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Antiarrhythmic drugs were withdrawn five days before procedure.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.