Abstract 17158: Intraoperative Electroanatomical Mapping and Histopathological Examination Revealed Mechanism of Monomorphic Ventricular Tachycardia associated with Primary Cardiac Tumor
Introduction: Ventricular tachycardia (VT) associated with a primary cardiac tumor is extremely rare. Complete resection of a tumor was reported to be effective in a treatment of this VT. However, the mechanism of the cardiac tumor-related VT (CT-VT) is still unknown, and the therapeutic strategy of the VT in patients with unresectable tumor is not determined.
Methods and Results: Four patients (20 ± 15 years, 3 males) with CT-VT (fibroma in 2, lipoma in 1, and hemangioma in 1 patient) were investigated. All four patients developed repetitive forms of monomorphic VTs, which were reproducibly induced by programmed ventricular stimulation and terminated by burst pacing. These VTs exhibited a right bundle branch block QRS morphology (QRS duration, 160 ± 28 ms) with a pseudo-delta wave (75 ± 10 ms) at a cycle length of 330 ± 86 ms. Intraoperative electroanatomical mapping showed a radially spreading activation pattern originating from the epicardial border of the tumor, where fractionated and late potentials were detected during sinus rhythm. Histopathological studies of the sections from this border area revealed tumor infiltration to the surrounding myocardium and myocardial cell disorganization exhibiting myocardial disarray. In 2 patients in whom the cardiac tumor was completely resected, cryoablation was added to the resection line. In the remaining 2 patients in whom complete resection of the tumor was unfeasible, encircling cryoablation to entirely isolate the unresectable tumor was effective in suppressing their VTs.
Conclusions: The mechanism of CT-VT is reentry localized at the epicardial border of the tumor. Myocardial disarray associated with infiltration of the cardiac tumor may be a substrate of this VT. Encircling cryoablation along the border of the tumor may be a therapeutic option for an unresectable CT-VT.
Author Disclosures: H. Murata: None. Y. Miyauchi: None. T. Nitta: None. K. Takahashi: None. I. Tsuboi: None. H. Hayashi: None. S. Uetake: None. K. Yodogawa: None. Y. Iwasaki: None. M. Hayashi: None. S. Sakamoto: None. S. Kunugi: None. W. Shimizu: None.
- © 2014 by American Heart Association, Inc.