Abrupt withdrawal of β-blockade therapy in patients with myocardial infarction: Effects on infarct size, left ventricular function, and hospital course

Abstract

The effects of abrupt withdrawal or continuation of β-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a β-blocker and randomly selected for withdrawal of β-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with β-blockers who were also randomly assigned to placebo therapy (group 2). There were no signficant differences between the two groups in MB creatine kinase isoenzyme (15.8 ± 10.9 vs 18.2 ± 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 ± 0.15 vs 0.47 ± 0.16) or 10 days later (0.42 ± 0.14 vs 0.47 ± 0.16), creatine kinase-determined incidence of infarct extention (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of β-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior β-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the β-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. β-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.