Left anterior fascicular block

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

The anatomy, clinical manifestations, differential diagnosis, prognostic implications, and treatment of LAFB will be reviewed here. Additional details regarding the ECG manifestations of LAFB 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 individuals, 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 median (also called medial or septal) fascicle to the interventricular septum. This 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 left anterior and median fascicles are supplied either by septal branches of the left anterior descending (LAD) artery or by the atrioventricular 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 — Estimates of the prevalence of LAFB in the general adult population range from 1 to 2.5 percent [5,6]. The incidence of LAFB increases with age and ranges from 0.2 percent in younger adults to 8.0 percent in patients older than 90 years of age [6,7].

ETIOLOGY — The left anterior fascicle is often a discrete ramus that crosses the left ventricular outflow tract and can be damaged by high flow, high pressure, and turbulence as occurs with aortic valvular disease, hypertension, and cardiomyopathies. LAFB can also occur in coronary heart disease, Chagas disease, infiltrative and inflammatory diseases, congenital heart diseases (including tricuspid atresia, endocardial cushion defects, single ventricle, spontaneous and surgical closure of a ventricular septal defect, and other disorders), and as part of primary sclerodegenerative processes ("Lenègre's and Lev's syndromes"), associated with fibrosis, and sometimes calcification of the proximal conduction system. Aortic valve surgery not uncommonly causes LAFB [8]. LAFB occurs in over 70 percent of patients with obstructive sleep apnea [9].

LAFB has been associated with significant disease in the left anterior descending (LAD) coronary artery and rarely has been induced by ischemia during exercise testing [10]. LAFB that develops during an acute inferior wall myocardial infarction may be an indicator of LAD lesions, multivessel coronary artery disease, and impaired left ventricular systolic function, and occurs more frequently in a left-dominant or balanced coronary artery system [11,12].

ELECTROCARDIOGRAPHIC FINDINGS — Left anterior and posterior 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 posterior fascicular block".)

Definition — The ECG features (waveform 1) of isolated LAFB include [13]:

●Frontal plane axis between -45° and -90° (ie, marked left axis deviation)

●qR pattern in lead aVL

●QRS duration less than 120 milliseconds

●R-peak time in lead aVL of 45 milliseconds or more (this criterion is not used as much as other three in a clinical setting, because it is difficult to assess on standard ECGs at usual gain)

These above criteria do not apply to patients with congenital heart disease in whom left axis deviation is present in infancy.

ECG activation patterns — The left anterior fascicle normally initiates activation in the upper part of the septum, the anterolateral left ventricular free wall, and the left anterior papillary muscle. The initial anterior paraseptal activation is absent in LAFB, while the remaining activation fronts caused by the posterior and median fascicles are normal. The net effect is a late leftward and superior vector and includes:

●S waves in the inferior leads, resulting in an rS pattern in II, III, and aVF.

●R waves in the leftward leads, resulting in a qR or R (depending upon the initial right or left orientation) pattern in leads I, aVL, V5, and V6.

●Because of the left axis deviation, the QRS complex in aVR and aVL ends in an R wave. There may also be a persistent terminal S wave in leads V5 and V6 due to the delayed activation of the high lateral wall that is normally activated by the left anterior fascicle. The S waves disappear if the precordial electrograms are recorded two interspaces higher.

The terminal vectors are more superior and also to the left and posterior. The very last terminal components may be directed slightly to the right or left. There is, however, a spectrum of LAFB that probably begins in the range of what is defined as having no axis deviation, through left axis deviation (-30° to -44°) to marked left axis deviation (-45° to -90°) [14].

QRS duration and T waves — The QRS duration in LAFB is often less than 100 milliseconds, although the World Health Organization/International Society and Federation of Cardiology Task Force allows up to 120 milliseconds or 20 milliseconds above the previous baseline [15]. The T waves are often normal, but the T wave vector may be directed anteriorly and downward.

LAFB may cause the S waves to disappear in leads I, aVL, and rarely in V5 and V6, thereby obscuring the diagnosis of right bundle branch block (RBBB). At times, the ECG pattern more resembles left bundle branch block (LBBB) than RBBB, which is one of the causes of RBBB simulating LBBB. (See "Right bundle branch block".)

DIFFERENTIAL DIAGNOSIS — The ECG in LAFB can mimic the findings seen in a number of other conditions. These include:

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

●An anteroseptal or even lateral MI may be suspected because of the QS pattern in V1 and V2 and the qR pattern in aVL. The Q waves in the precordial leads (eg, V1 and V2) are due to the inferior orientation of the initial vector. They may disappear in the precordial leads if the ECG leads are positioned one interspace lower.

●Small r waves in the inferior leads with the superior axis deviation may be confused with an inferior wall MI, particularly since approximately one-third of patients with an inferior infarct can reestablish small r waves in the inferior leads. There are a number of findings that help distinguish an inferior MI from LAFB.

•Persistent ST-T abnormalities suggest a prior inferior MI, while most patients with LAFB have normal T waves.

•Inferior MI is usually associated with Q waves.

Vectorcardiography may be helpful in this setting since the vector loop in the frontal plane is counterclockwise with LAFB versus clockwise with an inferior infarct. (See "ECG tutorial: Electrical components of the ECG", section on 'Electrical fields'.)

Left ventricular hypertrophy — The orientation of the midtemporal vector in LAFB may mimic left ventricular hypertrophy (LVH) in leads I and aVL and, conversely, may conceal signs of LVH in the left precordial leads. Debate continues to exist about whether LAFB alone may cause relatively tall R waves in I and aVL in the absence of LVH [16]. In general, LVH does not shift the axis more leftward than -30°. However, LVH and LAFB may coexist. Clues to concomitant LVH with a QRS axis of -45° or more leftward include evidence of left atrial abnormality, prominent precordial voltage, ST-T changes consistent with LV overload (formerly called the "strain" pattern), and possibly a QRS duration of 120 milliseconds or more. (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)

Pre-excitation — Pre-excitation can occasionally produce left 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'.)

Pulmonary disease — Severe chronic pulmonary disease (emphysematous type) may at times produce marked left axis deviation (approximately -90°). Findings suggestive of emphysema include a negative P wave in aVL, slow R wave progression reflecting right ventricular dilation, and downward displacement of the diaphragm. In addition, S waves may be present in leads I, II, and III.

Miscellaneous — A number of conditions may alter the appearance of the ECG and present diagnostic problems, including an anatomically horizontal heart, hypertrophic cardiomyopathy, straight back syndrome [17], and some types of congenital heart disease including corrected transposition, tricuspid atresia, single ventricle, endocardial cushion malformations, and Ebstein's disease. If the S wave in standard lead II is deeper than in lead III, the diagnosis of LAFB is unlikely. Not infrequently, other diagnostic approaches, such as echocardiography, radionuclide myocardial perfusion imaging, and, with suspected pre-excitation, electrophysiologic studies, are required to clarify these issues.

EVALUATION, TREATMENT, AND FOLLOW-UP — Patients with isolated LAFB are generally asymptomatic and do not require further diagnostic evaluation for LAFB 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 [18]. (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 LAFB 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 [HF], atrial fibrillation [AF], etc) should immediately be evaluated.

However, because LAFB is associated with a greater risk for subsequent development of AF and HF, patients should be aware of symptoms attributable to these conditions, and clinicians should consider further cardiac evaluation if there is any concerning history. (See 'Prognosis' below.)

PROGNOSIS

●Atrial fibrillation and heart failure – LAFB may be associated with heart failure (HF) and AF; however, this association may not be causal but instead due to a shared pathogenesis [19,20]. In the Cardiovascular Health Study, among 1614 persons without cardiovascular disease, 39 patients had isolated LAFB diagnosed by systematic study criteria [20]. Over 16 years of follow-up, those with LAFB had a higher risk of HF than those without LAFB (3.5 versus 1.6 per 100-person years; hazard ratio [HR] 2.4, 95% CI 1.4-4.1). Persons with LAFB also had a higher risk of AF (3.4 versus 1.8 per 100-person years; HR 1.9, 95% CI 1.1-3.2).

In a separate analysis from the same study cohort including those with cardiovascular disease, LAFB was associated with a twofold increased risk of developing AF even after accounting for other ECG indices (eg, QTc and atrial premature complexes [HR 2.1, 95% CI 1.1-3.9]) [19].

●Mortality – Evidence regarding the association between LAFB and mortality is mixed [20-22]. In the Cardiovascular Health Study described above, participants with LAFB had a somewhat increased risk of death over a median follow-up of 16 years (6.2 versus 4.5 per 100 person-years; HR 1.6, 95% CI 1.1-2.3) [20].

However, in a separate study of 358,000 primary care patients with a similar duration of follow-up, LAFB was not associated with increased mortality [21]. The latter study relied on electronic medical records (EMRs) compared with directly-read ECGs with standardized criteria to define LAFB; this may have led to misclassification of LAFB and a bias towards a null association with mortality [22].

●Progressive conduction system disease – In the EMR study of 358,000 primary care patients, LAFB was associated with an increased risk of third-degree heart block (HR 1.6, 95% CI 1.25-2.05) and pacemaker placement but not with right bundle branch block (RBBB; ie, development of bifascicular block) [21].

SUMMARY AND RECOMMENDATIONS

●Definition – Left anterior fascicular block (LAFB), 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 LAFB, with a resultant characteristic appearance on the ECG associated with marked left axis deviation (waveform 1). (See 'Introduction' above.)

●Epidemiology – Estimates of the prevalence of LAFB in the general adult population range from 1 to 2.5 percent. However, the incidence of LAFB increases with age and ranges from 0.2 percent in younger adults to 8.0 percent in patients older than 90 years of age. (See 'Epidemiology' above.)

●Electrocardiographic (ECG) findings – Isolated LAFB has the following features (waveform 1) on an ECG (see 'Definition' above):

•Frontal plane axis between -45 and -90 degrees (ie, marked left axis deviation)

•qR pattern in lead aVL

•QRS duration less than 120 milliseconds

•R-peak time in lead aVL of 45 milliseconds or more (this criteria is not used as much as other three in a clinical setting, because it is difficult to assess on standard ECGs at usual gain)

●Clinical implications – Patients with isolated LAFB are generally asymptomatic and do not require further diagnostic evaluation for LAFB or placement of a pacemaker or any other specific therapy. Therapy should be considered only in patients with persistent bifascicular or trifascicular block patterns or in certain neuromuscular disorders. (See 'Evaluation, treatment, and follow-up' above.)

Any symptoms consistent with the development of cardiac disease (eg, coronary heart disease, heart failure [HF], atrial fibrillation [AF], etc) should immediately be evaluated. (See 'Evaluation, treatment, and follow-up' above.)

●Prognosis – In longitudinal studies with 16 years of follow-up, LAFB appears to be associated with AF, HF, and progressive conduction system disease (ie, third-degree atrioventricular block and pacemaker placement). An association with mortality is uncertain. (See 'Prognosis' above.)