Left bundle branch block

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Left bundle branch block is a cardiac conduction abnormality seen on the electrocardiogram (ECG) whereby there is an impairment of transmission of the cardiac electrical impulse along the fibers of the left main bundle branch, or both the left anterior fascicle and left posterior fascicle. This conduction disturbance is characterized by wide (greater than or equal to 0.12 seconds) QRS complexes. In this condition, activation of the left ventricle is delayed, which results in the left ventricle contracting later than the right ventricle.

LBBB is uncommon among patients under 50 years of age (<0.5%). It occurs in 6% to 8% of patients over the age of 50.

On examination of the cardiovascular system, a paradoxical split of the second heart sound may be heard.

Asymptomatic patients with isolated left bundle branch block and no underlying heart disease require no treatment. Routine follow-up is required in such patients. In symptomatic patients treatment is directed at the underlying cause of left bundle branch block, such as ST elevation myocardial infarction. Patients withsyncope and LBBB may have a rhythm disturbance that requires a pacemaker. Given the dys-ynchrony that occurs with left ventricular contractility,cardiac resynchronization therapy in heart failure patients may be of benefit.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; J. Adrian Gutierrez [2]

The history of bundle branch block research illustrates the evolving understanding of cardiac electrophysiology. As early as 1909, researchers Eppinger and Rothberger were conducting experiments in dogs in which they injected silver nitrate to destroy portions of the myocardium and induce electrocardiographic changes. These studies provided some of the earliest evidence of the importance of the cardiac conduction system. They observed that extensive destruction of the ventricular free wall produced relatively little change on the ECG, whereas small lesions in the interventricular septum resulted in significant electrocardiographic abnormalities due to injury of the bundle branches ^[1]

In 1910, Eppinger and Stoerk described patients with bundle branch block who exhibited a positive QRS complex in lead I and negative complexes in leads II and III. Based on extrapolation from canine experiments, they interpreted this pattern as right bundle branch block. Similar conclusions were later supported by Lewis, who published what is now recognized as one of the earliest electrocardiograms of left bundle branch block but also misclassified it as right bundle branch block. These interpretations remained widely accepted until human mapping studies by Barker and colleagues in 1929 demonstrated that the pattern actually represented left bundle branch block. ^[1]

In 1979, Schneider and colleagues analyzed newly acquired LBBB in the Framingham Heart Study. They found that LBBB was commonly associated with hypertension, cardiomegaly, coronary heart disease, and heart failure, with only 11% of affected individuals remaining free of cardiovascular abnormalities during follow-up. These findings helped establish LBBB as a marker of underlying cardiovascular disease and adverse prognosis rather than a benign electrocardiographic finding. ^[2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Raviteja Guddeti, M.B.B.S. [3]; Aarti Narayan, M.B.B.S [4]

New LBBB is defined as the presence of a new left bundle branch block and:^{[1] [2]}

1. A prior ECG with normal QRS duration (<110 ms) within 24 hours before the LBBB tracing without T-wave abnormalities.
2. Acute-onset illness with LBBB on the admission tracing resolving within 24 hours without T-wave abnormalities on the subsequent narrow QRS tracings (to exclude LBBB lasting more than 24 hours) in patients with no history of LBBB.

An old LBBB is defined as an^[3] LBBB that has existed for more than 24 hours (by prior tracings or reports in the electronic medical record).

The LBBB duration is unknown on tracings obtained within the first 24 hours of admission in which there is not any prior EKG information.^[4]

Another classification system commonly used for LBBB is as follows:

The criteria to diagnose a complete left bundle branch block on an electrocardiogram includes the following:

1. The heart rhythm must be supraventricular in origin. A wide QRS complex that is not preceded by P waves would not qualify.
2. The QRS duration must be greater than or equal to 120 milliseconds.
3. There should be a QS or rS complex in lead V1.
4. There should be a monophasic R wave in lead I and lead V6.

The criteria for diagnosing an incomplete LBBB include:

1. QRS duration between 110 and 119 ms in adults, between 90 and 100 ms in children 8 to 16 years of age, and between 80 and 90 ms in children less than 8 years of age.
2. Presence of left ventricular hypertrophy pattern.
3. R peak time greater than 60 ms in leads V₄, V₅, and V₆.
4. Absence of Q wave in leads I, V₅, and V₆.
5. ST and T wave displacement opposite to the major deflection of the QRS complex.^[5][6][7][8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Raviteja Guddeti, M.B.B.S. [2]; Aarti Narayan, M.B.B.S [3]

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1. The normal cardiac conduction proceeds in a way so as to allow time for the atrium to relax during atrial diastole.
2. The electrical impulse generated in the SA node travels through the internodal pathways towards the AV node.
3. The conduction through the AV node is slowed down as it travels through it. This decrease in velocity of conduction allows time for the atrium to contract ahead of the ventricle so that the blood from the atria can fill up the ventricles through the atrio-ventricular valves.
4. As the impulse flows through the compact AV node, it rapidly conducts through the ventricular myocardial cells. Once the depolarization is complete, the ventricle relaxes during diastole in preparation for the next impulse.

• The conduction system of the heart consists of specialized cells designed to conduct electrical impulse faster than the surrounding myocardial cells.
• Anatomically, the AV node is divided into three regions as follows:
  • Transitional cell zone: This is the region where the internodal atrial pathways merge with the compact AV node.
  • Compact AV node: This region is located at the apex of the triangle of Koch, which is formed by the ostium of coronary sinus, tricuspid annulus and the tendon of Todaro.
  • Penetrating portion of the AV bundle: This region enters the tendon of Todaro and runs within the fibrous body of the membranous interventricular septum and eventually divides at the crest of the muscular interventricular septum into right and left branches.
• The left bundle branch penetrates the membranous portion of the interventricular septum and divides into several smaller branches. Parts of the left bundle branch include a pre-divisional segment, anterior fascicle/hemibundle and posterior fascicle/hemibundle. Rarely a median fascicle is present in some hearts.
  • The anterior fascicle supplies the anterior papillary muscle and the Purkinje network of the antero-lateral surface of the left ventricle.
  • The posterior fascicle supplies the posterior papillary muscle and the Purkinje network of the postero-inferior surface of the left ventricle.
  • Left bundle branch receives its blood supply from left anterior descending artery.

• Unlike right bundle branch block (RBBB), left bundle branch block completely modifies the way of depolarization of the conduction system of the heart. In LBBB the activation of the interventricular septum is from right to left due to uninterrupted conduction in the RBB.
• Then the electrical impulse propagates inferiorly to the left resulting in delayed depolarization and activation of the left ventricle especially the left lateral wall.^[1]
• In LBBB the right to left activation of the septum causes a small negative deflection (Q wave) in lead V₁ and a positive deflection (R wave) in lead V₆. Right ventricle depolarizes earlier than the left ventricle giving an R wave in lead V₁ and an S wave in lead V₆. Subsequent delayed depolarization of the left ventricle results in an S wave in lead V₁ and another R wave in lead V₆.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Raviteja Guddeti, M.B.B.S. [3]; Aarti Narayan, M.B.B.S [4]; Ogheneochuko Ajari, MB.BS, MS [5]

Left bundle branch block is a cardiac conduction seen on the electrocardiogram (ECG) whereby there is an impairment of transmission of the cardiac electrical impulse along the fibers of the left main bundle branch, or both the left anterior fascicle and the left posterior fascicle. Most causes of LBBB are the result of some form of cardiac disease but LBBB is also known to be associated with non cardiac causes.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Myocardial infarction

• Congestive heart failure
• Coronary heart disease^[1]
• Hypertension^[1]
• Hypertrophic obstructive cardiomyopathy^[1]
• Valvular heart disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

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LBBB must be differentiated from:

• Left anterior fascicular block (LAFB), which is when there is a block of the anterior fascicle.
• Left posterior fascicular block (LPFB), which is when there is a block of the posterior fascicle.
• Left ventricular hypertrophy, which also causes tall QRS complexes.
• Ventricular tachycardia and accelerated idioventricular rhythm
• Wolff-Parkinson-White syndrome
• Ventricular pacing

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] ; J. Adrian Gutierrez [3]

LBBB is uncommon among patients under 50 years of age (<0.5%). It occurs in 6% to 8% of patients over the age of 50.

Prevalence of LBBB in the general population ranges from 200 to 1100 per 100,000. ^[1]

Prevalence of LBBB increases with age. Large prospective studies have reported a mean age at diagnosis of approximately 70 years in men and 68 years in women. ^[2]

Among patients with heart failure with reduced ejection fraction (HFrEF), LBBB is a common conduction abnormality. In an analysis of the PARADIGM-HF and ATMOSPHERE trials, LBBB was present in 15.1% of 11,861 patients. ^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

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• Pulmonary arterial line placement ^[1] in a patient with LBBB can result in a complete heart block if the right bundle branch is traumatized during the process.
• Progression to higher degree AV block: It was shown in the Swedish study that the risk of progression was more pronounced in left block than in right bundle branch block.
• Bradycardia
• Delay in the diagnosis of MI: Presence of LBBB can delay the diagnosis of an acute MI.
• Sudden cardiac death is a potential complication when associated with a heart attack.

In asymptomatic patients under the age of 50, LBBB does not appear to be associated with an adverse prognosis.

It is notable that when LBBB is the presenting feature of an acute MI, the patient will not present with any chest pain half the time. Unfortunately, patients whose only manifestation of an acute MI is a left bundle branch block are less frequently treated with reperfusion therapy, and they have a worse prognosis.^[2] A large Swedish study in men more than 45 years old with LBBB who were followed-up for over 25 years, showed both a much higher risk for developing high degree atrioventricular block and a markedly higher hazard ratio for all-cause mortality than individuals with right bundle branch block.^[3]

Several clinical studies have shown that LBBB is associated with a grave prognosis in the presence of the following:

• Coronary artery disease: In patients with known or suspected CAD, LBBB is an independent predictor of all-cause mortality. As compared with diabetics without LBBB and patients with isolated LBBB, patients with LBBB and type II diabetes have more severe and extensive CAD and advanced LV dysfunction.
• Acute MI: Presence of LBBB in the setting of an acute MI can delay and complicate the diagnosis. Both short-term and long-term mortality have been shown to be higher in this association.
• Heart failure: LBBB results in left ventricular dys-synchrony, which compromises the left ventricular function leading to heart failure. Studies have shown LBBB as an independent risk factor for an increase in all-cause mortality and sudden death at one year. These patients could be treated with cardiac resychronization therapy with biventricular pacing.

Exercise-induced LBBB is a transient finding seen in approximately 0.5% of patients undergoing an exercise stress test. In one study of 17,277 exercise stress tests it was found that all-cause mortality and major cardiac events were significantly higher in patients with exercise-induced LBBB.^[4]

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