin resistance syndrome has been proposed as a major promotor of atherosclerotic disease and earlier studies have implied the hyperinsulinemia itself may enhance coronary vasomotor tone. In patients with vasospastic angina, previous studies have been inconclusive whether to basal coronary artery tone is elevated at the spasm related and nonspasm related artery. This study was performed to investigate whether basal coronary artery tone is elevated ans insulin resistance syndrome correlates to vasospastic angina. If insulin resistance syndrome correlates to vasospastic angina, we also investigated whether insulin resistance syndrome correlates to basal coronary artery tone.

The study comprised 27 patients with vasospastic angina(M/F ; 19/8, mean age ; 52±2 year) and 21 control subjects with atypical chest pain(M/F ; 9/8, mean age ; 47±3 year). We assessed basal coronary artery tone by obtaining the percent increase in coronary artery diameter induced by nitroglycerin and also examined glucose and insulin response to an oral glucose load of 75g.

1) There were no significant differences in body surface area, abdominal hip ratio, body mass index, incidence of hypertension, lipid profile, von-Willebrand factor, fibrinogen, and microalbumin except smorking incidence [vasospastic angia ; 16(50%) vs control ; 5(24%), p<0.05)] between vasospastic angina group and control. 2) Basal coronary artery tone was greater at the nonspastic site of the spasm-related artery(28.1±2.2% vs 13.1±0.9%, p<0.0001) and non-spasm related artery(23.7±1.6% vs 13.1±0.9, p<0.0001) in the patients with vasospstic angina than in control subjects. In the patients with vasospastic angina, high activity group had a greater basal coronary artery tone than low activity group at the nonspastic site of the spasm-related artery(31.7±2.6 vs 20.4±2.7%, p<0.001) and non-spasm related artery(26.8±2.0 vs 19.4±5.8%, p<0.001). 3) Plasma glucose and serum insulin response to an oral glucose load were similar between vasospastic angina group and control subjects, and glucose area, insulin area, and insulinogenic index(delta sigma Glucose / delta sigma Insulin)(330±12 vs 328±20 mg/dl *hour, 107±14 vs 96±17uU/ml*hour, and 2.18±0.33 vs 2.63±0.46, respectively, p=NS) also did not between both groups. 4) Two group did not differ siginificantly in the prportion of glucose intolerance but glucose area and insulin area were significantly high in vasospastic angina patients with glucose intolerance than in control subjects with normal glucose tolerance(366±22 vs 257±17mg /dl*hour, 127±19 vs 52±15uU*hour, respectively, p<0.05), but basal coronary artery tone did not differ significantly between vasospastic angina patients with glucose intolerance and control subjects with normal glucose tolerance.

1) These results revealed that basal coronary artery tone is elevated at the nonspastic site of the spasm related artery and non-spastic vessel, and the disease activity associated with elevated basal coronary artery tone in vasospastic angina. 2) But these results did not reveal the correlation of hyperinsulinemia with vasospastic angina, and so we did not determine the role of hyperinsulinemia as a pathogenesis of coronary spasm and the relation between hyperinsulinemia and basal coronary artery tone.