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  • br Discussion Compared to the right ventricular

    2019-04-26


    Discussion Compared to the right ventricular outflow tract, the LVOT has a more complicated anatomic structure, comprising the mitral annulus, aortic cusps, and LV basal myocardium. The AMC bridges the aortic and mitral valves with fibrous tissue, called the left fibrous trigone [3], and the extent of the fibrous tissue varies. A remnant of the atrioventricular conduction system (the “dead-end pathway”) was reported to be closely located, or even reaching, the AMC in some autopsied neonates or infants [4]. Particularly in the present case, the PP persists after the disappearance of the VA. A Purkinje fiber network may be present in the AMC that phosphodiesterase inhibitors forms a dead-end pathway. The AMC could serve as an independent arrhythmogenic substrate like focal Purkinje VT or verapamil-sensitive VT. Because we did not show response of the PP and VPC to the drug challenge test with adenosine, we could not tell what the PP really was. However, to our knowledge, no clear pathological or anatomical evidence demonstrates that the Purkinje fiber network forms a dead-end pathway in the AMC. Kurosawa et al. [3] described the direct continuation of the conduction axis itself, not referring the Purkinje fibers. In the present report, we demonstrated region of elongation the depolarization of the AMC was exceptionally directed by the upper conduction system based on the finding after successful RFCA. We speculated that the PP is a depolarization of the “dead-end” of the conduction axis continued from the AV node. The unique feature of the qrS pattern of the unipolar recordings would be formed by the depolarization of the focus deep inside the myocardium that propagated away from the catheter tip (“q”) and simultaneously toward the tip (“r”), and the depolarization of the endocardium, showing a deep S-wave. The r-S interval suggested a preferential pathway between the VA focus and the endocardial exit. Furthermore, the consecutive PP–PP intervals were consistent with the intervals of the preceding consecutive sinus rhythm, suggesting that depolarization of the VA focus depended on the sinus rhythm. We speculated that the AMC might provide a “missing” link to the conduction system. With an increased sinus rate, both the His-Purkinje and His-AMC axes can be activated. Non-sustained VT or frequent VPCs might be the result of an increased input frequency into the His-AMC conduction axis, manifesting as a non-reentrant mechanism [1].
    Conflict of interest