smad inhibitor br Commentary Recordings of the activation se

Commentary Recordings of the activation sequence from the CS during tachycardia are expected to help discriminate among atrial tachyarrhythmias [2]. During ongoing typical CCW AFL, most of the CS is activated from proximal to distal, because the CS musculature, by being continuous with the RA myocardium at the ostium and connected to the LA myocardium [3], is a major RA-to-LA connection [4–6]. However, several cases of typical CCW AFL with an atypical activation of the CS associated with changes in the morphology of FL waves have been described, probably because of changes in the interatrial connection caused by conduction block at the CS ostium [7–10], the mechanism of which remains unexplained. We recorded pacing from the ostium of CS in search of interatrial conduction along the CS. During pacing at a smad inhibitor length slightly longer than the AFL cycle length, the wavefront propagated in a proximal-to-distal CS activation sequence (Fig. 2), suggesting the presence of conduction across an interatrial electrical connection at the CS ostium. Moreover, during pacing at a cycle length close to that of AFL, the activation sequence became centrifugal and earliest at the mid CS (CS11–12), similar to that during AFL. Additionally, the interval between the pacing spike and the atrial deflection recorded at the bundle of His prolonged with an atypical Wenckebach periodicity, consistent with a spike-atrial conduction delay in the RA. The electrophysiological observations shown in Fig. 3 are explained as follows: (1) the wavefront of the S2- and S3-paced cycles passed through the ostium of the CS; (2) the S4-paced cycle was blocked because of refractoriness at the ostium of the CS (CS19–20 or more proximal), whereas another wavefront traveling in a caudal-to-cranial direction along the right-sided interatrial septum, returned via the Bachmann bundle, the interatrial septum, or both, in a cranial-to-caudal direction along the left-sided interatrial septum, reached the mid-CS (CS11–12), and finally encountered residual refractoriness at the CS ostium caused by the third paced RA-to-LA wavefront; (3) the S5-paced cycle was blocked at the ostium of the CS because of residual refractoriness caused by LA-to-RA concealed penetration from the S4-paced cycle; and (4) each new impulse was similarly blocked at the ostium of CS because of residual refractoriness from concealed penetration of the previous paced cycle (linking phenomenon) [11,12]. During captured pacing, the spike-atrial conductive properties represented atypical Wenckebach periodic conduction delay, followed by S10-atrial conduction block;(5) because of the cancellation of the linking phenomenon by the noncaptured S10 stimulus, the wavefront of the S11-paced cycle passed through the ostium of the CS again, although S12-, S13-, and S14 were similarly blocked at the ostium of the CS (not shown in Fig. 3). This pacing study suggests, therefore, that linking between dual conductive pathways of CS musculature and left atrial muscle was the mechanism responsible for the perpetuation of conduction block at the ostium of the CS. This may have diverted the activation wavefront from the right to the left atrium via alternate interatrial connections, such as Bachmann bundle, the interatrial septum, or both. A similar phenomenon may have occurred during ongoing AFL. The latency of the low RA conduction observed along the distal Halo catheter during ongoing AFL was consistent with the interval between atrial deflections at the ostium of the CS before encountering conduction block and that after bypassing the interatrial septum. If linking was not associated with the persistence of conduction block at the ostium of the CS, burst pacing might have induced 2:1 conduction block at that site, because of the all-or-none conduction properties of atrial muscle or CS musculature, similar to that of the atrioventricular accessory pathway. In addition, repetitive 1:1 phase 3 block at the ostium of the CS is unlikely, because of the frequency-dependent shortening of the action potential. To our knowledge, this is the first description of the linking phenomenon causing functional, repetitive conduction block over the CS musculature in humans. Transient changes in the interatrial conductivities induced by this phenomenon, like an on and off switch, might affect biatrial activation pattern in other atrial tachyarrhythmias [13].