Electroanatomical differences in Tetralogy of Fallot patients undergoing risk stratification

Julia Köbe (Münster)1, K. Wasmer (Münster)2, B. Rath (Münster)1, C. Ellermann (Münster)1, G. Frommeyer (Münster)1, P. S. Lange (Münster)1, F. Güner (Münster)1, L. Eckardt (Münster)1

1Universitätsklinikum Münster Klinik für Kardiologie II - Rhythmologie Münster, Deutschland; 2Clemenshospital Klinik für Kardiologie Münster, Deutschland

 

Abstract:

The overall survival of patients with Tetralogy of Fallot (ToF) has improved considerably. Nevertheless, patients are at risk for ventricular arrhythmias and sudden cardiac death. Electroanatomical mapping (EAM) and identification of slow conducting isthmuses has recently shown to be predictive in identifying ToF patients at risk for ventricular arrhythmias. The study aimed at carving out differences in EAM of ToF patients and their impact on arrhythmic risk. 

 

Methods:

Patients with corrected ToF, double outlet right ventricle (DORV) and pulmonary valve atresia referred for EAM and risk stratification for ventricular arrhythmias are included. Clinical data was taken from the hospital files. All patients underwent 3D EAM (CARTO system, Biosense Webster, substrate settings: dense scar < 0.5 mV, border zone 0.5-1.5 mV). Programmed ventricular stimulation (CL 500/430/370/330 S2 and S3, minimum 150 msec and CL 450/350 S5) was performed. In case of slow conducting isthmuses or clinical ventricular tachycardia, ablation was performed. After ablation re-mapping and proof of block was pursued. RV volumes and length, width, and area of the transannular patch and the ventricular septal defect patch were measured with the EAM tools. Besides, distance between VSD patch and pulmonary valve was measured. Measurements were correlated to inducibility. 

 

Results:

N=59 patients (n=25 male, mean age 39.9 ±15.0 years) are included. Underlying defect was DORV in n=5, pulmonary valve atresia in n=1, the rest were ToF patients. N=34 had at least one prior pulmonary valve replacement. EAM was performed 31.6±12.9 years after initial total correction. N=11 patients presented with documented sustained ventricular tachycardia (VT), n=48 patients received EAM due to risk factors (syncope, non-sustained VTs, etc.). 

EAM revealed slow conducting isthmuses between ventricular septum defect (VSD) patch and pulmonary valve in n=23 (39%) and were consecutively ablated, n=1 patient presented with VT in relation to a slow conducting isthmus between ventriculotomy and tricuspid valve and was successfully ablated. Right ventricular volumes were 192±57.8 ml, the transannular patch measured 12.6±11.1 cm2, the VSD patch 1.6±1.2 cm2. The most relevant isthmus between VSD patch and pulmonary valve measured 1.8±0.7 cm. A shorter isthmus between VSD patch and pulmonary valve and larger RV volumes tended to be prognostic for VT induction without reaching statistical significance. 

 

Conclusion:

As described earlier, the isthmus between VSD patch and pulmonary valve encounters for most of ventricular arrhythmias in ToF patients. In our cohort 39% presented with slow conduction in this area. A shorter distance between VSD patch and pulmonary valve and a higher RV volume tended to be prognostic for a higher VT risk. 

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