Because sudden death has been an important concern in patients who have undergone intracardiac repair of Fallot’s tetralogy, electrophysiological interest has understandably focused on high-degree heart block and ventricular arrhythmias. High-degree heart block has yielded to ventricular tachycardia as the probable cause of sudden death. By reason of the attention devoted to ventricular electrical instability, comparatively little attention has been paid to disturbances in atrial rhythm. The timely study from the Adult Congenital Heart Disease Clinic of the Thorax Center, Rotterdam, addressed this important deficiency and put into perspective the incidence and significance of atrial arrhythmias in adults after repair of Fallot’s tetralogy. The relatively early era of cardiac surgery reflected in the report was a necessity, not a shortcoming, because the data were derived from an adult patient population after a mean follow-up of 17.5 years (1.4 to 32 years). The observations are therefore based on a wide variety of surgical techniques, a relatively broad age range at time of operation, and a substantial follow-up. Significantly, the surgical and follow-up data were derived entirely from patients at a single center.
The authors “carefully sifted through all available material in search of rhythm disturbances as they appeared on monitor strips, routine ECG tracings, and Holter records.” Access to multiple Holter monitor tracings increased the probability of arrhythmia detection. Perioperative atrial arrhythmias as well as those occurring during cardiac catheterization were appropriately excluded. The diligence with which atrial arrhythmias were sought goes a long way in explaining their relatively high incidence. Both bradyarrhythmias and tachyarrhythmias were identified. Sinus node dysfunction was present in 36% of patients, and atrial tachyarrhythmias—supraventricular tachycardia, atrial fibrillation, or atrial flutter—in 34%. The authors pointed out that surface ECGs did not permit separation of AV node reentry from ectopic atrial foci or accessory pathways. They also took care to warn against misinterpreting supraventricular tachycardia for ventricular tachycardia in a patient population with a high prevalence of QRS prolongation (postoperative prolongation of right ventricular activation).
Importantly, when atrial tachyarrhythmias were removed from the analysis of patients with concomitant ventricular tachycardia, the incidence of palpitations did not reach significance. The practical corollary of this observation is that palpitations were likely to reflect disturbances in atrial rather than ventricular rhythm. The relation between palpitations and atrial arrhythmias argues for the use of event recorders, which promise to increase the yield still further. Exercise stress testing was a useful means of provoking ventricular ectopic rhythms but was not useful in provoking atrial tachyarrhythmias, which were more readily recovered in the Holter monitors.
The cause of sinus node dysfunction in 47 of the 53 patients was in all probability related to superior vena caval cannulation. The cause or causes of the atrial tachyarrhythmias were less clear. There was no apparent relation between atrial arrhythmias and right atrial size or the presence and degree of tricuspid regurgitation. In fact, right atrial enlargement was present in 98% of patients. Accordingly, arrhythmic origin in the right atrium (or atrial septum) was more likely to have been a result of atriotomy and/or closure of a coexisting interatrial communication (atrial septal defect or patent foramen ovale). The authors then called attention to potential origin of the arrhythmias in the left atrium. Three of 4 patients with echocardiographic left atrial enlargement had atrial fibrillation or atrial flutter. None had mitral regurgitation. An enlarged left atrium was more likely to have been due to the surgical shunts—Blalock-Taussig, Potts, or Waterston—or to a residual postoperative ventricular septal defect. Twenty-seven of the 53 patients did in fact have shunt operations—16 Blalock-Taussig, 10 Waterston, and 1 Potts. Surgical shunts might have set the stage for left atrial tachyarrhythmias even though the present study did not identify a postoperative increase in left atrial size. All 4 patients with left atrial enlargement had residual ventricular septal defects, which, however, were considered small. The authors found a significant correlation between the incidence of atrial arrhythmias and left ventricular abnormalities that were probably residua of volume overload due to the surgical shunts or to inadequate myocardial protection during early-era intracardiac repairs.
The importance of the authors’ observations is underscored by the main sources of morbidity in their adult patients after intracardiac repair of Fallot’s tetralogy, namely, the atrial arrhythmias. Recurrences of atrial fibrillation or atrial flutter are potential risks for cerebral emboli, which occurred in 4 of the patients. Prophylactic anticoagulants carry an associated risk of hemorrhage.
Sinus node dysfunction required permanent pacemaker implantation in 4 patients. The atrial tachyarrhythmias were managed pharmacologically. Intracardiac mapping techniques may clarify the precise arrhythmic mechanisms in this patient population and establish the exact anatomic foci of atrial ectopic tachycardia, reentrant supraventricular tachycardia, and atrial flutter. Radiofrequency catheter ablation of the tachyarrhythmias promises to extend the therapeutic armamentarium.
The study from the Thorax Center dealt with disturbances in atrial rhythm in patients with Fallot’s tetralogy who were operated on during the past two decades. For patients operated on today, we can anticipate, during the next two decades, a lower incidence of bradyarrhythmias previously caused by sinus node injury and a lower incidence of tachyarrhythmias originating in the left atrium in response to shunt-induced volume overload of the left heart.
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
- Received February 9, 1995.
- Accepted February 9, 1995.
- Copyright © 1995 by American Heart Association