br Discussion We describe an additional diagnosis to

Discussion We describe an additional diagnosis to consider when BVT is identified. One of the proposed mechanisms of BVT include elevated intracellular calcium, causing delay after depolarization in anatomically separate parts of the conducting system. Baher et al. [1] proposed that two separate foci, with different rate thresholds for delayed after depolarization–induced ventricular bigeminy, were present in a rabbit model. When the ventricular rate exceeded the lower threshold, bigeminy would develop. This would effectively double the retinoic acid receptor rate, increasing the overall ventricular rate above the second threshold. Once this had developed, the two competing sites would simply alternate on a beat-to-beat basis. This is likely the mechanism underlying BVT observed with digitalis toxicity and catecholaminergic polymorphic VT. The other proposed mechanisms for BVT include an alternating bundle branch block related to bifocal automaticity and inscribed in opposite directions, or scar-mediated reentry around a circuit with two alternating exit sites. This latter is likely the underlying mechanism in our case. More recently, Sung et al. described a mechanism including retrograde conduction over the mid septal fascicular pathway, with alternating block in the left anterior or posterior fascicles, to explain polymorphic fascicular VT patterns [2]. Cardiac sarcoidosis causes ventricular inflammation and scarring due to focal non-caseating granulomas. Scarring is typically patchy, with a predilection for the basal septum, anterior wall, and perivalvular regions of the left ventricle. It may also be confluent, affecting the right ventricular epicardium or endocardium. In sarcoidosis, it is plausible that multiform or bidirectional premature ventricular contractions (PVCs) are due to multiple exits from the areas of inflammation and/or scarring. Conduction disturbances in cardiac sarcoidosis are not uncommon, and often affect the His-Purkinje system [3]. In our case, the patient had an intraventricular conduction delay at baseline, with prolonged QRS complexes at relatively low atrial rates (Fig. 1A). The majority of the retrospective data suggest that immunosuppression reduces the burden of arrhythmias, especially in the early phases of the disease [4]. Previous case series have reported various success rates with VT ablation in patients with cardiac sarcoidosis, likely due to the small number of patients in each series, with varying degrees of disease burden. The most common circuit for VT in one report was reentry in the peritricuspid area, which can be safely ablated [5]. In another study, abolishing all inducible tachycardias was not always feasible because of septal intramural circuits, extensive right ventricular scarring, or sites of origin in close proximity to the left anterior descending, the ramus intermedius arteries, or the para-Hisian region, which prohibit safe ablation [6]. In the current case, it is likely that the presence of a septal focus leads to alternate exits into the right or left ventricle which shows the observed electrocardiogram pattern. Although the septal involvement was not visible by imaging until a year after diagnosis, it might have been present initially, but was microscopic in nature. This is consistent with previous autopsy studies that have shown a heterogeneous distribution of sarcoid granulomas in the myocardium [7]. The recent expert consensus document is an excellent resource for management and risk stratification for cardiac sarcoidosis patients [8]. ICD implantation for primary prevention is commonly performed due to the high burden of VT events (estimated incidence rate of 15% per year) in patients with cardiac sarcoidosis [9]. In the current case, ICD implantation was recommended due to the high burden of nonsustained VT episodes, left and right ventricular dysfunction, and the presence of fibrosis and active inflammation by imaging studies.
Conflict of interest
Case report