• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • However the patient was later


    However, the patient was later re-admitted with frequent palpitation symptoms similar to those exhibited prior to the initial RFCA. Despite oral class I antiarrhythmic drug and beta-blocker treatment, ECG revealed incessant ATs and symptomatic AF (Fig. 2), so repeat RFCA was performed. Intravenous bolus infusion of ATP did not produce dormant electrical reconduction in either the left or right PVs, but incessant AF/ATs were induced. The earliest atrial activation site initiating incessant AF/ATs was consistently observed from the electrodes placed between the superior vena cava (SVC) and the upper right atrium, which was the location identical to that observed in the initial procedure. To identify the precise ectopic origin, a circular multielectrode-mapping catheter was positioned superior to the atriocaval junction within the SVC based on venography. During repetitive ATs, the activation recorded from the mapping catheter was consistently the earliest, and AT was diagnosed as being triggered by a non-PV focus within the SVC (Fig. 3). Electric isolation of the SVC was therefore performed (Fig. 4), after which AF/ATs were no longer inducible. Only dissociated potentials from the mapping catheter in the SVC were observed, despite repeated ATP bolus injections with and without concomitant ISP infusion. The patient did not exhibit any AF/ATs during a follow-up period of approximately 6 months.
    Discussion Adenosine is known to hyperpolarize atria cells via activation of the A1 adenosine receptor-mediated inwardly rectifying potassium currents (IKAdo), which shorten the bosentan duration (APD) and the effective refractory period [9]. While established, the mechanisms behind the association of these ionic interactions, adenosine-induced PV (and/or non-PV) trigger activation, and clinical AF remain unclear. Several reports have indicated that adenosine (in the form of ATP) can generate autonomic activation of PV triggers. Cheung et al. [10] presumed that adenosine-induced PV triggers were in part elicited by activation of parasympathetic triggers because adenosine and acetylcholine (ACh), both of which are parasympathetic neurotransmitters with cardiac stimulatory actions, act on identical cell signaling pathways to produce significant antiadrenergic effects [11]. Adenosine and ACh share similar G-protein receptor-effector coupling systems (class A18 rhodopsin-like; adenosine interacts with the A1 receptor, and ACh with muscarinic [M2] receptor). Activation of these systems generates the outward potassium currents IKAdo and M2 receptor-mediated inwardly rectifying potassium currents, respectively, resulting in hyperpolarization of the cardiac cell membrane and shortening of the atrial APD and refractory period. Such ionic interactions would provide a favorable substrate for atrial arrhythmogenic activities such as AF/ATs. With respect to ACh, several reports have described the relevance between the ACh-mediated cholinergic effect, which stimulates the intrinsic cardiac autonomic nervous system (ICANS), and PV and/or non-PV triggers. In dogs, administration of ACh into the ganglionated plexi (GP) fat pad, a major ICANS situated at the PV–LA junction, induced spontaneous PV triggers and AF [12]. In addition, Lu et al. [13] demonstrated that the hyperactivity of the SVC-aorta-GP axis, another major ICANS, induced by direct injection of ACh could lead to rapid firing from the SVC. Under the existence of both efferent parasympathetic and sympathetic neurons in the GPs, stimulation of these major ICANSs would sympathetically produce a high cytosolic Ca2+ enhanced by calcium transients and parasympathetically induce APD shortening. Subsequently, enhanced intracellular Ca2+ accumulation occurs at membrane voltages negative to the equilibrium potential for the sodium–calcium exchanger (NCX) due to enhanced repolarization, which acts as its forward mode resulting in an inward current, leading to generation of an early after depolarization (EAD), and re-excitation of the myocardium, causing PV and/or non-PV firing [14].