Serial signal-averaged electrocardiograms were recorded every 72 hours in 60 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 61.6% (37 patients) during hospitalization. Of these 37 patients, late potentials appeared transiently in 20 (54%), while in 9 patients (24%), once late potentials had appeared, they tended to persist. No specific clinical characteristics were related to the development of late potentials (site of infarction, peak creatine kinasa activity, Killip class, thrombolytic therapy). The presence of late potentials did not identify patients who developed clinically significant ventricular tachyarrhythmias (primary ventricular fibrillation, ventricular tachycardia). The abnormal late potentials were modified by the administration of lidocaine. This lack of correlations suggests that the abnormal signal averaged electrocardiogram and complex ventricular arrhythmias during acute myocardial infarction have different electrophysiological bases. Late potentials could be only a bystander electrophysiological phenomenon without clinical correlation in this clinical phase.

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[Induction of a double nodal pathway in dogs by transcatheter ablation with high frequency currents].

A dog weighing 15 kg and anesthetized with intravenous sodium thiopental was subjected to transcatheter ablation of the AV junction with high-frequency currents, in order to induce a partial alteration in AV conduction (first degree AV block). Two conventional bipolar electrode-catheters were introduced through the right femoral vein and used one for atrial pacing and the other for His bundle recording and current delivering. The catheter used for ablation was situated in the AV junction where the distal monopolar recording of the His bundle electrogram showed an A/V ratio close to one in the presence of His bundle deflection. Three discharges were delivered under continuous electrocardiographic monitoring. The output power used was 15 watts and current application time was up to five seconds after attaining complete AV block; 1:1 AV conduction was quickly restored on concluding discharge. After the second discharge, a discontinuous nodal function curve of the dual AV nodal pathway type was obtained (absent in control and after first discharge studies). Following the third discharge the conduction through the slow pathway was abolished. The study was repeated after four weeks, an a dual AV nodal pathway type curve similar to that found during the acute phase was obtained. The histologic findings showed a collagen scar partially replacing nodal tissue and creating a partial septation of the AV node. To conclude: The structural alterations of the AV node may induce a dual AV nodal pathway response.

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