Atrial fibrillation is a common arrhythmia in Wollf-Parkinson-White (WPW) syndrome and the QRS complex during atrial fibrillation (Af) is usually wide due to delta wave. In the patient with WPW syndrome described here, the QRS complex was wide during normal sinus rhythm (NSR) and was normal during Af.
case report
A 40-year-old businessman complained of a ten-year history of occasional bouts of palpitation.
No abnormalities were detected on physical examination.
The chest X-ray and laboratory data were wi thin normal limits. The 12-lead electrocardiogram during Af showed normal QRS complexes (0.08 sec.) but during NSR. (79 beats/min.) QRS complexes (0.13 sec.) were wide with delta wave and P-R interval of 0.09 sec. which was typical typical type B WPW syndrome.
His bundle electrogram sho wed H-V interval of 50.0 msec. during Af. During NSR A-H interval was 86.2 msec and H-V interval 39.6 msec. Right atrial pacing with progressive reduction in the cycle length resulted in A-H prolongation. H deflection was buried in V deflection at a pacing rate of 128.4/min. and 3: 1 or 4: 1 A-V block occured at 167.8/min.
The atria were stimulated with the basic cycle length of 810.8 msec. LBBB like p attern occured at A1-A2 intervals of 410.0 msec. H deflection was buried in V defletion at 370.0msec and QRS was normalized at 325.0 msec. An effective refractory period (ERP) of accessory pathway (AP) and AV node was 353.0 and less than 315 msec., respectively.
AV-A conduction time during ventricular pacing remained constant.
A reciprocating tachycardia could not be induced during the electrophysiological study.
comment
Conduction of the Af impulses to the ventricules occures through normal conduction pathways and/or AP. In most cases A-V conduction occures through AP and QRS complexes are wide with delta wave. The QRS complex is entirely normal when A-V conduction occurs only through normal conduction pathways. However this phenomenon is very rare and only few cases have been reported. Although 'the mechanism is not fully understood, it may be partly explained by: 1) ERPAP>ERPAV node 2) retrograde concealede conduction to AP were postulated. There are several other possible mechanisms. Due to various direction, rhythm or strength of fibrillation impulse, the fibrillation impulses: 1) cannot input into the AP; 2) are blocked within the AP and 3) cannot stimulate the large ventricular muscles (mismatch impedance). However, more studies are required to corroborate them.
