A small percentage of patients presenting with acute myocardial infarction are found to have angiographically normal or near normal coronary arteries. Thrombus, coronary spasm or coronary embolism have been thought to cause myocardial infarction in these circumstances. Acetylcholine(Ach) may dilate coronary arteries indirectly by releasing EDRF(endothelium derived relaxing factor), but constrict arterial smooth muscle when endothelium is dysfunctional or denuded. In this study, we observed Ach responses of infarct related arteries with and without stenotic leisions to clarify the possible etiologic role of vasospasm in ischemic heart disease.

Seven to ten days after acute myocardial infarction. Ach(100ug for left and 50ug for right )responses of infarct-related coronary was studied in 16 patients with angiographically normal coronary arteries(Group 1) and 15 patients with significant stenotic lesions(Group 2). Ach responses was also studied in 27 noninfarct related arteries(NIRA) of group 1 and 29 NIRAs of group2. The positive response was defined as total or subtotal occlusion after Ach injection. In 6 patients of group 1 with Ach(+), intravenous ergonovine(Erg) test was also performed after completion of Ach test.

1) Ach(+) responses of IRAs with or without significant coronary artery disease was more frequent(70%) than that of NIRAs(14%). 2) Ach(+) response of IRAs with angiographically normal coronary artery (87.5%) was more common than that with significant fixed disease(45.4%). 3) ACh and ergonovine induced vasospasm at the same site in 4 of group 1.

In the majority of patients with normal coronary artery and acute myocardial infarction(AMI), Ach induced vasospasm in the IRAs. Ach(+) response occured more frequently in normal coronary arteries. These findings suggest that coronary vasospasm might etiologic role for AMI. especially in thoses patients with normal coronary artery. However our investigation failed clarify whether the those responses of IRAs to Ach was a cause or a result of myocardial infarction due to the post-ischemic injured endothelium.

Ach and Erg induced vasospasm at the same site in 4 of group 1 which suggests that local hyperreactivity might be related to coronary spasm.