The link in Linking.

We present 2 cases of the slow-fast form of AVNRT with initially narrow QRS complexes followed by sudden unexpected transition to persistently wide QRS complexes due to aberrant intraventricular conduction. Introduction of a properly timed extrastimulus in one case and critical oscillations in cycle length due to short-long coupling in the second case set the stage for the initial bundle branch block. However, persistence of the aberrancy pattern once the initial event abated was maintained by the "linking" phenomenon. Delayed, retrograde concealed activation from the contralateral bundle branch perpetuated the initial bundle branch block.

another 2:1 sequence, one to one conduction is initiated with firstly narrow followed by persistent left bundle branch block (LBBB). What is the mechanism of LBBB?

Commentary
In both cases typical narrow complex AVNRT transforms into persistent BBB morphology following an ipsilateral BBB beat.
In case 1, the premature RV depolarization retrogradely activated the right bundle as demonstrated by the earlier retrograde His bundle activation (arrow). This premature activation of the right bundle branch (Figure 1B), with a short-long sequence produced a prolongation of the right bundle refractoriness [1] with the result that the next QRS shows an incomplete right bundle branch block. After that, block in the RBB is perpetuated by repeated retrograde invasion by the impulses coming from the left bundle, the so called "linking phenomenon" [2][3]. In this concept, it is the delayed retrograde activation of the bundle that extends its refractory period and thus perpetuates the antegrade bundle block. This has been demonstrated in accessory A-V pathways [4].
In case 2, during the 2:1 AV conduction a premature beat with a RBBB pattern occurs which is most likely due to aberrant conduction in the RBB (with a long HV interval indicating slow conduction in the other bundle). Right bundle branch block is the most frequently observed aberrancy in premature supraventricular beats [1] and the beat fulfils the Ashman phenomenon "long-short coupling interval" rule of aberrancy [2]. With this in mind, one can assume that the LBB is activated first by this premature beat, but what is occurring at the same instance in the RBB? If the impulse completely fails to depolarize the RBB, and there was no "concealed" retrograde invasion of the RBB, the subsequent diastolic interval of the RBB will be prolonged, thus prolonging its action potential, its refractoriness and facilitating RBB aberrancy when 1:1 AV conduction occurs. However, this is not the case, as the 1:1 conduction has LBBB aberrancy. This implies that the RBB has been invaded retrogradely by the "premature" impulse via antegrade activation of the LBB ("linking"). Thus the RBB's next diastolic interval would be shorter than that of the LBB, promote a shorter refractory period and thus permit conduction via the RBB whilst block would occur in the still refractory LBB (i.e. LBBB aberrancy). By comparison, the cycle length sequence experienced by the LBB would be (i) "short" in the premature LBB beat (ii) "long" between the premature LBB beat and the subsequent SVT beat, and then (iii) "short" in the second beat of the 1:1 AV conduction run. This sequence of "short-long-short" cycle lengths, previously described by Denker et al1 and termed the "Akhtar phenomenon" by Rosenbaum et al [3], explains the mechanism of LBBB aberrancy that was then perpetuated by a "linking" mechanism.
In summary, these cases demonstrate that different initial events can give rise to functional bundle branch block during AVNRT. In one case, a properly applied ventricular extrastimulus preexcited one bundle branch that subsequently blocked antegradely, while in the other case oscillations in cycle length with short-long sequence gave rise to the first QRS with bundle branch block. However, perpetuation of block was not due to the initial event, but rather was secondary to active interaction with the contralateral bundle branch, such that concealed, delayed retrograde activation from the contralateral bundle branch acted to maintain the functional antegrade block; a phenomenon known as "linking" phenomenon [2][3][4].