OBJECTIVES: We investigated the efficacy of percutaneous coronary intervention (PCI) in patients with coronary spastic angina (CSA) and severe organic stenosis. BACKGROUND: Coronary spasm occurs at the site of organic stenosis in most patients with CSA and severe stenosis, whereas multivessel spasm occurs frequently in those with normal coronary arteries. The incidence of multivessel spasm and the efficacy of PCI in patients with CSA and severe stenosis have not been fully elucidated. METHODS: Forty-five patients with CSA and severe stenosis underwent spasm provocative testing with intracoronary acetylcholine before and 7 +/- 3 months after PCI (20 patients had angioplasty and 25 patients had stenting), when all patients were free of restenosis. RESULTS: Spasm was induced at the site of severe stenosis in 30 patients (66.7%) with (n = 12) or without (n = 18) spasm induced in another vessel. In the remaining 15 patients, spasm was induced at a different site in the stenotic vessel and/or in another vessel. Repeat provocative tests were performed in 43 of 45 patients. Although spasm was never induced at exactly the same site of the initial stenosis that had been dilated, spasm was induced at a different site in the dilated vessel and/or in another vessel, in 33 (76.7%) of 43 patients. Multivessel spasm occurred in 28 (62.2%) of 45 patients on one or both provocations. CONCLUSIONS: Spasm was frequently induced at a site different from the initial stenosis, even in the absence of restenosis after PCI. Calcium antagonists should be continued in most patients with CSA who show no restenosis after PCI.
OBJECTIVES: We investigated the efficacy of percutaneous coronary intervention (PCI) in patients with coronary spastic angina (CSA) and severe organic stenosis. BACKGROUND:Coronary spasm occurs at the site of organic stenosis in most patients with CSA and severe stenosis, whereas multivessel spasm occurs frequently in those with normal coronary arteries. The incidence of multivessel spasm and the efficacy of PCI in patients with CSA and severe stenosis have not been fully elucidated. METHODS: Forty-five patients with CSA and severe stenosis underwent spasm provocative testing with intracoronary acetylcholine before and 7 +/- 3 months after PCI (20 patients had angioplasty and 25 patients had stenting), when all patients were free of restenosis. RESULTS:Spasm was induced at the site of severe stenosis in 30 patients (66.7%) with (n = 12) or without (n = 18) spasm induced in another vessel. In the remaining 15 patients, spasm was induced at a different site in the stenotic vessel and/or in another vessel. Repeat provocative tests were performed in 43 of 45 patients. Although spasm was never induced at exactly the same site of the initial stenosis that had been dilated, spasm was induced at a different site in the dilated vessel and/or in another vessel, in 33 (76.7%) of 43 patients. Multivessel spasm occurred in 28 (62.2%) of 45 patients on one or both provocations. CONCLUSIONS:Spasm was frequently induced at a site different from the initial stenosis, even in the absence of restenosis after PCI. Calcium antagonists should be continued in most patients with CSA who show no restenosis after PCI.