Swiss Interventional Study on Silent Ischemia Type II - SWISSI II
The goal of the trial was to evaluate the effect of percutaneous coronary intervention (PCI) on clinical outcomes among patients with silent ischemia after a myocardial infarction (MI).
Patients Screened: 1,057
Patients Enrolled: 201
Mean Follow Up: Mean follow-up, 10.2 years
Mean Patient Age: Mean age, 55 years
Documented, first ST-segment elevation MI or non-ST-segment elevation MI in the prior 3 months; no malignancy; undergo a maximal symptom-limited exercise test without chest pain; significant ST depression as a sign of silent ischemia; silent ischemia confirmed by stress imaging; and one- to two-vessel coronary artery disease at coronary angiography suitable for PCI
MACE, defined as cardiac death, nonfatal MI, or symptom-driven revascularization
Individual components of the primary endpoint, noncardiac mortality, all-cause mortality, and angina not leading to revascularization
Patients were randomized to PCI (n = 96) or intensive medical therapy (n = 105). Medical therapy included either 5-10 mg/d of bisoprolol, 5-10 mg/d of amlodipine, 4-12 mg of molsidomine twice daily, or a combination of these, with the goal of eliminating or maximally reducing silent ischemia during bicycle ergometry. In the PCI group, complete revascularization was to be performed (i.e., no residual stenosis >75%).
Aspirin (100 mg/d) and a statin
At baseline, the mean number of lesions >75% was 2.0 in the PCI group and 2.3 in the medical therapy group. The large majority of patients were smokers (73%), and 45% had hypertension. By design, more patients in the medical therapy group at final follow-up were taking a beta-blocker (84.2% vs. 39.1%, p < 0.001), calcium antagonist (31.6% vs. 17.4%, p = 0.09), and nitrates (44.7% vs. 4.3%, p < 0.001).
The primary endpoint of major adverse cardiac events (MACE) at a mean follow-up of 10 years was lower in the PCI group compared with the medical therapy group (3.2% vs. 9.5, hazard ratio [HR] 0.35, p < 0.001). The components of the composite endpoint were also lower in the PCI group, including cardiac death (3/1019 vs. 22/1048, HR 0.14, p = 0.01), nonfatal MI (11/938 vs. 40/856, HR 0.26, p = 0.002), and symptom-driven revascularization (26/846 vs. 46/735, HR 0.52, p = 0.008). Angina not leading to revascularization was also lower in the PCI group (11/973 vs. 32/948, HR 0.33, p = 0.009).
Among patients with silent ischemia after an MI, performance of PCI was associated with a reduction in MACE at an average 10-year follow-up compared with intensive, anti-ischemic medical therapy.
Asymptomatic patients with documented ischemia following MI represent a small but potentially high-risk population. Results of the present study differ from those of the recent OAT trial, which demonstrated no clinical benefit of PCI among stable patients with a persistently occluded infarct artery after MI. However, the populations studied differed somewhat in that in the OAT trial, there was no requirement to show ongoing ischemia, whereas in the present study, patients had to have silent ischemia on stress testing.
Erne P, Schoenenberger AW, Burckhardt D, et al. Effects of percutaneous coronary interventions in silent ischemia after myocardial infarction: the SWISSI II randomized controlled trial. JAMA 2007;297:1985-91.
Keywords: Myocardial Infarction, Follow-Up Studies, Constriction, Pathologic, Percutaneous Coronary Intervention, Molsidomine, Coronary Angiography, Chest Pain, Nitrates, Amlodipine, Bisoprolol, Hypertension, Exercise Test
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