Abstract
Ventricular tachyarrhythmias are known sequelae among adults with repaired tetralogy of Fallot. The incidence of sustained ventricular tachycardia and sudden cardiac death in patients 35 years after corrective surgery is estimated at 11.9% and 8.3%, respectively.1 Studies have shown that right ventricular enlargement resulting from chronic pulmonic regurgitation is the most common hemodynamic substrate.2 QRS prolongation (>180 milliseconds) is one of the most sensitive ECG predictors and in turn correlates with right ventricular (RV) dilation.3 The exact mechanism is not as well studied as that of left ventricular arrhythmias, but it is purported that volume overload leads to RV myocardial stretching and RV fibrosis and hence serves as an arrhythmogenic focus. The anatomic location of the RV pathology leading to ventricular tachyarrhythmias after tetralogy of Fallot surgical repair is not well defined. The basal portions of the RV …
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