Idiopathic focal epicardial ventricular tachycardia originating from the crux of the heart

Background Idiopathic ventricular tachycardia (VT) can arise from the epicardium, usually near the summit of the left ventricle (LV). Objective The purpose of this study was to describe a distinct syndrome of epicardial VT that arises from the crux of the heart. Methods Among 340 patients with idiopathic VT referred for ablation, four were identified with VT that was mapped to the epicardium at the crux. Results VT was sustained in all patients and was associated with syncope or presyncope in three. Rapid VT (mean cycle length 264 ms) was induced with programmed stimulation or burst pacing from the ventricle but required isoproterenol infusion in three. ECG during VT demonstrated a left superior axis QRS morphology with a precordial maximal deflection index ≥0.55 in all patients (mean 0.61). Intracardiac mapping revealed earliest activation in the middle cardiac vein or proximal coronary sinus at the crux in all patients. Irrigated radiofrequency ablation in the middle cardiac vein or proximal coronary sinus was attempted in all patients and successfully abolished VT in one. Percutaneous epicardial radiofrequency ablation was attempted in 2 of 3 remaining patients and successfully abolished VT in both. Simultaneous coronary angiography demonstrated the site of earliest activation within 5 to 10 mm of the proximal posterior descending coronary artery, with no acute narrowing of that artery following ablation. Conclusion Idiopathic VT may arise by a focal mechanism from the epicardium at the crux in close proximity to the posterior descending coronary artery. This syndrome can result in rapid, catecholamine-sensitive VT and requires careful attention to the posterior descending coronary artery during ablation. Idiopathic ventricular tachycardia (VT) can arise from the epicardium, usually near the summit of the left ventricle (LV). The purpose of this study was to describe a distinct syndrome of epicardial VT that arises from the crux of the heart. Among 340 patients with idiopathic VT referred for ablation, four were identified with VT that was mapped to the epicardium at the crux. VT was sustained in all patients and was associated with syncope or presyncope in three. Rapid VT (mean cycle length 264 ms) was induced with programmed stimulation or burst pacing from the ventricle but required isoproterenol infusion in three. ECG during VT demonstrated a left superior axis QRS morphology with a precordial maximal deflection index ≥0.55 in all patients (mean 0.61). Intracardiac mapping revealed earliest activation in the middle cardiac vein or proximal coronary sinus at the crux in all patients. Irrigated radiofrequency ablation in the middle cardiac vein or proximal coronary sinus was attempted in all patients and successfully abolished VT in one. Percutaneous epicardial radiofrequency ablation was attempted in 2 of 3 remaining patients and successfully abolished VT in both. Simultaneous coronary angiography demonstrated the site of earliest activation within 5 to 10 mm of the proximal posterior descending coronary artery, with no acute narrowing of that artery following ablation. Idiopathic VT may arise by a focal mechanism from the epicardium at the crux in close proximity to the posterior descending coronary artery. This syndrome can result in rapid, catecholamine-sensitive VT and requires careful attention to the posterior descending coronary artery during ablation.