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Updated: Aug 11, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left
Insights
Abruptly stopping beta-blockade therapy during acute myocardial infarction did not significantly impact infarct size or mortality. Recurrent chest pain was slightly higher initially but did not pose a major clinical problem.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Beta-blockade therapy is commonly used in cardiovascular conditions.
- The potential effects of abruptly withdrawing beta-blockers during acute myocardial infarction (AMI) were not well-established.
Purpose of the Study:
- To evaluate the clinical outcomes of abrupt beta-blocker withdrawal versus continuation in patients with AMI.
Main Methods:
- A study involving 326 patients in the Multicenter Investigation of the Limitation of Infarct Size (MILIS) trial.
- Comparison of patients previously on beta-blockers randomly assigned to withdrawal versus placebo, against patients not on beta-blockers assigned to placebo.
- A subgroup analysis compared withdrawal versus continuation of beta-blockade.
Main Results:
- No significant differences in infarct size, left ventricular ejection fraction, infarct extension, congestive heart failure, ventricular fibrillation, or in-hospital mortality between groups.
- Patients withdrawing from beta-blockers experienced more recurrent ischemic chest pain within 24 hours, but this was not linked to rebound hemodynamic changes.
- Subgroup analysis showed similar outcomes.
Conclusions:
- The beta-blockade withdrawal phenomenon is not a significant clinical issue in acute myocardial infarction.
- Abrupt discontinuation of beta-blockade therapy during AMI is clinically acceptable if indicated.
Abstract:
The effects of abrupt withdrawal or continuation of beta-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 beta-blocker and randomly selected for withdrawal of beta-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with beta-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant 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 extension (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 beta-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior beta-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the beta-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. beta-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.
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