What are the etiology and ECG (electrocardiogram) findings of Left Anterior Fascicular Block (LAFB)?

Left Anterior Fascicular Block (LAFB): Etiology and ECG Findings

ECG Diagnostic Criteria

The diagnosis of LAFB requires four mandatory electrocardiographic criteria: left axis deviation between -45° and -90°, qR pattern in lead aVL, R-peak time in aVL ≥45 ms, and QRS duration <120 ms. 1, 2

Specific ECG Features

Axis and Morphology:

• Frontal plane QRS axis must be between -45° and -90° 1, 2
• Characteristic qR pattern in lead aVL is required 1, 2
• R-peak time (intrinsicoid deflection) in aVL must be ≥45 ms 1, 2
• QRS duration remains <120 ms, distinguishing it from complete bundle branch block 1, 2

Vector Changes:

• The QRS vector shifts posteriorly and superiorly, producing larger R waves in leads I and aVL 1, 3
• Smaller R waves but deeper S waves appear in leads V5 and V6 1, 3
• Small q waves followed by tall R waves characterize the lateral high leads (I and aVL) 2

Important Diagnostic Pitfalls

Before diagnosing LAFB, exclude other causes of left axis deviation:

• Left ventricular hypertrophy must be ruled out 2
• Age-related leftward axis shift in elderly patients can mimic LAFB 1, 2
• Congenital heart defects, particularly atrioventricular canal defects, cause left axis deviation from infancy 1, 2

Critical caveat: Left axis deviation alone should not be considered synonymous with LAFB—the delayed intrinsicoid deflection in aVL is essential for diagnosis 4. Studies show only 41% of ECGs with axis at -30° demonstrate delayed activation in aVL, increasing to 100% at -75° or greater 4.

Etiology

Pathophysiologic Mechanisms

LAFB results from conduction block in the anterior fascicle of the left bundle branch, with multiple potential etiologies: 1

Common causes include:

• Degenerative/fibrotic disease of the conduction system (most common) 1
• Ischemic heart disease and myocardial infarction 1, 3
• Hypertensive heart disease 2, 3
• Infiltrative diseases 1
• Inflammatory/infectious processes 1
• Congenital heart defects (atrioventricular canal defects) 2, 3
• Genetic/hereditary conduction disorders (Lenegre disease) 2
• Traumatic injury 1

Clinical Context and Prevalence

• Prevalence is 0.5-1.0% in the general population under 40 years 2
• More common in males and increases with age 2
• May be isolated and benign in patients without structural heart disease 2, 3
• In acute myocardial infarction, LAFB indicates more severe coronary disease and worse outcomes 3

Impact on Other ECG Interpretations

LAFB significantly affects interpretation of left ventricular hypertrophy:

• R-wave amplitude in leads I and aVL are unreliable for LVH diagnosis when LAFB is present 1, 3
• Criteria incorporating S-wave depth in left precordial leads (V5, V6) improve LVH detection in the presence of LAFB 1, 3

LAFB can mask or mimic other conditions:

• Small Q waves in V2 may simulate anteroseptal infarction 5
• Inferior and anterior myocardial infarctions may be masked by R waves replacing Q waves 5

Clinical Evaluation and Management

When LAFB is detected, perform:

• Thorough cardiological evaluation including exercise testing, 24-hour ECG monitoring, and cardiac imaging to identify underlying structural disease 2, 3
• Echocardiography if structural heart disease is suspected 1
• ECG screening of siblings in young patients with bifascicular block patterns to exclude genetic progressive conduction disease 2, 3

Prognostic implications:

• Isolated LAFB without other conduction abnormalities is generally benign 2, 3
• When associated with other conduction abnormalities, there is increased risk of developing clinically significant AV block requiring monitoring for progression 2, 3
• In acute MI context, more vigilant monitoring is warranted due to potential progression to higher-grade AV block 3