Ventricular tachycardia originating from the posteroseptal process of the left ventricle with inferior wall healed myocardial infarction.

Ventricular tachycardia (VT) substrates may form in preferential locations and similar electrocardiographic patterns may be observed when ventricular activation starts from a particular site. We examined the role of the posterior inferior process of the left ventricle in the mechanism of VT occurring after inferior wall myocardial infarction. We reviewed isochronal maps of 40 VTs obtained at surgery in 13 patients, with a 128-electrode system using epicardial sock and endocardial balloon electrode arrays. Based on the epicardial to left endocardial relation we observed 7 tachycardias in 7 patients with onset of activation over the crux of the heart. This activation mimicked excitation through a posteroseptal accessory pathway. Endocardial activation maps showed breakthroughs occurring 6 to 40 ms later and did not give evidence in favor of macroreentry. In all but 1 VT, left-axis deviation was present (-30 to -75 degrees) with a positive concordance from leads V2 to V6 (QRS wave patterns were variable in V1). These tachycardias, which were clinical in 3 of 7 cases, were interpreted as arising from the posterior inferior process of the left ventricle and successfully ablated by left septal and epicardial cryolesions. In another patient, this concept was further validated by percutaneous radiofrequency ablation of a tachycardia with the previously described morphology. In conclusion, VT may originate from the posteroseptal process of the left ventricle with inferior wall healed myocardial infarction. Because these tachycardias can be successfully eliminated, their characteristic morphologies may provide clinical markers for the identification of patient candidates to surgical or nonsurgical ablative therapy.