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.
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.
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.
The LBBBM-AVRT is observed in a minority (7.1%) of the cases referred for RFCA of AP. (ABSTRACT TRUNCATED)