Ischemic ventricular tachycardia from below the posteromedial papillary muscle, a particular entity: Substrate characterization and challenges for catheter ablation.

BACKGROUND

In patients with ischemic ventricular tachycardia (VT), substrate may be "protected" by the posteromedial papillary muscle (PMPM), explaining failure of endocardial-only ablation.

OBJECTIVE

We sought to characterize the arrhythmogenic substrate and ablation approach in patients with ischemic VT mapped to the inferior left ventricle in which endocardial ablation failed because of inaccessible substrate underlying the PMPM.

METHODS

We included 10 patients with recurrent ischemic VT, evidence of inferior scar, and failed endocardial ablation. In all patients, epicardial mapping was performed via a percutaneous (n = 9) or surgical (n = 1) approach, and VT elimination was achieved by ablation opposite to the PMPM. Clinical characteristics, electrocardiographic characteristics, and procedural data were analyzed.

RESULTS

In all patients, intracardiac echocardiography showed hyperechoic scar below the PMPM, and 5 exhibited a pattern characterized by subendocardial basal scar that became intramural and epicardial at distal segments. In 4 patients, VT remained inducible despite endocardial scar isolation, manifested by the absence of electrograms, dissociated potentials, and/or exit block. Eleven inducible VTs were mapped to the epicardium underlying the PMPM: 8 had a right bundle branch block configuration with variable transition, while 3 exhibited left bundle branch block with negative concordance. An inferior QS pattern was present in 10 of 11 VTs. Noninducibility was achieved in 8 patients, and 7 patients remained arrhythmia-free after a mean follow-up of 27 ± 23 months.

CONCLUSION

In patients with inferior ischemic scar, VT may arise from the area underneath the PMPM, limiting endocardial ablation. Intracardiac echocardiography accurately defines the substrate distribution, and an epicardial approach may eliminate VT. A pattern of "basal-endocardial/apical-epicardial" ischemic involvement is described.