Left bundle branch block

INTRODUCTION — Left bundle branch block (LBBB), a pattern seen on the surface electrocardiogram (ECG), results when normal electrical activity in the His-Purkinje system is interrupted (figure 1). The normal sequence of activation is altered dramatically in LBBB, with a resultant characteristic appearance on the ECG (waveform 1).

LBBB most often occurs in patients with underlying heart disease and may be associated with progressive conducting system disease. However, LBBB can also be seen in asymptomatic patients with a structurally normal heart. The presence of LBBB complicates the diagnosis of myocardial ischemia/infarction and interferes with the interpretation of exercise testing. In patients with significant LV dysfunction, LBBB results in left ventricular dyssynchrony and may contribute to heart failure (HF).

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

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. The components of the left bundle branch are (figure 1) [1-5]:

●A predivisional segment.

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

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

●In some hearts, a median fascicle to the interventricular septum.

Blood supply — The left anterior descending artery provides the primary blood supply for the left bundle branch, particularly for the initial portion (figure 2). As is true for the right bundle branch, there may be some collateral flow from the right and circumflex coronary systems.

Electrophysiology — The main left bundle and its fascicles consist of Purkinje fibers that transmit impulses at a rate of 1 to 3 m/sec resulting in virtual simultaneous depolarization of the terminal His Purkinje system and the adjacent ventricular myocardium. Pathological studies in LBBB have suggested that the block may be proximal (particularly in diffuse myocardial disease), distal, or a combination of both [6]. The precise anatomical location of block is an important aspect for left bundle branch (LBB) pacing [7]. LBB pacing has been shown to reverse LBBB through stimulation distal to the site of block [8].

Electrophysiologic studies have revealed multiple and complicated patterns of myocardial activation, the heterogeneity of which depends upon the function or dysfunction of the distal specialized conduction system [9]. Changes in myocardial activation only affect the left ventricle in LBBB; thus, changes in the morphologic features of local electrograms can be recorded in the left, but not the right, ventricle [10].

An LV activation pattern study in patients with chronic HF and LBBB on ECG was studied in seven patients with an LV ejection fraction of less than 35 percent [11]. Three patients had preserved activation of the left bundle despite LBBB on the ECG. Four had conduction block. The remainder had homogeneous depolarization propagation within the LV. These findings suggest that there are variable patterns of LV endocardial activation, which may be important in cardiac resynchronization therapy. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system", section on 'Rationale for CRT'.)

EPIDEMIOLOGY — The prevalence of LBBB increases with age, occurring in less than 1 percent of the general population, with estimates ranging from 0.2 to 1.1 percent [12-17]. LBBB occurs infrequently in young healthy subjects [18-21]. As an example, a study of 237,000 airmen under age 30 found only 125 cases of LBBB, representing a prevalence of 0.05 percent [20]. Ninety percent of these subjects had no apparent structural heart disease, and an isolated LBBB in young males was generally benign.

The increase in LBBB prevalence with age was illustrated in a prospective study of 855 Swedish males in the general population who were 50 years of age and followed for 30 years [18]. The prevalence of LBBB was 0.4 percent at age 50, 2.3 percent by age 75, and 5.7 percent by age 80. In this otherwise healthy population, there was no significant association with risk factors for or the presence of ischemic heart disease, myocardial infarction or cardiovascular deaths, suggesting that LBBB is more commonly a marker of a slowly progressive degenerative disease of the conduction system. Among 66,450 participants in the Women's Health Initiative trial, 714 had LBBB at study entry, representing a prevalence of 1.1 percent [15].

In contrast to the Swedish study, other studies have suggested an association between the new onset of LBBB and underlying advanced and/or advancing heart disease, particularly in older adults. This is illustrated in the following examples:

●Among 5209 persons from the Framingham Heart Study followed for 18 years, 55 subjects developed LBBB at a mean age of 62 years [22]. Patients who developed LBBB had significantly higher rates of antecedent hypertension, cardiomegaly, and coronary heart disease. Coincident with or subsequent to the onset of the LBBB, 48 percent developed clinically apparent coronary disease or HF for the first time. Over the period of follow-up, only 11 percent of those who developed LBBB remained free of cardiovascular disease compared to 50 percent in an age-matched control group without LBBB.

●Among 110,000 Irish subjects who underwent screening for cardiovascular disease, 112 were found to have LBBB [23]. At a mean follow-up of 9.5 years, patients with LBBB demonstrated a significantly increased prevalence of cardiovascular disease (21 versus 11 percent in patients without LBBB).

The incidence of underlying cardiovascular disease is lower in younger subjects with LBBB [18,20]. However, because of the association of LBBB with the subsequent development of cardiovascular disease, even in otherwise asymptomatic patients, careful evaluation and follow-up are indicated. When LBBB is present, patients should be evaluated for hypertension, coronary disease, and other disorders that have been associated with LBBB (eg, myocarditis, valvular heart disease, cardiomyopathies) [6,24,25]. (See 'Evaluation' below.)

ETIOLOGY — Similar to the right bundle branch, conduction in the left bundle branch can be compromised by both structural and functional factors.

Structural heart disease — Excepting cases of acute anterior MI, LBBB is not generally the result of a single clinical entity but rather results from slowly progressive degenerative disease involving the conduction system. As such, numerous chronic conditions which contribute to myocardial fibrosis (eg, hypertension, coronary artery disease, cardiomyopathies) can contribute to the development of LBBB.

LBBB may result following an acute myocardial insult such as myocardial ischemia, myocardial infarction, endocarditis with abscess formation, or myocarditis and in such circumstances is usually associated with a worse prognosis. (See 'Prognosis' below and "Conduction abnormalities after myocardial infarction" and "Complications and outcome of infective endocarditis", section on 'Perivalvular abscess' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Electrocardiogram'.)

LBBB may also develop following certain cardiac surgeries (eg, septal myectomy) or procedures (eg, transcatheter aortic valve implantation). (See "Transcatheter aortic valve implantation: Complications", section on 'High degree heart block' and "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Septal reduction therapy'.)

Functional LBBB — LBBB may be functional, as a result of a long preceding R-R interval following by a short cycle ("rate-related bundle branch block"). Functional LBBB may be sustained if, after the initial aberration, the impulse traveling down the right bundle branch reenters the left bundle branch rendering it again refractory, and this pattern repeats for several cycles.

Ventricular tachycardia may mimic LBBB, as in repetitive monomorphic ventricular tachycardia originating from the right ventricular outflow tract or in bundle branch reentrant ventricular tachycardia (see "Ventricular tachycardia in the absence of apparent structural heart disease" and "Bundle branch reentrant ventricular tachycardia").

Hyperkalemia can depress conduction in the His-Purkinje system and rarely causes LBBB [26,27]. (See "ECG tutorial: Miscellaneous diagnoses", section on 'Hyperkalemia'.)

ECG FINDINGS AND DIAGNOSIS — The abnormalities in conduction and activation of the myocardium in persons with LBBB result in two major changes: loss of normal early septal forces, and the development of large and prolonged QRS complexes in the leftward leads (I, avL, and V6).

A task force from the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society has defined the electrocardiographic features of LBBB. These criteria incorporate the activation forces described above and include [28]:

●QRS duration greater than or equal to 120 ms in adults, greater than 100 ms in children 4 to 16 years of age, and greater than 90 ms in children less than four years of age.

●Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6 attributed to displaced transition of QRS complex.

●Absent q waves in leads I, V5, and V6, but in the lead aVL, a narrow q wave may be present in the absence of myocardial pathology.

●R peak time greater than 60 ms in leads V5 and V6 but normal in leads V1, V2, and V3, when small initial r waves can be discerned in the above leads.

●ST and T waves usually opposite in direction to QRS complex.

●Sometimes positive T wave in leads with upright QRS complexes may be normal ("positive QRS-T" concordance).

●However, depressed ST segments and/or negative T waves in leads with negative QRS ("negative QRS-T" concordance) are generally abnormal, and may be a sign of underlying ischemia.

●The appearance of LBBB may change the mean QRS axis in the frontal plane to the right, to the left, or to a superior, in some cases in a rate-dependent manner.

IMPACT OF LBBB ON THE ABILITY TO DIAGNOSE OTHER CONDITIONS — The electrocardiographic changes in LBBB can cause diagnostic problems in a variety of clinical conditions:

●Ventricular hypertrophy – The diagnosis of left ventricular hypertrophy (LVH) can only be established by echocardiography in the setting of LBBB since the two disorders produce similar ECG changes:

•The unmasking of left ventricular forces in LBBB (due to lack of counteracting right ventricular forces) results in increased QRS voltage in the leads used for the voltage criteria for LVH.

•The ST-T vectors in both LVH and LBBB are directed opposite to the QRS vector.

The diagnostic issues are different in right ventricular hypertrophy (RVH). This disorder may cause the leftward directed initial vector characteristic of LBBB to shift to the right, resulting in "pseudonormalization" of the initial vector and the reappearance of q waves in I, aVL, and V6. Echocardiography can be used to determine RVH and ventricular function in this setting. (See "ECG tutorial: Chamber enlargement and hypertrophy".)

●Myocardial ischemia – LBBB masks the ability to identify ischemia during exercise because of the associated ST and T wave abnormalities; as a result, exercise perfusion imaging or echocardiography is usually preferred when such patients are evaluated for CHD. It has been suggested that ST segment changes of ≥0.5 mm from baseline in leads II and AVF are predictive of ischemia in the setting of left bundle branch block [29]. However, this observation does not change the recommendation to use other exercise modalities. (See "Selecting the optimal cardiac stress test".)

●Acute myocardial infarction – LBBB complicates and often prevents the electrocardiographic diagnosis of acute myocardial infarction. This important issue is discussed elsewhere. (See "Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm".)

DIFFERENTIAL DIAGNOSIS — While LBBB has a fairly characteristic appearance on ECG, there are other conditions in which the ECG may have a similar appearance that need to be excluded prior to the diagnosis of LBBB, including other causes of prominent T wave inversions (table 1).

Incomplete LBBB — Incomplete LBBB is characterized by a QRS duration of 0.10 to 0.12 sec, a diminutive or absent q in I and V6 that is frequently replaced by a slurred initial upstroke (pseudo-delta wave), a QRS morphology reminiscent of complete LBBB, a delayed intrinsicoid deflection (time from beginning of QRS to its maximal amplitude in V6), and usually increased voltage. Canine studies suggest that incomplete LBBB may be a form of left septal (median) fascicular block [30].

Ventricular tachycardia and accelerated idioventricular rhythm — If the dominant ventricular rhythm originates from a pacemaker in the ventricle, the QRS will be widened and can have the appearance of a LBBB. However, both ventricular tachycardia (heart rate greater than 100 beats per minute) (waveform 2) and accelerated idioventricular rhythm (heart rate between 60 and 100 beats per minute) (waveform 3) are associated with atrioventricular (AV) dissociation, which should distinguish the rhythm from a supraventricular rhythm with aberrant conduction seen with LBBB. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation" and "ECG tutorial: Ventricular arrhythmias", section on 'Accelerated idioventricular rhythm'.)

Ventricular pacing — Ventricular pacing from the right ventricle typically results in a QRS complex resembling that seen with LBBB on the surface ECG. In nearly all patients, however, the presence of pacemaker spikes preceding the QRS complex differentiates a paced complex from LBBB.

Ventricular preexcitation (Wolff-Parkinson-White syndrome) — In some patients with manifest right-sided accessory pathways, the preexcitation pattern can mimic LBBB. In Wolff-Parkinson-White syndrome, however, the PR interval is typically short, which is generally not the case with LBBB.

PROGNOSIS — The prognosis in patients with LBBB is related largely to the type and severity of any concurrent underlying heart disease and to the possible presence of other conduction disturbances [17]. As an example, patients who also have type II second degree atrioventricular (AV) block or multi-fascicular block generally have more significant myocardial disease and a guarded prognosis. (See "Second-degree atrioventricular block: Mobitz type II" and "Chronic bifascicular blocks".)

Asymptomatic patients — LBBB appears to have a minimal effect on outcomes in younger, apparently healthy subjects, while LBBB in older individuals has been associated with an increase in mortality. Two large cohorts of younger asymptomatic persons have reported no increase in mortality in subjects with LBBB [20,23], while three other cohorts have reported increases in sudden cardiac death and overall mortality among those with LBBB [15,16,31-33].

●In the cohort of 237,000 healthy young males discussed above, the presence of LBBB was not associated with cardiovascular disease or an increase in mortality [20].

●Similarly, in a cohort of 110,000 subjects discussed above, the development of LBBB was associated with a higher incidence of subsequent cardiovascular disease without any increase in subsequent mortality [23].

●In contrast, among 53,377 females without cardiovascular disease at baseline (excluding those with RBBB) who participated in the Women's Health Initiative trial, there was a significantly greater risk of death from coronary heart disease (adjusted hazard ratio [HR] 2.17, 95% CI 1.37-3.43) and a trend toward higher death from any cause (adjusted HR 1.18, 95% CI 0.90-1.55) among females with LBBB compared with no BBB [15].

●In a study evaluating 202,268 subjects >40 years of age in a primary care population in Copenhagen, the presence of LBBB was associated with increased risk of myocardial infarction, HF, and pacemaker requirement in both males and females over a mean follow up of 7.8 years. In addition, LBBB was associated with an increased risk of cardiovascular death in males but not females (HR 1.80, 95% CI 1.38-2.35) [33].

●Among 8527 participants in the NHANES study (87 percent White Americans, 53 percent female, 16 percent with coronary heart disease at baseline), cardiovascular mortality was significantly higher in those with LBBB at baseline (adjusted HR 2.4 compared with those without BBB, 95% CI 1.3-4.7) [16].

●Similarly, in a Swedish primary prevention study that followed 7392 middle-aged males for 28 years, a higher mortality rate was demonstrated among the 46 males (0.6 percent) with LBBB [31]. Compared with males without bundle branch block, those with LBBB had significant increases in progression to high-degree AV block (adjusted HR 12.9, 95% CI 4.1 to 40.2) and all-cause mortality (adjusted HR 1.9, 95% CI 1.2 to 3.0) that was primarily due to out-of-hospital sudden death. The findings in the Swedish cohort are consistent with those seen in a cohort of 3983 asymptomatic Canadian males, 29 (0.7 percent) of whom developed LBBB during 30 years of follow-up [32]. The presence of LBBB was associated with a higher mortality and a 10-fold increase in sudden death.

Patients with coronary heart disease — LBBB is an independent predictor of all-cause mortality in patients with known or suspected coronary heart disease (CHD). This has been illustrated in several studies:

●In a review of 7073 adults referred for nuclear exercise testing, 2 percent of the subjects had LBBB [34]. After a mean follow-up of nearly seven years, those with LBBB had a greater mortality than those without LBBB (24 versus 11 percent; adjusted HR 1.5, 95% CI 1.1 to 2.0).

●In a post-hoc analysis of the 15,609 subjects with known CHD enrolled in the Coronary Artery Surgery Study (CASS), the presence of LBBB was associated with a more than fivefold increase in mortality after two years of follow-up [35].

●In the Heart Outcomes Prevention Evaluation (HOPE) cohort of 9541 patients with cardiovascular disease or diabetes in the absence of HF, the presence of LBBB was associated with a significantly higher risk for major cardiovascular events, cardiovascular death, HF, sudden death, and all-cause mortality [36].

●Among 12,354 females with cardiovascular disease (excluding those with RBBB) who participated in the Women's Health Initiative trial, there was a significantly greater risk of death from coronary heart disease (adjusted HR 2.92, 95% CI 2.08-4.08) and death from any cause (adjusted HR 1.43, 95% CI 1.11-1.83) among females with LBBB compared with no BBB [15].

In addition, individuals with type II diabetes mellitus and LBBB have more severe and extensive CHD and advanced left ventricular dysfunction as compared with diabetics without LBBB and in individuals with isolated LBBB [37].

Patients with acute myocardial infarction — The presence of LBBB is associated with higher short-term and long-term mortality following an acute myocardial infarction (MI). In addition, the presence of LBBB in a patient presenting with chest discomfort can delay or complicate the diagnosis of acute myocardial infarction (MI). Both of these situations are discussed in greater detail elsewhere. (See "Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm" and "Overview of the acute management of ST-elevation myocardial infarction" and "Conduction abnormalities after myocardial infarction", section on 'Bundle branch block'.)

Patients with heart failure or cardiomyopathy — Even in the absence of associated structural heart disease, LBBB is associated with dyssynchronous left ventricular activation, which reduces the efficiency of left ventricular contraction. The magnitude of the effect on left ventricular dyssynchrony was illustrated in a report in which 18 patients with isolated LBBB were compared with 10 normal controls [38]. Isolated LBBB was associated with dyssynchronous contraction and a significantly lower left ventricular ejection fraction than the controls (54 versus 62 percent, respectively).

The adverse effect of ventricular dyssynchrony due to LBBB is more pronounced in the presence of HF, possibly even serving as a primary cause of HF [39]. Several studies have reported that LBBB is an independent risk factor for mortality in patients with HF and is associated with increased all-cause mortality and sudden death at one year [39-41]. Other studies, however, have not shown an association with LBBB and mortality over longer periods of follow-up [42,43].

The development of a new LBBB during treatment for dilated cardiomyopathy may be a poor prognostic sign. Among a single-center cohort of 608 patients with dilated cardiomyopathy followed for a median of 122 months, 189 patients (31 percent) had LBBB at baseline diagnosis while 47 patients (11 percent) developed a new LBBB during follow-up [43]. While there was no significant increase in mortality related to baseline LBBB status, total mortality was markedly higher among patients with new LBBB compared with patients without new LBBB (49 versus 25 percent; adjusted HR 3.2; 95% CI 1.9-5.3).

Worse outcomes in heart-failure patients with LBBB may be expected due to dyssynchronous left ventricular activation [44,45]. This observation provides the rationale for the use of cardiac resynchronization therapy with biventricular pacing in patients with HF who have an intraventricular conduction delay, primarily due to LBBB. Worse outcomes, including mortality and likelihood of implantable cardioverter-defibrillator placement, have also been suggested in patients with LBBB and mildly reduced left ventricular ejection fraction (LVEF; 36 to 50 percent) who are not typically candidates for cardiac resynchronization therapy [46]. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system" and "Cardiac resynchronization therapy in heart failure: Indications and choice of system", section on 'Rationale for CRT'.)

Exercise-induced LBBB — Exercise-induced LBBB occurs transiently in approximately 0.5 percent of patients undergoing an exercise stress test. The prognostic value of exercise-induced LBBB was long debated. However, exercise-induced LBBB appears to be predictive of higher rates of mortality and cardiac events. In one study of 17,277 exercise stress tests, during which 70 episodes of exercise-induced LBBB occurred, death from any cause and major cardiac events were significantly more common in the group with exercise-induced LBBB [47]. (See "Exercise ECG testing: Performing the test and interpreting the ECG results", section on 'Bundle branch block'.)

Painful LBBB syndrome — Chest discomfort associated with the development of new LBBB in the absence of myocardial ischemia can rarely present as "painful LBBB syndrome." Clinically, painful LBBB syndrome has most commonly been reported as a "new" LBBB associated with otherwise unexplained chest pain [48]. The working hypothesis is that some patients are sensitive to the dyssynchronous ventricular contraction. This rare condition has been successfully treated with His bundle pacing and cardiac resynchronization therapy [49-51].

Patients undergoing noncardiac surgery — In patients undergoing noncardiac surgery, the presence of a LBBB is not associated with an increase in postoperative cardiac complications but is associated with a nonsignificant increase in perioperative mortality as a result of non-cardiovascular complications [52]. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Initial evaluation'.)

EVALUATION — When LBBB is present, patients should be evaluated for hypertension, coronary disease, HF, and other disorders that have been associated with LBBB (eg, myocarditis, valvular heart disease, cardiomyopathies). In most patients, this can be accomplished with a careful history and physical examination. An assessment of LVEF, usually with echocardiography, is typically warranted [53,54]. Focused additional testing (ie, stress testing with imaging) may be indicated for a subset of patients directed by findings from the history, exam, or other data [54]. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Stress testing in patients with left bundle branch block or a paced ventricular rhythm".)

TREATMENT — For asymptomatic patients with an isolated LBBB and no other evidence of cardiac disease, no specific therapy is required. However, permanent pacemaker insertion is indicated for patients who develop symptomatic conduction system disturbances, such as third degree or Mobitz type II second degree AV block, which is not associated with a reversible or transient condition. Patients with LBBB and syncope felt to be cardiac in nature may also be considered for treatment with a permanent pacemaker [54]. In addition, patients with LBBB and HF with reduced LVEF are generally candidates for treatment with cardiac resynchronization therapy [53,55]. These are discussed in more detail separately. (See "Permanent cardiac pacing: Overview of devices and indications" and "Third-degree (complete) atrioventricular block" and "Second-degree atrioventricular block: Mobitz type II" and "Cardiac resynchronization therapy in heart failure: Indications and choice of system".)

On rare occasions, insertion of a temporary pacemaker may be indicated for patients with LBBB. A temporary pacemaker may be considered for a patient undergoing right heart catheterization because of the potential for transient complete heart block associated with catheter manipulation. Temporary pacing is also indicated for a LBBB in association with an acute myocardial infarction, particularly when a first degree AV block is also present. The management of patients with a LBBB who have a myocardial infarction and those undergoing surgery is discussed elsewhere. (See "Temporary cardiac pacing" and "Conduction abnormalities after myocardial infarction".)

SUMMARY AND RECOMMENDATIONS

●Definition – Left bundle branch block (LBBB) results when normal electrical activity in the His-Purkinje system is interrupted, thereby altering the normal sequence of activation, resulting in the characteristic ECG appearance of a widened QRS complex and changes in the directional vectors of the R and S waves (waveform 1). (See 'Introduction' above and 'ECG findings and diagnosis' above.)

●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 (figure 1). The left bundle branch penetrates the membranous portion of the interventricular septum under the aortic ring and then divides into several fairly discrete branches, receiving most of its blood supply from the left anterior descending coronary artery (figure 2). (See 'Anatomy and electrophysiology' above.)

●Prevalence – The prevalence of LBBB, which appears to increase with age, has been estimated between 0.2 to 1.1 percent of the general population. (See 'Epidemiology' above.)

●Causes – Various clinical conditions are associated with the development of LBBB, although LBBB most commonly results not from a single clinical entity but rather from slowly progressive degenerative disease involving the conduction system. LBBB may result following an acute myocardial insult such as myocardial ischemia, myocardial infarction, or myocarditis. In addition, LBBB may be functional as a result of a long preceding R-R interval following by a short cycle ("rate-related bundle branch block"). (See 'Etiology' above.)

●ECG features – The ECG features of the QRS complex which define LBBB in adults include QRS duration greater than or equal to 120 ms; broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6; absent q waves in leads I, V5, and V6; R peak time greater than 60 ms in leads V5 and V6 but normal in leads V1, V2, and V3; and ST and T waves usually opposite in direction to QRS complex (waveform 1). (See 'ECG findings and diagnosis' above.)

●Impact on diagnosis of other conditions – LBBB interferes with the correct ECG-based diagnoses of ventricular hypertrophy, myocardial ischemia, and acute myocardial infarction. (See 'Impact of LBBB on the ability to diagnose other conditions' above.)

In patients with chest discomfort and LBBB, the diagnosis of acute myocardial ischemia or infarction may be delayed due to the challenges of interpreting the ECG changes. (See 'Patients with acute myocardial infarction' above.)

●Differential diagnosis – Ventricular rhythms and ventricular pacing, conditions in which the QRS complex has a similar morphology to LBBB, need to be excluded prior to making the diagnosis of LBBB. (See 'Differential diagnosis' above.)

●Prognosis – The prognosis in patients with LBBB is related largely to the type and severity of any concurrent underlying heart disease and to the possible presence of other conduction disturbances:

•Effect of age – Among asymptomatic patients, LBBB appears to have minimal effect on outcomes in younger, apparently healthy subjects, while LBBB in older individuals has been associated with an increase in mortality. (See 'Asymptomatic patients' above.)

•With coronary artery disease – LBBB is an independent predictor of all-cause mortality in patients with known or suspected coronary heart disease. The presence of LBBB is associated with higher short-term and long-term mortality following a myocardial infarction. (See 'Patients with coronary heart disease' above and 'Patients with acute myocardial infarction' above and "Overview of the acute management of ST-elevation myocardial infarction" and "Conduction abnormalities after myocardial infarction", section on 'Bundle branch block'.)

•With heart failure – LBBB is an independent risk factor for mortality in patients with heart failure and is associated with increased all-cause mortality and sudden death at one year. (See 'Patients with heart failure or cardiomyopathy' above.)

●Evaluation for concurrent conditions – When LBBB is present, patients should be evaluated for hypertension, coronary disease, and other disorders that have been associated with LBBB (eg, myocarditis, valvular heart disease, cardiomyopathies). In most patients, this can be accomplished with a careful history and physical examination. (See 'Evaluation' above.)

●Management

•If asymptomatic – For asymptomatic patients with an isolated LBBB and no other evidence of cardiac disease, no specific therapy is required.

•If develop symptomatic AV block – Permanent pacemaker insertion is indicated for patients with LBBB who develop symptomatic conduction system disturbances, such as third degree or type II second degree AV block, which is not associated with a reversible or transient condition. (See 'Treatment' above and "Permanent cardiac pacing: Overview of devices and indications".)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.