INTRODUCTION: AV nodal reentrant tachycardia is routinely cured using radiofrequency catheter ablation techniques. However, there remains controversy as to whether the reentrant circuit for this tachycardia exists solely in the AV node or whether perinodal atrial tissues are vital to the circuit. In addition, the effects of radiofrequency ablation of the slow pathway of AV nodal reentrant tachycardia on the AV node are not known. We examined an autopsy specimen to determine the anatomical location and extent of AV nodal damage of radiofrequency slow pathway ablation for cure of AV nodal reentrant tachycardia. METHODS AND RESULTS: A 64-year-old woman with confirmed AV nodal reentrant tachycardia underwent a successful "slow pathway" AV modification with a single radiofrequency application. Five months after the procedure, the patient died from a spontaneous intracranial hemorrhage. Postmortem gross pathological examination of the heart was performed. The heart was then sectioned and stained for histologic examination. On gross examination, a pale lesion 0.5 cm in diameter was seen on the endocardial surface adjacent to the tricuspid annulus, approximately 0.85 cm anterior to the coronary sinus os and 1.15 cm from the apex of the triangle of Koch where the AV node resides. Histologic examination revealed a right atrial lesion composed of connective tissue and fat. The compact AV node and surrounding transitional cells were unaffected histologically, with normal atrial cells lying between the AV node and the lesion. CONCLUSION: Ablation of the slow pathway to cure AV nodal reentrant tachycardia does not produce any gross or histologic damage to the AV node, suggesting that the AV nodal reentrant circuit does not exist in its entirety in the AV node.
INTRODUCTION: AV nodal reentrant tachycardia is routinely cured using radiofrequency catheter ablation techniques. However, there remains controversy as to whether the reentrant circuit for this tachycardia exists solely in the AV node or whether perinodal atrial tissues are vital to the circuit. In addition, the effects of radiofrequency ablation of the slow pathway of AV nodal reentrant tachycardia on the AV node are not known. We examined an autopsy specimen to determine the anatomical location and extent of AV nodal damage of radiofrequency slow pathway ablation for cure of AV nodal reentrant tachycardia. METHODS AND RESULTS: A 64-year-old woman with confirmed AV nodal reentrant tachycardia underwent a successful "slow pathway" AV modification with a single radiofrequency application. Five months after the procedure, the patient died from a spontaneous intracranial hemorrhage. Postmortem gross pathological examination of the heart was performed. The heart was then sectioned and stained for histologic examination. On gross examination, a pale lesion 0.5 cm in diameter was seen on the endocardial surface adjacent to the tricuspid annulus, approximately 0.85 cm anterior to the coronary sinus os and 1.15 cm from the apex of the triangle of Koch where the AV node resides. Histologic examination revealed a right atrial lesion composed of connective tissue and fat. The compact AV node and surrounding transitional cells were unaffected histologically, with normal atrial cells lying between the AV node and the lesion. CONCLUSION: Ablation of the slow pathway to cure AV nodal reentrant tachycardia does not produce any gross or histologic damage to the AV node, suggesting that the AV nodal reentrant circuit does not exist in its entirety in the AV node.