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J Thorac Cardiovasc Surg 1995;109:303-310
© 1995 Mosby, Inc.


SURGERY FOR CONGENITAL HEART DISEASE

Arrhythmias and intracardiac conduction after the arterial switch operation

Larry A. Rhodes, MD*, Gil Wernovsky, MD, John F. Keane, MD, John E. Mayer, Jr., MD, Allison Shuren, RN, MSN, PNP, Christine Dindy, CCT, Steven D. Colan, MD, Edward P. Walsh, MD


Boston, Mass.

Supported in part by grant HL 41786 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

Received for publication April 1, 1994. Accepted for publication August 15, 1994. Address for reprints: Gil Wernovsky, MD, Children's Hospital of Philadelphia, 34th St. and Civic Center Blvd., Philadelphia, PA 19104.

Abstract

Intraatrial baffling procedures such as the Mustard or Senning repair of transposition of the great arteries have been associated with a high incidence of cardiac arrhythmias. These abnormalities are thought to arise from trauma to the sinus node and atrial muscle during the procedure. In the arterial switch operation, there is little intraatrial manipulation other than the repair of the atrial septal defect. In theory, rhythm disturbances after the arterial switch operation should be less prevalent. From January 1, 1983, to December 31, 1990, 390 patients (230 with intact ventricular septum and 160 with a coexisting ventricular septal defect) underwent an arterial switch operation. Electrocardiograms and 24-hour Holter monitor studies were obtained in the 364 survivors at hospital discharge and during follow-up. Limited intracardiac electrophysiologic studies were performed 6 to 12 months after the operation. Results: Atrioventricular node function was preserved in most patients; seven patients (2%) had first-degree, two (0.7%) second-degree, and five (1.7%) had complete atrioventricular block (all with coexisting ventricular septal defect). All five patients with complete heart block received a permanent pacemaker. In those patients not having a permanent pacemaker, sinus rhythm was present in 96% on the surface electrocardiogram and 99% during 24-hour Holter monitor studies (1 month to 8.5 years, mean 2.1 years after the operation). Intracardiac electrophysiologic studies (n = 158) demonstrated normal corrected sinus node recovery times and AH intervals in 97% of patients. Atrial ectopy was present in 152 of 172 (81%) patients, with the majority (64%) of patients having only occasional premature beats without repetitive forms. Ventricular ectopy was a frequent finding during 24-hour monitoring. At hospital discharge 70% had ventricular ectopy; these values fell to 57% (in patients with intact ventricular septum) and 30% (in patients with a coexisting ventricular septal defect) at follow-up. In the early postoperative period, there were 25 episodes of supraventricular tachycardia (14 of which required therapy), 6 episodes of junctional ectopic tachycardia, and 9 episodes of ventricular tachycardia. The incidence of supraventricular tachycardia had fallen to 5% at follow-up, with no atrial flutter or fibrillation noted. Three patients had ventricular tachycardia on follow-up Holter studies. In summary, our results confirm the theoretical advantages of anatomic correction over atrial level correction of transposition of the great arteries with respect to preservation of sinus node function and low incidence of clinically significant tachyarrhythmias. (J THORAC CARDIOVASC SURG 1995; 109: 303-10)




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