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Five patients with recurrent syncope or pre-syncope due to rapid supraventricular tachycardias underwent electrophysiological study. In each patient, an AV nodal re-entrant tachycardia could be induced. By leaving a coronary sinus catheter in place, the effects of drugs on the ability to induce tachycardia could be tested on sequential days. Drug effects were highly variable, but in each patient it was possible to determine a drug which prevented induction of tachycardia. Patients treated with this drug have had no recurrent symptoms or tachycardias with a followup of 4-21 months. Although AV nodal re-entry is highly dependent on autonomic tone, electrophysiological study appears to be a useful means of selecting therapy in patients with severe, symptomatic tachycardias.

Eight patients with ventricular aneurysms and ventricular tachycardia refractory to drugs were studied. Each patient underwent intraoperative epicardial and endocardial mapping during stable sinus rhythm. After aneurysmectomy, areas of the endocardial border zone which demonstrated fragmented activity were excised. Mapping was then repeated to ensure that major areas of fragmentation did not remain. Mapping was completed in less than 20 minutes in each patient. One patient died of pump failure before hospital discharge and a second patient, who was arrhythmia-free, died of pump failure 12 months postoperatively. Six patients are alive and free of ventricular tachycardia 5 to 25 months (mean 11.5) postoperatively. We conclude that excision of areas of fragmented electrical activity in the endocardial border zone of ventricular aneurysms is a useful approach to surgical therapy for ventricular tachycardia. This approach allows an excision directed to arrhythmogenic areas without the need for tachycardia induction in the operating room.

We evaluated the effectiveness of oral verapamil therapy for control of ventricular rate in digitalized patients with atrial fibrillation (AF) with three clinical problems: chronic AF with rapid rate at rest (four patients), chronic AF with accelerated rate during modest exercise (five patients), and rapid rates during paroxysmal AF (four patients). Patients in the first two categories were evaluated both by open-label dosage titration and by a randomized, double-blind, cross-over protocol. In chronic AF with rapid rate of rest, there was a significant reduction in resting heart rate (from 125 +/- 7 to 87 +/- 14, P less than 0.01) and in peak exercise heart rate (from 162 +/- 33 to 126 +/- 25, P less than 0.01). In chronic AF with rapid rate during exercise, there was also a significant decrease in resting heart rate (from 90 +/- 7 to 66 +/- 4, P less than 0.01) and in peak exercise heart rate (from 126 +/- 19 to 101 +/- 15, P less than 0.01). These effects continued during longterm follow-up of one to 12 months (mean seven months). In patients with paroxysmal AF, verapamil slowed the ventricular response from 16- +/- 24 to 72 +/- 4 P less than 0.01) with only some amelioration of symptoms. Therapy was well tolerated despite a high prevalence (seven of 13 patients) of radiographic cardiomegaly (cardiothoracic ratio greater than 0.55). We conclude that verapamil is a safe and useful drug for control of ventricular rate in digitalized patients with chronic and paroxysmal AF.

To determine the effects of left ventricular hypertrophy on epicardial activation of the human heart, intraoperative epicardial mapping of 40 to 66 points was performed in 10 patients undergoing aortic valve replacement. Mean calculated left ventricular mass was 364 +/- 98 g. All patients had normal left ventricular contraction. Earliest epicardial activation occurred in the anterior right ventricle in all patients. In 9 patients, it was the only epicardial breakthrough point. One patient had a single inferior left ventricular breakthrough point. Epicardial activation spread from the right ventricle towards the left ventricle in both the anterior and inferior direction. Latest epicardial activation occurred at the base of the left ventricle in 9 patients and the base of the right ventricle in 1. When compared with patients with coronary artery disease, normal ventricular contraction, and no left ventricular hypertrophy, patients with hypertrophy had fewer left ventricular breakthrough points (p less than 0.001) and were more likely to have latest activation at the left ventricular base (p less than 0.0010. We conclude that left ventricular hypertrophy is associated with marked changes in the pattern of epicardial activation. These changes may reflect delay in spread from endocardium due to the increased wall thickness.

Endocardial mapping was performed on 16 patients undergoing coronary artery bypass surgery, and the results were correlated with ventriculography. Bipolar electrograms were recorded from 25 to 30 left ventricular (LV) endocardial sites by a specially designed probe which was inserted through the LV vent. Electrograms were evaluated for timing and presence of fragmentation. Five patients had normally contracting ventricles, four had areas of hypokinesis, six had areas of akinesis, and one had an area of dyskinesis. In each patient earliest endocardial activation was in the septum, most often the middle portion. Latest activation was in the lateral basal area in 13 patients and in the lateral apical area in three patients. Fragmented electrograms were not found in any normal or hypokinetic zones but were found in three of six akinetic segments, and in the one dyskinetic segment. These findings describe endocardial activation of the LV and the changes seen with regional contraction abnormalities.