Self-vasodilating Ability at the Spastic Site of Patients with Vasospastic Angina

Abstract

SUMMARYDeficient 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 µg) 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]) ×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. (Jpn Heart J 2003; 44: 299-311)

The Incidence of Stent-edge Spasm After Stent Implantation in Patients With or Without Vasospastic Angina Pectoris

“…This finding suggests the clinical importance of newly occurring stent-edge spasm. The diagnosis of VSA is sometimes difficult because some patients with severe coronary spasm complain of only chest discomfort without typical rest angina or chest pain on effort 11) and the disease activity of coronary spasm may be related to the results of spasm provocation testing. 16) Therefore, it is very difficult to completely exclude the possibility of a patient having VSA in our patients without VSA.…”

“…The diagnosis of VSA was based on previously reported criteria (rest angina, induction of total or subtotal spasm, and ischemic electrocardiographic change during spasm provocation test). 11) In these patients, coronary stent implantation was performed as the treatment of organic stenotic lesions >75% diameter stenosis. We did not perform stent implantation for the treatment of coronary spasm itself in any of the patients with VSA.…”