Left posterior fascicular block

INTRODUCTION — Left posterior fascicular block (LPFB), a pattern (formerly called left posterior hemiblock) 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 LPFB, with a resultant characteristic appearance on the ECG, associated with marked right axis deviation (waveform 1).

The anatomy, clinical manifestations, differential diagnosis, prognostic implications, and treatment of LPFB will be reviewed here. Additional details regarding the ECG manifestations of LPFB are discussed separately. (See "ECG tutorial: Intraventricular block", section on 'Left anterior fascicular block'.)

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 pre-excitation), 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.

●A left median (also called medial or septal) fascicle to the interventricular septum is found in nearly 65 percent of people and can arise from the common left bundle or from the anterior, posterior, or both fascicles.

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 [3,4]. 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 proximal part of the left posterior fascicle is supplied by the artery to the atrioventricular (AV) node and, at times, by septal branches of the left anterior descending (LAD) artery (figure 2). The distal portion has a dual blood supply from both anterior and posterior septal perforating arteries. The left anterior and median fascicles are supplied either by septal branches of the LAD or by the AV nodal artery.

EPIDEMIOLOGY — Isolated LPFB is a rare finding, particularly among otherwise healthy persons, with estimates of its prevalence ranging from 0.1 to 0.6 percent [5,6].

●In a cohort study involving 358,958 primary care patients, 0.8 percent presented with isolated LPFB [7].

●Among a cohort of 6416 people participating in a Finnish public health study, only eight persons (0.12 percent) were identified with isolated LPFB [5].

●In a study of 2254 patients with heart failure, only 14 (0.6 percent) had isolated LPFB [8].

●Among a cohort of 2160 patients with acute myocardial infarction, the prevalence of LPFB was 0.4 percent [9].

●In a cohort of 888 older adult subjects (age ≥90 years), there were only three with isolated LPFB [6].

LPFB is most often seen in association with right bundle branch block, as one of the manifestations of "bifascicular block." This is discussed in detail separately. (See "Chronic bifascicular blocks".)

ETIOLOGY — The left posterior fascicle branch is the first branch of the left bundle and is large in its initial course. It then fans extensively throughout the posterior and inferior left ventricle. The left posterior fascicle is exposed to lower pressures and less turbulence than the left anterior fascicle; it also has a dual blood supply. These characteristics probably explain why isolated LPFB is an uncommon finding. (See 'Epidemiology' above.)

Isolated LPFB can, however, be seen in the setting of extensive arteriosclerotic cardiovascular disease, as an association with inferior myocardial infarction and extensive coronary disease has been suggested [10]. LPFB can also occur with cardiomyopathies, including those that result from hypertension and Chagas disease, myocarditis, hyperkalemia, acute cor pulmonale, and chronic degenerative and fibrotic processes of the conducting system. Transient LPFB is quite rare but also suggests extensive coronary artery disease [11].

ELECTROCARDIOGRAPHIC FINDINGS — Left posterior and anterior fascicular blocks mainly affect the direction but not the duration of the QRS complex because the conduction disturbance primarily involves the early phases of activation. (See "Left anterior fascicular block".)

Definition — The ECG features (waveform 1) of isolated LPFB include [12]:

●Frontal plane axis between 90° and 180° in adults

●rS pattern in leads I and aVL

●qR pattern in leads III and aVF

●QRS duration less than 120 milliseconds

ECG activation patterns — The left posterior fascicle normally initiates activation of the lower part of the septum, the inferolateral wall, and the posteromedial papillary muscle. The ECG criteria for LPFB (also called left posterior hemiblock) are depicted on the ECG (waveform 1). The changes that are seen reflect alterations in the different phases of activation.

●Early activation – Early activation by the normally conducting anterior and septal fascicles causes the initial vector to be directed to the left, anteriorly, and superiorly producing initial small r waves in leads I, V1, and V6.

●Mid-temporal and terminal activation – The mid-temporal and terminal vectors in LPFB are directed to the right, posteriorly, and inferiorly due to delayed depolarization of the areas normally activated by the left posterior fascicle. This leads to the characteristic rightward axis of +90° to +180° [13]. As a result, there is a qR morphology in leads II, III, and aVF and an rS morphology in leads I and aVL.

QRS duration and T waves — The QRS duration usually does not exceed 100 milliseconds, although the World Health Organization/International Society and Federation of Cardiology (WHO/ISFC) Task Force allows up to 120 milliseconds, or 20 milliseconds above the previous baseline [13]. The T waves are often normal, but the T wave vector may be directed posteriorly and upward.

DIFFERENTIAL DIAGNOSIS — By contrast to left anterior fascicular block, LPFB is very rare as an isolated finding. The ECG in LPFB can mimic the findings seen in a number of other conditions. These include:

Right ventricular hypertrophy — The ECG criteria for LPFB apply only in the absence of other causes for a rightward axis, such as right ventricular hypertrophy (RVH) due to valvular heart disease or lung disease with cor pulmonale. Right axis deviation (axis >+90° to 100°) is often present with RVH. The RV forces become predominant in patients with RVH (especially due to a pressure load as with pulmonic outflow obstruction or severe pulmonary hypertension), producing tall R waves in the right precordial leads (V1 and V2) and deep S waves in the left precordial leads (V5 and V6). There also may be associated right atrial overload and ST segment and T wave abnormalities in the right precordial leads.

Old myocardial infarction — Prior myocardial infarction (MI), with resulting Q waves, may appear similar to LPFB on an ECG. (See "ECG tutorial: Myocardial ischemia and infarction", section on 'Prior Q wave myocardial infarction'.)

●A high lateral or anterolateral MI can mimic LPFB. With an infarct, however, the initial r wave in leads 1 and aVL is absent, and only a Q wave is seen.

●The small q waves in the inferior leads in LPFB may cause confusion with an inferior wall MI.

The presence of right bundle branch block (RBBB) might suggest right axis deviation because of the deep terminal S wave in leads 1, aVL and V5, and V6. However, these S waves reflect delayed RV activation, not left ventricular forces. An additional potential source of confusion is that RBBB can occur in association with LPFB (table 1).

Pre-excitation — Pre-excitation can occasionally produce right axis deviation. The presence of pre-excitation is indicated by a short PR interval, a delta wave, and a widened QRS complex. This pattern often has Q waves in leads II, III, and aVF and not infrequently is misdiagnosed as an inferior wall MI. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.)

Miscellaneous — Isolated LPFB is a diagnosis of clinical exclusion, requiring that other more common causes of rightward QRS axis be ruled out. Once RVH, prior MI, and pre-excitation have been excluded, other conditions to exclude include misplacement of the ECG leads, typically with limb lead reversal, or the presence of a normal ECG variation (especially in younger adults).

EVALUATION, TREATMENT, AND FOLLOW-UP — Patients with isolated LPFB are generally asymptomatic and do not require further diagnostic evaluation for LPFB 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 other disorders (eg, neuromuscular disorders, Anderson-Fabry disease, etc). (See "Chronic bifascicular blocks".)

A number of neuromuscular diseases are associated with fascicular block. These include myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and a peroneal muscular atrophy. These patients represent a special class and are treated more aggressively with pacemakers due to the potential for unpredictably rapid progression of conduction disease [14]. (See "Inherited syndromes associated with cardiac disease" and "Permanent cardiac pacing: Overview of devices and indications", section on 'Neuromuscular diseases'.)

Patients with isolated findings of LPFB on the surface ECG do not require any specific follow-up aside from routine care. Any symptoms consistent with the development of cardiac disease (eg, coronary heart disease, heart failure, atrial fibrillation, etc) should immediately be evaluated.

PROGNOSIS — Isolated LPFB is very rare and thus, unlike left anterior fascicular block, left bundle branch block, and right bundle branch block, there are limited studies evaluating this ECG pattern with subsequent atrial fibrillation or other cardiovascular morbidity risk.

In the above cited cohort study evaluating ECGs in 358,958 primary care patients, there was an observed increase in mortality among patients with isolated LPFB compared with those without any fascicular block over a 10-year follow-up period (hazard ratio 2.09, 95% CI 1.87-2.32) [7].

SUMMARY AND RECOMMENDATIONS

●Left posterior fascicular block (LPFB), 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 LPFB, with a resultant characteristic appearance on the ECG associated with marked right axis deviation (waveform 1). (See 'Introduction' above.)

●Isolated LPFB is a rare finding, particularly among otherwise healthy persons, with estimates of its prevalence ranging from 0.1 to 0.6 percent. (See 'Epidemiology' above.)

●Isolated LPFB has the following features on an ECG (see 'Definition' above):

•Frontal plane axis between 90° and 180° in adults (in the absence of other factors known to cause a rightward QRS axis)

•rS pattern in leads I and aVL

•qR pattern in leads III and aVF

•QRS duration less than 120 milliseconds

●Patients with isolated LPFB are generally asymptomatic and do not require further diagnostic evaluation for LPFB 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 'Evaluation, treatment, and follow-up' above.)

●Patients with isolated findings of LPFB on the surface ECG do not require any specific follow-up aside from routine care. 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.)