Fascicular Ventricular Arrhythmias

Ventricular arrhythmias involving the fascicular system may be seen in both structurally normal and abnormal hearts. Idiopathic fascicular ventricular tachycardia represents almost 10% to 15% of idiopathic ventricular tachycardia related to the left ventricle. Cohen et al and subsequently Zipes et al first described these arrhythmias in the 1970s as relatively narrow right bundle left axis arrhythmias that arose close to the posterior fascicle and could be induced with atrial pacing. Belhassen et al later described the responsiveness of these arrhythmias to verapamil. Although initial studies focused on arrhythmias related to the left posterior fascicle, it is possible for arrhythmias to arise from any portion of the fascicular system and in both structurally normal and abnormal hearts. Furthermore, when approaching the patient presenting with arrhythmias arising from the His-Purkinje system, it is important to consider the unique complexities related to mapping and ablation. In this review, we will focus on the mechanisms of such arrhythmias, relevant embryology, anatomy and physiology, and approaches to management in both the presence and absence of other structural heart disease. Broadly, fascicular ventricular tachycardia in the absence of other structural heart disease will be termed idiopathic fascicular ventricular tachycardia (IFVT), whereas that related to structural disease will be discussed in the context of the relevant disease state. Generally, IFVT is separated into 3 types—left posterior fascicular with a right bundle branch block pattern and left axis deviation, left anterior with a right bundle branch block and right axis deviation pattern, and left upper septal fascicular with a narrow QRS and normal axis but often with a right bundle branch block morphology. There are rare reported cases of left bundle branch block pattern, V 3 –V 4 transition IFVT with a normal axis arising from the right bundle branch. In addition, we will touch on other Purkinjeand fascicular-related arrhythmias because they relate in diagnosis and mapping to IFVT. However, by far, the most common form of IFVT is the posterior fascicular type (≈90% of cases) (Table 1). We will exclude consideration of premature ventricular contraction– triggered ventricular fibrillation that may similarly involve abnormalities in the His-Purkinje system from this review. Electrophysiological and Anatomical Characteristics In ablation of fascicular ventricular arrhythmias, an understanding of the normal anatomical course of the fascicles is critical. However, variation in the anatomical course is common. In the normal human heart, the penetrating bundle of His arises from the atrioventricular node and runs in the central fibrous body as a cord-like structure, typically dividing into the left and right bundles at the junction of the membranous septum and the crest of the muscular interventricular septum. The right bundle then arises at an obtuse angle with the distal third of the right bundle being more superficial and coursing to the right ventricular free wall in the moderator band. The left bundle tends to be broader than the right bundle and emerges just beneath the noncoronary cusp of the aortic valve, giving rise to a thinner anterior fascicle and broader posterior fascicle. Almost 60% of people may also have a third fascicle termed the left septal, upper, or median fascicle. The left bundle anatomy can exhibit considerable variation in the normal human heart with potential for significant cross-linking between fascicles and variability in the width, length, and degree of arborization (Figure 1). The fascicular system ultimately terminates in a mesh-like Purkinje network. The Purkinje fibers vary in density throughout the heart, largely seen around the papillary muscles and midventricle, and less so at the base of the heart. Furthermore, they can penetrate as deep as a third of the myocardial thickness. Functionally, the electrophysiological tendency for the fascicular–Purkinje system to participate in tachycardia may be because of the unique physiology that allows the system to overcome source–sink mismatch. On the basis of all existing data, electrical propagation from Purkinje to ventricular myocyte depends on direct charge transfer. Thus, transmission at the Purkinje–myocyte junction always has the potential to be bidirectional (ie, anterograde and retrograde). In fact, given the larger ventricular mass, the potential for retrograde activation may actually be higher than anterograde activation. This has been demonstrated by work done by Joyner et al. One