We thank Dr. Weiss for his interest in our recent article. Theophylline was to be administered at a rate of 100 mg/min until conversion to normal sinus rhythm occurred or until a maximum of 250 mg was administered. As noted by Dr. Weiss, although two patients converted to normal sinus rhythm after receiving 100 mg of theophylline, a total of 250 mg was administered by the treating physicians. It is now our practice, however, to empirically administer 250 mg of theophylline as a slow intravenous bolus when hemodynamically significant atrioventricular block occurring as a complication of myocardial infarction is recognized. Using this approach, we have safely and promptly converted another two patients (one patient with third-degree atrioventricular block and one with high-grade second-degree atrioventricular block) to normal sinus rhythm. None of these 10 patients (8 in the study and 2 thereafter) had recurrence of the bradyarrhythmia, required further treatment with theophylline, required temporary or permanent pacing, or had electrophysiologic testing. All eight patients in the study were discharged from the hospital. One of the two latter patients died 5 days after his initial myocardial infarction and bradycardic event of severe left ventricular dysfunction and congestive heart failure.

Despite the small number of patients studied, we believe that these data clearly support the hypothesis that the occurrence of atrioventricular block soon after an inferior-wall myocardial infarction is mediated by endogenous adenosine. Moreover, we plan to pursue the application of more potent and specific A₁-adenosine receptor antagonists as a pharmacologic approach to ischemia-related atrioventricular block.