LABORATORY INVESTIGATION VENTRICULAR ARRHYTHMIA Myocardial injury and induction of arrhythmia by direct current shock delivered via endocardial catheters in dogs

Although electrical ablation of ventricular tachycardia via percutaneous catheters has been recently accomplished in human beings, little is known of its pathologic or arrhythmogenic effects. We studied 21 open-chest anesthetized dogs in which an endocardial electrode catheter was percutaneously introduced into the left ventricle. Direct current (DC) shock was delivered by a standard defibrillator through the distal electrode to a back paddle. Cross-sectional two-dimensional echocardiographic studies were performed in the plane of the catheter (confirmed by epicardial metal beads), and blood flow was determined by the microsphere technique before DC shock and when the animals were killed 2 to 8 days later. Of 1 1 dogs receiving a total of 100 to 400 J, only three survived 48 hr compared with nine of 10 receiving 50 J and all three control dogs. Holter monitoring demonstrated sustained ventricular tachycardia (VT) (-30 sec) in all 1 1 dogs monitored (six received 100 J), beginning within 5 hr of the DC shock; three control dogs had no VT. Two dogs that died suddenly while being monitored showed ventricular fibrillation. Histologic examination revealed hemorrhagic contraction band necrosis in the shock zone, a type of injury similar to that observed in reperfusion necrosis. Necrosis of the left ventricle was 0.5% to 5%. There was no significant difference in necrosis between dogs receiving 100 J or more and those receiving 50 J (2.5 vs 1.7 g; p > 10). Percent systolic thickening determined in eight equally divided regions around the left ventricle showed no difference between the shock zone, perishock zone, or remote normal zone in dogs receiving 50 J. Blood flow was diminished in the shock zone by 21 + 6% (p < .005) but was unchanged elsewhere. Thus DC shock with as little as 50 J through an endocardial catheter results in localized nontransmural hemorrhagic necrosis. Despite its involvement of a relatively small portion of the left ventricle, this lesion is markedly arrhythmogenic, resulting in sustained VT/sudden death during the first week after DC shock. Circulation 69, No. 5, 1006-1012, 1984. THERAPEUTIC interventions to treat medically refractory ventricular tachyarrhythmias include experimental antiarrhythmic drugs, antitachycardiac pacemakers, endocardial resection, and the automatic implantable defibrillator. IA Recently, closed-chest ablation in the His bundle was successfully performed in patients with medically refractory supraventricular tachyarrhythmias by delivery of a direct current (DC) shock through a standard electrode catheter.5 6 Reasoning that high-energy discharge would also interrupt From the Cardiology Division, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore. Supported by grant HL-17655-07 (SCOR in Ischemic Heart Disease) from the NHLBI, National Institutes of Health. Address for correspondence: Bruce B. Lerman, M.D., University of Virginia School of Medicine, Cardiology Division, Box 158, Charlottesville, VA 22908. Received Nov. 14, 1983; revision accepted Jan. 18, 1984. Presented in part at the 56th Annual Scientific Sessions of the American Heart Association, November 1983, Anaheim, CA. 1006 reentrant pathways responsible for ventricular tachycardia (VT), Hartzler7 has also used this procedure in the ventricle for ablation ofVT in human beings. However, the hemodynamic and electrophysiologic consequences of DC shock on endocardium are unknown. Previous studies limited to either transthoracic or epicardial DC shock have reported impaired ventricular function,8-13 myocardial necrosis,'4 15 and ventricular arrhythmias.16, 17 This study was therefore designed to assess the longterm effects of DC shock delivered through an endocardial catheter on regional structure, function, and cardiac rhythm of the canine left ventricle.