Multicenter randomized trial and a systematic overview of lidocaine in acute myocardial infarction.

BACKGROUND: More than 20 randomized trials and 4 meta-analyses have been conducted on the use of prophylactic lidocaine in acute myocardial infarction (MI). The results suggest that lidocaine reduces ventricular fibrillation (VF) but increases mortality rates in acute MI. METHODS AND RESULTS: Patients with ST-elevation MI who were examined <6 hours after symptom onset (n = 903) were randomly assigned to either lidocaine or no lidocaine and to either streptokinase and heparin or heparin alone. Lidocaine was given as 4 boluses of 50 mg each every 2 minutes, then an infusion of 3 mg/min for 12 hours, then 2 mg/min for 36 hours. We compared the incidence of in-hospital death and ventricular arrhythmias. We then performed a meta-analysis of prophylactic lidocaine in acute MI that included these and prior trial results. The rates of VF and death with and without lidocaine were calculated for each trial, then odds ratios (OR) with confidence intervals (CI) were calculated for the risk of these events overall with and without lidocaine. Patients given lidocaine in the randomized study had significantly less VF (2.0% vs 5.7% without lidocaine, P =.004) and a trend toward increased mortality rates (9.7% vs 7.0%, P =.145). Meta-analysis revealed nonsignificant trends toward reduced VF (OR 0.71, 95% CI 0.47 to 1. 09) and increased mortality rates (OR 1.12, 95% CI 0.91 to 1.36) with lidocaine. CONCLUSIONS: Lidocaine reduces VF but may adversely affect mortality rates. The routine use of prophylactic lidocaine in acute MI is not recommended.

Lack of effect of amiodarone on survival after extensive infarction. Polish Amiodarone Trial.

BACKGROUND: The purpose of this study was to elucidate whether the reduction of mortality with amiodarone after myocardial infarction depended on ejection fraction. METHODS: The data from the Polish Amiodarone Trial were analysed retrospectively. Patients with acute myocardial infarction and contraindications to beta-blockers were randomized on days 5-7 after admission to receive amiodarone (n = 305) or placebo (n = 308). Short and long-term (46 months) mortality were analysed comparing the groups with impaired (ejection fraction < 40%) and preserved (ejection fraction > or = 40%) left ventricular function. A subset of patients (n = 523) with available echocardiograms were subjected to this analysis. RESULTS: Long-term and sudden cardiac mortality were significantly reduced with amiodarone in the group of patients with ejection fraction > or = 40% (amiodarone versus placebo, respectively: 9.1 versus 16.5%, P < 0.05; 3.4 versus 8.2, P < 0.05). No beneficial effect of amiodarone was observed in the group with low ejection fraction (cardiac and sudden cardiac mortality: amiodarone versus placebo, 20.8 versus 19.3% and 7.8 versus 5.7% respectively). One-year mortality also revealed a favourable trend only in amiodarone-allocated patients with ejection fraction > or = 40%. CONCLUSION: Amiodarone decreased long-term and sudden cardiac mortality after myocardial infarction only in patients with preserved left ventricular function. No benefit was observed in patients with decreased ejection fraction.

Effect of amiodarone on mortality after myocardial infarction: a double-blind, placebo-controlled, pilot study.

OBJECTIVES: The goal of this study was to evaluate the effect of amiodarone on mortality, ventricular arrhythmias and clinical complications in high risk postinfarction patients. BACKGROUND: No therapy has been shown to reduce sudden death in patients ineligible to receive beta-adrenergic blocking agents after myocardial infarction. METHODS: Patients who were not eligible to receive beta-blockers were randomized to receive amiodarone (n = 305) or placebo (n = 308) for 1 year. RESULTS: There were 21 deaths in the amiodarone group compared with 33 in the placebo group (odds ratio 0.62, 95% confidence interval [CI] 0.35 to 1.08, p = 0.095). There were two noncardiac deaths in the amiodarone group and none in the placebo group; thus, the difference in cardiac mortality (19 vs. 33, respectively) was statistically significant (odds ratio 0.55, 95% CI 0.32 to 0.99, p = 0.048). There was a significant decrease in Lown class 4 ventricular arrhythmias (7.5% vs. 19.7%, respectively, p < 0.001). Adverse effects developed in 30% of amiodarone-treated patients and 10% of placebo-treated patients. Pulmonary toxicity, which was mild and reversible, occurred in only one patient in the amiodarone group but in no patient in the placebo group. CONCLUSIONS: This trial demonstrated a significant reduction in cardiac mortality and ventricular arrhythmias with amiodarone treatment. However, given the wide confidence intervals and borderline statistical significance of our trial, larger trials are needed to confirm or refute this view.