Correspondence and reprint request:
Mahdi Moeini, Department of Cardiac electrophysiology, Rajaie Cardiovascular Medical and Research Center, Vali-Asr St., Ayatollah Hashemi-Rafsanjani Blvd, Tehran, 1996911151 Iran
Tel: +98 21 2392 3822
Fax: +98 21 2392 2340
Abstract
A 34 years old man with refractory symptoms and unresponsive to antiarrhythmic drug therapy referred to our center. Electrophysiological study and diagnostic maneuvers confirmed the diagnosis of orthodromic reciprocating atrioventricular tachycardia using a slowly and decrementally conducting AP as orthodromic arm and slow AV nodal pathway as antidromic arm. AP was successfully ablated radiofrequency application through retrograde approach at Aorto- mitral continuity. The response of this arrhythmia to diagnostic maneuvers at an unusual location of AP offers insight to electrophysiological properties of this type of accessory pathways.
Introduction
Slowly and decrementally conducting accessory pathways (Aps) responsible for induction of a specific type of reciprocating reentrant tachycardia called permanent junctional reciprocating tachycardia (PJRT).(1) PJRT often in the form of incessant tachycardia more commonly seen in early ages. The tachycardia is characterized by a narrow QRS rhythm with variable rates, a retrograde P wave axis, and an RP interval that is longer than the PR interval. In many patients, PJRT is fairly difficult to control medically. Catheter ablation has now become as a highly effective technique for eliminating these accessory pathways with minimal risk of AV block (2). Although the anatomic origin in majority of cases are localized to posteroseptal area but few cases with uncommon location has been reported. In this report we introduce an uncommon location with electrophysiological properties at Aorto-Mitral continuity.
Case presentation
A 34 years old man with history of frequent palpitations refractory to drug therapy referred to our center. He had documented tracing of a narrow QRS tachycardia terminated after Adenosine injection. Clinical examination, chest x -Ray and echocardiography revealed no abnormality.
Patient brought to electrophysiology Lab after obtaining formal consent, in sinus rhythm. Procedure was performed under conscious sedation. Antiarrhythmic drugs were withdrawn five days before procedure.
Three standard quadripolar and decapolar diagnostic catheters were introduced through left and right femoral veins and placed in right atrium (HRA), right ventricle (RV) and coronary sinus (CS) positions. His bundle (HB) potential was recorded using mapping catheter. Twelve lead ECG during sinus rhythm showed normal PR interval with no manifest pre-excitation. The basic parameters of AH and HV interval were 85msec and 49msec, respectively. There was the evidence of dual AV node physiology manifested as atrioventricular (AV) nodal jump. A narrow complex tachycardia with long RP-short PR could be initiated after extarstimulation from HRA following an AV nodal jump. The earliest retrograde atrial activation during tachycardia was recorded from His bundle position. RV apical pacing showed decremental with earliest atrial activation at the His area, although no fused V-A potential was recorded in either CS or His position. Notably, we were able to induce the arrhythmia with RV apical extrastimulation.
Diagnostic maneuvers were performed. His synchronous pacing from RV apex failed to advance or reset the arrhythmia on multiple attempts. However, Morady maneuver by RV overdrive pacing repeatedly terminated the tachycardia.