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Low-dose aspirin reduced the incidence of first nonfatal myocardial infarction in patients with stable angina pectoris

ACP J Club. 1993 May-June;118:73. doi:10.7326/ACPJC-1993-118-3-073

Source Citation

Juul-Möller S, Edvardsson N, Jahnmatz B, et al. Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. Lancet. 1992 Dec 12;340:1421-5.



To study whether low-dose aspirin given to patients with chronic stable angina pectoris reduces the rate of first myocardial infarction (MI) and sudden death.


Randomized, double-blind, placebo-controlled trial with median follow-up of 50 months.


94 primary care centers in Sweden.


2035 patients (mean age 67 y, 52% men) with chronic stable angina pectoris (exertional chest pain for at least 1 month) were studied. Exclusion criteria were treatment with aspirin, anticoagulants, verapamil, nonsteroidal anti-inflammatory agents, high-dose diuretics, or class I antiarrhythmic drugs; heart rate < 55 per minute; previous MI; atrioventricular block (II/III); obstructive lung disease; peptic ulcer; hypersensitivity to aspirin; or juvenile or uncontrolled, late-onset diabetes. Follow-up was 99.5%.


All patients initially received sotalol and were randomized after at least 3 weeks of anginal symptom control. 1009 patients were randomized to aspirin, 75 mg/d, and 1026 to placebo.

Main outcome measures

First MI (World Health Organization criteria) or sudden death. Secondary end points were vascular events and deaths, all-cause mortality, and stroke. Patients were examined every 3 to 6 months.

Main results

Compared with patients taking placebo, patients taking aspirin had fewer primary end points (P = 0.003) consisting of fewer nonfatal MIs (P = 0.006) and a trend toward fewer sudden deaths (P = 0.1) (Table). Vascular events (first MI, stroke, or vascular death) were similarly reduced (P < 0.001) (Table). The groups (aspirin vs placebo) did not differ for all-cause mortality (82 vs. 108 deaths, P = 0.103) or nonhemorrhagic adverse events (174 vs 168 events). Treatment was stopped in 362 patients in the aspirin group and 417 patients in the placebo group. Independent relative risks for MI or sudden death were women versus men, 0.44 (95% CI 0.33 to 0.61); no diabetes versus diabetes, 0.45 (CI 0.27 to 0.72); cholesterol < 6.5 versus ≥ 6.5 mmol/L, 0.70 (CI 0.51 to 0.96); and aspirin and sotalol versus placebo and sotalol, 0.68 (CI 0.49 to 0.9), respectively.


Low-dose aspirin taken by patients with stable angina pectoris on sotalol reduced the incidence of first non-fatal myocardial infarction and vascular events.

Source of funding: Not stated.

For article reprint: Dr. S. Juul-Möller, Cardiology Section, Department of Medicine, General Hospital, S-21401 Malmö, Sweden. FAX 46-40-336-281.

Table. Sotalol plus aspirin vs sotalal plus placebo in patients with stable angina pectoris*

Outcome at a median of 50 months Sotalol plus aspirin Sotalol plus placebo RRR (95% CI) NNT (CI)
Primary endpoints (fatal, nonfatal MI, and sudden death) 8 % 12% 34% (13 to 49) 25 (15 to 69)
Nonfatal MI 5% 8% 39% (13 to 57) 34 (20 to 115)
Sudden deaths 2% 3% 38% (-9 to 64) Not significant
Vascular events 11% 16% 32% (14 to 46) 20 (13 to 49)

*Abbreviations defined in Glossary; RRR, NNT, and CI calculated from data in article.


Juul-Möller and colleagues state that the Swedish Angina Pectoris Aspirin Trial is a study of primary prevention because documented previous MI was an exclusion criterion. All patients, however, were presumed to have coronary artery disease for an average of 4.7 years, based on "symptoms of chronic stable angina pectoris." The extent and severity of coronary artery disease is not defined. The number of patients who had coronary angiography or revascularization is also not stated, although patients already on or requiring aspirin were excluded. The intervention is more rightly considered secondary prevention because event rates were presumed and shown to be higher than in healthy persons. As such, the findings add to the already compelling body of data showing that aspirin reduces infarction, stroke, and death in patients with atherosclerotic disease.

The trial is noteworthy in several respects. First, important reductions in the primary and secondary end points were seen with an aspirin dose of 75 mg/d, lower than that given in other trials of secondary prevention after infarction. Second, unlike many trials that enroll men exclusively or predominantly, almost half the participants in this study were women. The effect of aspirin on the primary end points appeared to be the same in both sexes. Regrettably, a formal subgroup analysis was not presented. Finally, although no reduction in total mortality was seen, the sample size was too small to exclude such an effect. The reduction in MI, stroke, and total mortality far outweighed the slight excess of major or fatal bleeding.

Physicians already have sufficient reason for treating patients with stable angina with aspirin. Whether 75 mg/d is as effective at reducing risk as higher doses must await a direct comparison.

Steven Borzak, MD
Henry Ford Heart and Vascular InstituteDetroit, Michigan, USA