Objective This study was designed to discuss the mechanism, critical isthmus, the characteristics of surface electrocardiogram (ECG) and the strategy of ablation of ventricular tachycardia (VT) after repair of congenital heart disease in order to increase the success rate and safety of radiofrequency catheter ablation (RFCA).
Methods Eleven consecutive patients (9 men and 2 women, aged 6∼41 years) with recurrent and symptomatic VT after repair of congenital heart disease were investigated. Nine patients had undergone surgical repair of tetralogy of Fallot (TOF), 1 patient had an operation for severe congenital pulmonary stenosis and patch closure of ventricular septal defect (VSD) and suture of atrial septal defect (ASD), and the remaining patient had repair of trilogy of Fallot combined with right ventricular cardiomyopathy. The ECG showed sustained VTs in 10 patients and unsustained VTs in 1 patient, and 4 patients had the histories of syncope. Substrate mapping of the right ventricle during sinus rhythm was performed in all 11 patients. Unexcitable tissue identified from bipolar voltage (<0.5 mV) and uncaptured ventricular regions was defined as the scar or surgical patch, and the possible conduction channel between scar/patch and valve annulus (tricuspid annulus and pulmonary annulus) was defined as anatomic isthmus. Five possible isthmuses were as follows: (1) the tricuspid annulus and scar/patch in the anterior right ventricular outflow (isthmus 1), (2) the pulmonary annulus and right ventricular free wall scar/patch (isthmus 2), (3) the pulmonary annulus and septal scar/patch (isthmus 3), (4) the septal scar/patch and tricuspid annulus (isthmus 4), and (5) the scar/patch in the anterior right ventricular outflow and septal scar/patch (isthmus 5). The methods for mapping and ablating VT were as follows. If the induced VTs were hemodynamically stable, the VT mapping techniques included activation mapping and voltage mapping, combined with entrainment mapping and diastolic potentials mapping to ablate critical isthmuses. For VTs that were unstable or could not be induced, high density substrate mapping was performed at potentially critical isthmuses of the right ventricle, radiofrequency energy was delivered as linear lesions based on the location of the best pace map and the sites with special potentials to anatomic boundaries.
Results In 9 patients after surgical repair of TOF, 19 different monomorphic VTs (cycle length, 170∼350 ms) could be induced; 15 were documented as clinical VTs, 2 VTs were hemodynamically unstable. In 1 patient of having an operation for severe congenital pulmonary stenosis and patch closure of VSD and suture of ASD, 1 nonsustained VT could be induced, the clinical 2 VTs could not be induced. Five morphologies of nonsustained VT could be induced in the remaining patient who had repair of trilogy of Fallot combined with right ventricular cardiomyopathy. In 10 patients who had surgical repair of TOF or severe congenital pulmonary stenosis and patch closure of VSD and suture of ASD, mapping and ablation was performed during VTs in 4 patients. In the other 6 patients, mapping and ablation was performed during sinus rhythm. The sites of surgical correction of the right ventricle were associated with the origins of VTs in these 10 patients. Combined with QRS morphology during VT and the results of mapping and ablation, anatomic isthmus 2 were ablated in 8 patients, isthmus 3 ablated in 8 patients, isthmus 5 ablated in 4 patients, and isthmus 4 ablated in 1 patient. Isthmus 2 and 3 as the reentry circuit critical isthmuses were more common. In the patient of having repair of trilogy of Fallot combined with right ventricular cardiomyopathy, 5 morphologies of nonsustained VTs (cycle length, 250∼310 ms, left bundle-branch block) could be induced, 2 were clinical VTs. Combined with the information of surgical operation method and the result of electroanatomic mapping, these VTs were considered being relevant with right ventricular cardiomyopathy, but not the surgical operation of congenital heart disease. Radiofrequency energy was delivered around the scar of the right ventricle apex and at the sites with late potential within the scar. All the 25 VTs induced in the 11 patients were caused by scar related reentry. Catheter ablation achieved acute success in 10 patients, including elimination of all VTs in 9 patients, and elimination of the clinical VTs in 1 patient. Ablation of VTs failed in the remaining patient with TOF because of lacking of inferior vena cava. During 3 months to 9 years of follow up, VTs recurred in 3 patients. Two of them had a successful ablation of VTs in the second procedure, and 1 patient had success in the third procedure.
Conclusions Reentry circuit isthmuses in VTs late after repair of congenital heart disease are located within anatomically defined isthmuses bordered by unexcitable tissue of scar, patch or valve annulus. The isthmuses between the pulmonary annulus and right ventricular free wall scar/patch (isthmus 2), and between the pulmonary annulus and septal scar/patch (isthmus 3) were more common. In addition, the boundary between the scar/patch in the anterior right ventricular outflow and septal scar/patch (isthmus 5) could also be the critical isthmus of VT. RFCA of these 3 isthmuses could increase the success rate of VT after repair of congenital heart disease. The information of surgical operation prior to ablation and ventricular angiogram during the procedure were very important to predict critical isthmuses and direct electroanatomic mapping. Based on the electroanatomic mapping, RFCA of critical isthmuses of VTs in patients after repair of congenital heart disease might have a high success rate and a low recurrence, especially for unmappable VTs.
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