P357Epicardial abnormal electrical activity in unselected patients with ischemic ventricular tachycardia: a pilot mapping study

Background radiofrequency catheter ablation (RFA) on the endocardial ventricular surface is widely used for post-myocardial infarction (post-MI) ventricular tachycardia (VT) treatment. It has been described that about 10% of patients with post-MI require additional epicardial ablation for successful VT termination. However, there is still lack of data regarding the extent of scarring and the presence of local abnormal ventricular electrical activity (LAVA, low-voltage and/or fractionated signals) on the epicardial surface in patients with ischemic VT. Purpose to assess the extent of epicardial electrophysiological substrate in patients with remote myocardial infarction and indications for VT ablation. Methods thirteen out of 59 patients with sustained ischemic VT (12 men; mean age 59,9 ± 9,5) and without previous cardiac surgery signed an informed consent to undergo epicardial mapping and comprized the study population. Endocardial access was used previously as primary method in 4 patients ICD/ CRT-D had been previously implanted in 11 patients: mean left ventricle ejection fraction was 38,8 ± 10,6 %: hemodynamically unstable VT was present in 10 patients; the most frequent scar localization by ECG and transthoracic echocardiography – left ventricle (LV) inferior wall (10 patients), LV lateral wall – (7 patients). All patients underwent full clinical evaluation. Electrophysiological procedure and catheter ablation was performed under general anesthesia. Epicardial access was obtained through percutaneous subxyphoid puncture. Voltage mapping of endocardial and epicardial surfaces was performed. Maps were evaluated for the presence of LAVA. Ablation was performed at sites of LAVA on either side of the ventricular wall. Results epicardial access was successful in 12 patients. Bi- and unipolar mapping was successfully performed and analyzed in 11 subjects. LAVA was present in all but one patient on endocardial surface and in 9 (82%) out of 12 patients on epicardial surface. Localization of endocardial and epicardial LAVA coincided in 8 (67%) patients suggesting transmural ischemic scar. One patient had only epicardial scar, 1 patient had septal endocardial scar without LAVA on the epicardial surface. In one patient LAVA sites were localized on different left ventricle walls. More extensive unipolar than bipolar endocardial scar area was found (11,8 (IQR:2,0;31,6) vs 45,8 (IQR:17,1;86,5) сm2; р=0,03). Epicardial unipolar scar area prevailed over bipolar scar area: median 46.0 cm2 (IQR: 15.9;55.5) vs 107.7 cm2 (IQR: 84.3;168.9) р=0,04. LAVA epicardial area was wider than endocardial: 19.7 cm2 (IQR: 2.3; 29.7) vs 4.1 cm2 (IQR: 0.4; 23.8) р=0.03. Conclusion according to the results of our pilot study in unselected patients with ischemic VT, epicardial arrhythmogenic substrate was detected in 82% of cases. Epicardial LAVA area significantly prevailed over endocardial LAVA area.