Left septal fascicular block

INTRODUCTION — Left septal fascicular block (LSFB; also called left middle or left median fascicular block) results when one of the earliest phases of normal electrical activity in the His-Purkinje system is delayed or interrupted (figure 1). Since the normal sequence of activation is altered in LSFB, it may be associated with alteration in the electrocardiogram (ECG). This form of block is one of the causes of a "counterclockwise rotation" pattern (early R wave transition) in the precordial leads and is quite variable, sometimes associated with a loss, not a gain, of anterior forces (waveform 1). This variability has contributed to some of the controversies and unresolved issues regarding LSFB. (See 'Electrocardiographic findings' below.)

The anatomy, clinical manifestations, differential diagnosis, prognostic implications, and treatment of LSFB will be reviewed here. In the discussion that follows, it is assumed that the reader understands the general concepts of cardiac vectors, asynchronous activation of the ventricles (delayed as in fascicular or bundle branch block or early as in preexcitation), and the effects that asynchrony has on the duration, morphology, and amplitude of the QRS complex. (See "ECG tutorial: Physiology of the conduction system" and "General principles of asynchronous activation and preexcitation".)

ANATOMY AND ELECTROPHYSIOLOGY

Anatomy — The bundle of His divides at the juncture of the fibrous and muscular boundaries of the interventricular septum into the right and left bundle branches. The main left bundle branch penetrates the membranous portion of the interventricular septum under the aortic ring and then divides into several fairly discrete branches (figure 1) [1]. There is a large amount of individual variability in the size and distribution of the left fascicles [2]. However, in most patients, there are two main fascicles:

●The left anterior fascicle that crosses the left ventricular outflow tract and terminates in the Purkinje system of the anterolateral wall of the left ventricle.

●The left posterior fascicle that fans out extensively inferiorly and posteriorly into Purkinje fibers.

●In up to 65 percent of hearts, a left septal fascicle (also called left middle or left median fascicle) to the interventricular septum. This has been reported in nearly 65 percent of people and can arise from the common left bundle or from the anterior, posterior, or both fascicles. The anatomy of the septal fascicle, when found, is more variable than the other fascicles, with a large number of interconnections [2,3].

Support for the trifascicular nature of the left bundle comes from the observation in animals and humans that depolarization of the left ventricle begins in three areas corresponding to the terminal portions of the anterior, posterior, and septal fascicles [4,5]. In the normal heart, the three fascicles of the left bundle are simultaneously depolarized. Further evidence of simultaneous activation of the fascicles can be found with routine electroanatomic mapping of a structurally normal heart. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.)

Blood supply — The left anterior and septal fascicles are supplied either by septal branches of the left anterior descending (LAD) artery or by the atrioventricular (AV) nodal artery (figure 2). The proximal part of the left posterior fascicle is supplied by the artery to the AV node and, at times, by septal branches of the LAD artery. The distal portion has a dual blood supply from both anterior and posterior septal perforating arteries.

EPIDEMIOLOGY — ECG findings consistent with isolated LSFB are an extremely rare finding, particularly among otherwise healthy persons. There are only a few reported estimates of isolated LSFB. In a review of some 26,000 ECGs, criteria for LSFB were found in approximately 0.5 percent, a prevalence similar to left posterior fascicular block (between 0.1 and 0.6 percent) but less than left anterior fascicular block (between 1 and 2.5 percent) [6].

ETIOLOGY — A variety of underlying disorders may be responsible for LSFB, including ischemic or hypertensive heart disease, hypertrophic cardiomyopathy, and diabetes mellitus. LSFB can be induced by ischemia, fibrosis, or sclerodegenerative changes, which are generally associated with alterations in the other fascicles [2,7-10]. In addition, patients with no known structural heart disease can have transient LSFB with premature atrial ectopy [11]. Patients with prior catheter ablation of fascicular arrhythmias may also have LSFB as a consequence of the ablative treatment.

ELECTROCARDIOGRAPHIC FINDINGS — Similar but even more subtly than left anterior and posterior fascicular blocks, LSFB mainly affects the direction, but not the duration, of the QRS complex because the conduction disturbance primarily involves the early phases of activation (waveform 1). The major clinical implication of LSFB is that the ECG mimics the changes induced by a septal or posterior myocardial infarction. (See "Left anterior fascicular block" and "Left posterior fascicular block".)

Definition — A task force from the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society has defined the ECG features of left anterior and posterior fascicular blocks. This document acknowledges the lack of universally accepted criteria for LSFB, and therefore this condition was not electrocardiographically defined by this group [12]. In a separate consensus report, LSFB was specifically addressed with recognition of a lack of true universal ECG criteria [13]. There are several proposed ECG criteria including the loss of a septal q wave with an R pattern in leads V5 and V6 and the presence of an RS pattern in V1 to V2 indicating a gain in prominent anterior forces. However, because there are other conditions that can result in these ECG patterns, the consensus document is in agreement with the aforementioned task force conclusions.

ECG activation patterns — Myocardial activation may be affected in two ways by a conduction disturbance in the left septal fascicle: apparent loss or gain of anterior forces. In fact, the demonstration of these changes was one of the early observations suggesting the existence of a left septal fascicle. The ECG pattern seen with LSFB is probably determined by the differences in the sites of insertion of the septal, anterior, and posterior fascicles:

●Apparent gain of anterior forces with early precordial transition/counterclockwise rotation (CCWR) – In marked contrast, prominent R waves are seen in the right precordial leads when LSFB leads to a gain of anterior forces [8,14]. These changes are similar to those that occur in true posterior (dorsal) myocardial infarction. The prominence of the R waves may be increased when LSFB occurs in association with right bundle branch block.

The relationship between shift of the transitional zone on the standard 12-lead ECG and anatomic rotation of the heart in one plane was studied by cardiac computed tomography (CT) [15]. The left-sided angle between the interventricular septum and horizontal axis of the body (the septal angle) was determined on the cardiac CT. The mechanism of CCWR could be attributed to the septal angle in approximately two-thirds of the cases, but the remainder was thought to be due to LSFB.

In one description of transient LSFB occurring during proximal occlusion of the left anterior descending artery, an acute gain of anterior forces was observed along with preservation of septal q waves [16].

●Apparent loss of anterior forces – Functional or hyperkalemia-induced dysfunction in the left septal fascicle can lead to the loss of anterior forces, resulting in the transient development of q waves in leads V1 and V2, which normally have a positive initial deflection due to septal depolarization [17,18]. Similar changes occur with permanent LSFB and are indistinguishable from septal fibrosis or infarction.

EVALUATION, TREATMENT, AND FOLLOW-UP — Patients with an ECG raising consideration of isolated LSFB are generally asymptomatic and do not require further diagnostic evaluation or placement of a pacemaker or any other specific therapy. Therapy should be considered only in patients with persistent bifascicular or trifascicular block or in certain neuromuscular disorders. (See "Chronic bifascicular blocks".)

Any symptoms consistent with the development of cardiac disease (eg, coronary heart disease, heart failure, atrial fibrillation, etc) should immediately be evaluated.

PROGNOSIS — Similar to isolated left posterior fascicular block, isolated LSFB is very rare. Thus, unlike left anterior fascicular block, left bundle branch block, and right bundle branch block, there are no studies evaluating this ECG pattern with subsequent atrial fibrillation or other cardiovascular morbidity risk.

SUMMARY AND RECOMMENDATIONS

●Left septal fascicular block (LSFB; also called left middle or left median fascicular block), a pattern seen on the surface electrocardiogram (ECG), results when normal electrical activity in the His-Purkinje system is delayed or interrupted (figure 1). The normal sequence of activation is altered in LSFB, with a frequent counterclockwise rotation and a resultant appearance on the ECG that is variable, sometimes manifesting with a gain of anterior forces, but at other times with an apparent loss of anterior forces. (See 'Introduction' above.)

●Among experts and professional societies, there is an acknowledgment of the lack of universally accepted criteria for LSFB. Proposed ECG criteria include the loss of a septal q wave with an R pattern in lead V5 and V6 and presence of an RS pattern in V1 to V2 indicating a gain in anterior forces. However, there are other conditions that can result in these nonspecific ECG patterns. (See 'Electrocardiographic findings' above.)

●Isolated LSFB is an extremely rare finding, particularly among otherwise healthy persons. Criteria for LSFB have been reported only in approximately 0.5 percent of the general population. (See 'Epidemiology' above.)

●Patients with an ECG raising consideration of isolated LSFB are generally asymptomatic and do not require further diagnostic evaluation or placement of a pacemaker or other specific therapy. Any symptoms consistent with the development of cardiac disease (eg, coronary heart disease, heart failure, atrial fibrillation, etc) should immediately be evaluated. (See 'Evaluation, treatment, and follow-up' above.)