Peer-review started: August 28, 2022
First decision: November 21, 2022
Revised: December 4, 2022
Accepted: December 21, 2022
Article in press: December 21, 2022
Published online: January 26, 2023
Coronary spasm can be divided into two types: Focal spasm and diffuse spasm, but the prognosis for focal spasm is reported to be worse than that for diffuse spasm.
The cause of the worse prognosis in focal spasm is unclear, and although the degree of myocardial ischemia may be more severe in focal spasm, no method has been established to evaluate the severity of coronary spasm.
The objective of the present study was to investigate such relationships using a pressure wire during the spasm provocation test (SPT) in patients with vasospastic angina (VSA).
Eighty-seven patients with VSA (average age: 67 years; 50 men, 37 women) underwent SPT. During SPT, a pressure wire was advanced into the distal portion of the right coronary artery and the left anterior descending coronary artery, and the ratio of intracoronary pressure to aortic pressure (Pd/Pa) was continuously monitored. An SPT was performed with acetylcholine (ACh), and the presence of coronary spasm was defined as the presence of > 90% arterial narrowing in response to an ACh infusion, with the usual chest symptoms and/or ischemic ECG changes. Focal spasm was defined as total or subtotal spasm within one segment of the AHA classification, while diffuse spasm was defined as > 90% spasm with two or more segments. The group with focal spasm in at least one major coronary artery was classified as the focal group, and the group without focal spasm as the diffuse group.
Among 87 patients, the frequencies of metabolic syndrome and coronary atherosclerosis were higher in the focal group (n = 33) than in the diffuse spasm group (n = 54, P < 0.05). In vessel analyzes, in these 134 spastic segments, diffuse and focal spasms were detected in 100 and 34 vessels, respectively. Pd/Pa at baseline was similar in both groups (diffuse: 0.96 ± 0.05, focal: 0.95 ± 0.05, P = 0.35); however, Pd/Pa during coronary spasm was lower in focal spastic vessels (0.66 ± 0.20) than in diffuse spastic vessels (0.76 ± 0.11, P < 0.01), and the reduction in Pd/Pa during an SPT was also lower in focal spastic vessels (-0.29 ± 0.20) than in diffuse spastic vessels (-0.18 ± 0.11, P < 0.01). The presence of focal spasm was a significant factor responsible for the reduction in Pd/Pa during SPT.
These findings suggest that focal spasm may be more severe than diffuse spasm, judging by intracoronary pressure during coronary spasm. This mechanism may be involved in the poor prognosis of focal spasm, and careful measures, such as intensified drug therapy, should be taken when focal spasm is detected.
In recent years, more patients have been evaluated for coronary microvascular dysfunction using pressure wires and then for coronary artery spasm induced by ACh, and it is possible that pressure wires will be used more frequently to induce coronary artery spasm. It will be important to confirm the findings of this study in more cases.