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Background: In the fibrinolytic era, several studies have suggested that the rate of atrioventricular block (AVB) in the setting of acute myocardial infarction (MI) is high and is associated with increased short-term mortality. We sought to delineate predictors of AVB and determine long-term mortality of patients developing AVB in the setting of ST-segment elevation MI (STEMI) treated with thrombolytic therapy., Methods: We combined data on patients from 4 similar studies of STEMI. We identified independent predictors of AVB and compared the 6-month and 1-year mortality rates of patients with AVB (5251) to the rates of patients without AVB (70 742)., Results: The incidence of AVB was 6.9%. Significant independent predictors of AVB included inferior MI, older age, worse Killip class at presentation, female sex, enrollment in the United States, current smoking, hypertension, and diabetes. Adjusted mortality was significantly higher in patients with AVB than in patients without AVB within 30 days (OR 3.2, 95% CI 2.7-3.7), 6 months (OR 1.6, 95% CI 1.5-1.8), and 1 year (OR 1.5, 95% CI 1.3-1.6). For patients with AVB and inferior MI, mortality odds ratios (ORs) were 2.2 (95% CI 1.7-2.7), 2.6 (95% CI 2.4-2.9), and 2.4 (95% CI 2.2-2.6) within 30 days, 6 months, and 1 year, respectively. For patients with AVB and anterior MI, mortality ORs were 3.0 (95% CI 2.2-4.1), 3.5 (95% CI 3.1-3.8), and 3.3 (95% CI 3.0-3.7) within 30 days, 6 months, and 1 year, respectively., Conclusions: In the thrombolytic era, AVB in the setting of STEMI is common and associated with higher mortality. Future studies should focus on determining therapies that are effective at reducing mortality rates in such patients.

To assess the efficacy and safety of current pharmacologic therapy for supraventricular tachycardia (SVT) in infants, we reviewed 112 infants treated between July 1985 and March 1993. The SVT mechanism was determined by esophageal electrophysiologic study and involved an accessory pathway in 86, atrioventricular (AV) node reentry in 10, atrial muscle reentry in 11, and an ectopic atrial tachycardia in 5 patients. Of six infants not treated, none had clinical recurrences of SVT. Of the 106 patients treated, 70% remained free of tachycardia while receiving digoxin, propranolol, or both. Class I antiarrhythmic agents were necessary for 13 patients, and class III agents were required for another 13 infants. Verapamil was used in one infant with AV node reentry tachycardia. Nine infants with complex clinical presentations were believed to have failed medical management and underwent radiofrequency ablation. Five patients died, four of complications related to structural heart disease and one shortly after radiofrequency ablation was performed. No deaths appeared to be related to antiarrhythmic medications. No drug-related side effects requiring medication change occurred, and no proarrhythmia was observed. Thus medical therapy appears to be effective and safe in infants with SVT. Radiofrequency ablation should be reserved for rare infants who fail aggressive medical regimens or when the situation is complicated by ventricular dysfunction, severe symptoms, or complex congenital heart disease.

DPH is highly effective against both atrial and ventricular arrhythmias resulting from digitalis toxicity and should be considered one of the primary antiarrhythmic drugs in this clinical situation. Clinical studies have indicated that DPH, for the most part, is effective against atrial arrhythmias and not markedly effective against ventricular arrhythmias associated with acute or chronic cardiac disease. For the latter ventricular arrhythmias, DPH is usually considered only after other antiarrhythmic drug therapy has failed. Studies on the mechanisms responsible for the antiarrhythmic effects of DPH are, as yet, inconclusive, There is good evidence that its actions differ from those of the commonly used drugs with local anesthetic effects. The extent to which it exerts direct effects on the heart which are therapeutically relevant remains to be demonstrated; further, there is solid evidence that its effects on the central nervous system may be of prime importance in its antiarrhythmic efficacy.

The acute electrophysiologic effects of a bolus injection of 100 mg. of lidocaine were investigated in 39 patients with impulse formation and conduction defects by means of His-bundle recording and were correlated with plasma lidocaine levels. The effects of therapeutic plasma levels on conduction intervals and refractory periods were subsequently studied during sinus rhythm and atrial pacing. The sinus-node function was studied by measurement of the sino-atrial recovery time. Seventeen patients had conduction defects in or distal to the His bundle, six exclusively proximal to the His bundle, and nine at both levels. Nine patients had pre-existent sinus-node malfunction. Ten out of 39 patients suffered from acute myocardial infarction. Two patients were studied twice because of changed A-V conduction. Intravenous injection of 100 mg. of lidocaine within 20 seconds produced peak arterial plasma levels (mean 26.6 mug per milliliter) 60 seconds after the beginning of the injection. Seven out of 26 patients showed transient progression of their pre-existent infra-His conduction impairment, coincident with peak plasma levels, apparently due to drug toxicity. Even at therapeutic plasma levels, five out of 26 patients showed decremental intraventricular conduction during atrial pacing when compared to control tracings. His-Purkinje refractoriness was not shortened in these patients and increased in two. Lidocaine had no effect on ventricular automaticity in three patients with complete heart block. Lidocaine had no consistent effects on sinus rate, SART, atrial refractoriness, or A-V nodal conduction as measured by pooled AH intervals and the Wenckebach point, and on A-V nodal refractoriness. It is concluded that lidocaine is safe in patients with high degrees of A-V nodal block and in patients with impulse formation disturbances. However, patients with intraventricular conduction defects are prone to deterioration of their conduction disturbance due to drug toxicity. The drug should be given to such patients preferably if monitoring and pacemaker facilities are available and by the intramuscular route to avoid peak plasma levels.

The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:1 supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:1 AV conduction, but despite prompt termination of tachycardia in both cases, 2:1 AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block--that is, the "final common pathway" of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node.