Self-vasodilating ability at the spastic site of patients with vasospastic angina: estimation by acetylcholine delayed phase.

Deficient nitric oxide (NO) release is thought to be the principal mechanism of coronary spasm, however, the precise mechanisms are unknown. Although acetylcholine (ACh) is used for provocation of coronary spasm, ACh is also used for the augmentation of blood flow and flow-mediated vasodilation is induced. We estimated the self-vasodilating ability (endothelial function) at the spastic site of coronary arteries in patients with vasospastic angina (VSA) during the provocation test of coronary spasm by ACh. This study included 93 patients with VSA and 77 patients with atypical chest pain (ACP). Intracoronary injection of ACh (20, 50, and 100 microg) was performed over 30 seconds and the coronary artery diameter of the spastic site was measured 3 to 4 minutes after ACh injection (delayed phase). The ability of dilation (AOD) was calculated as: ([diameter of delayed phase-baseline diameter]/[diameter after isosorbide dinitrate-baseline diameter]) x 100 (%). No significant difference was noted between the AOD in patients with ACP and VSA (28 +/- 36 vs 15 +/- 60%, respectively). The AOD values of 49% of patients with VSA were greater than the mean value of AOD of patients with ACP. At least almost half of the patients with VSA may have preserved self-vasodilating ability at the spastic site, and an abnormality other than endothelial dysfunction is involved in the mechanism of coronary spasm in these patients.