Background: Among patients (pts) with atrioventricular accessory pathway (AP), some cases show wide complex arrhythmias with different QRS morphology. In a subset of these pts, an atrioventricular reentrant tachycardia with left bundle branch block morphology (LBBBM-AVRT) is observed. The aim of this study is: 1) to identify the substrate and the reentrant mechanism underlying the LBBBM-AVRT in pts undergoing radiofrequency catheter ablation (RFCA) of AP; 2) to report the results achieved by RFCA of the identified substrate.
Methods: From May 1991 to April 1993, among the 168 pts who underwent RFCA for arrhythmias related to an AP, 12 (7.1%) (8M, 4F, mean age 35 +/- 21 yrs, range 8-65) showed LBBBM-AVRT, alone or associated with other arrhythmias. Pts, in whom LBBBM was rate-related during orthodromic AVRT, were excluded from this study. During sinus rhythm, QRS complex was normal in 1 pt, while ventricular preexcitation due to a right-sided Kent bundle (KB) was present in 4 pts; among the other pts without preexcitation, 3 showed left bundle branch block (LBBB) and 4 right bundle branch block. In 2 pts, an Ebstein disease was present, while dilated cardiomyopathy was observed in another. The LBBBM-AVRT was iterative in 3 pts and in 6 pts it was the only arrhythmia observed; the mean tachycardia cycle length was 341 +/- 49 msec (range 250-428). In 1 pt, the LBBBM-AVRT was induced only after successful RFCA of a right-sided AP, responsible for orthodromic AVRT. All pts underwent diagnostic electrophysiologic study and RFCA during the same session.
Results: In 6/12 pts one or more KBs were observed, while in the remaining 6 an atrioventricular or atriofascicular "Mahaim like" bundle (MB) was present; the patient population was divided into 4 groups on the basis of the substrate and the reentrant mechanism responsible for LBBBM-AVRT. In Group 1, 3 pts were included: the LBBBM-AVRT was an orthodromic AVRT involving the nodal conduction antegradely (showing LBBB also during sinus rhythm) and a left-sided unidirectional KB, retrogradely. In all the 3 pts, the LBBBM-AVRT was iterative and not controlled by antiarrhythmic agents and RFCA of the KB abolished the arrhythmia. Two further pts were included in Group 2: in these pts with multiple bilateral KBs, the LBBBM-AVRT involved a right-sided KB antegradely and a left-sided one, retrogradely. In these 2 pts both KBs were successfully ablated. In 1 pt, considered in Group 3, the LBBBM-AVRT was sustained by an antidromic circuit involving a right-sided KB antegradely and the nodal conduction retrogradely; in this pt the KB was completely interrupted after two RFCA procedures. The remaining 6 pts with MB were included in Group 4: at least one associated electrophysiologic abnormality was present in all (dual A-V nodal pathway in 4/6 and a right-sided KB in 4/6); Ebstein disease was also observed in 2 of them. In 4/6 pts the LBBBM-AVRT was an antidromic tachycardia involving the nodal conduction retrogradely and the MB antegradely; in 3/4 pts the MB was ablated (along with a nodal reentrant tachycardia in 1 pt), while in the remaining pt in whom the non-sustained LBBBM-AVRT, inducible only after RFCA of a right-sided KB, had not been clinically observed, no further ablation was mandatory. In the remaining 2 pts in Group 4, the LBBBM-AVRT was due to the involvement of MB in other arrhythmias such as an AVRT due to a right-sided KB and a "slow-slow" nodal reentrant tachycardia, respectively; the LBBBM-AVRT were abolished by RFCA of these two underlying arrhythmias. All pts are asymptomatic during a 7.9 +/- 6.9 months follow-up.
Conclusions: The LBBBM-AVRT is observed in a minority (7.1%) of the cases referred for RFCA of AP. (ABSTRACT TRUNCATED)