ReviewImplications of Left Bundle Branch Block in Patient Treatment
Section snippets
Anatomy and Electrocardiographic Recognition
Anatomically, the left bundle arises from the His bundle on the left endocardial side of the muscular septum.1 On rare occasions, when the His bundle lies on the right side of the interventricular septum, it might actually traverse through the septum.2 The proximal portion of the left bundle might vary in width, from 1 to 14 mm, a variability that is also influenced by the location of the His bundle in relation to the septum. The left bundle then broadens as it travels apically and divides into
Epidemiology and Natural History
LBBB is rare in those <50 years of age and almost never occurs in those <35 years of age, suggesting that it is an acquired disorder. In population studies, its prevalence increases steadily from <1% at age 50 to ∼6% by 80 years.8, 9 Factors that have been associated with its development include LV hypertrophy on the electrocardiogram, an increased cardiac volume, hypertension, valvular heart disease, cardiomyopathies, myocarditis, and coronary artery disease.9, 10, 11 Some, however, develop
Acute Myocardial Infarction
The prevalence of LBBB in patients who present to the emergency department with clinical suspicion for AMI is relatively low and varies from 1% to 9%.16, 17, 18 Furthermore, <50% of these patients actually have an occluded epicardial coronary artery and/or elevated biomarkers. Even in patients with LBBB who present with an occluded epicardial coronary artery, the LBBB often might not be caused by the AMI. It is very rare for an anterior AMI to cause complete LBBB, given the dual supply from
Left Ventricular Dyssynchrony
LBBB results in an altered pattern of LV activation and subsequent contraction. Under normal circumstances, impulse conduction spreads rapidly down the His bundle branches, followed by the Purkinje system and most of the LV endocardial surface is activated synchronously or within 40 ms. This results in efficient contraction at the expense of minimal energy. These dynamics are altered in the presence of LBBB, because conduction through the myocardium occurs at a slower pace than by the
Cardiac Resynchronization Therapy
Large, randomized, multicenter trials have shown symptom and mortality benefit with CRT in patients with advanced HF and LV dyssynchrony as measured by a prolonged QRS duration (Table 2).37, 38, 39, 40, 41, 42, 43, 44 Current guidelines give a class I recommendation for CRT for patients who have a LV ejection fraction of ≤35%, a QRS duration of ≥0.12 second, sinus rhythm, and New York Heart Association functional class III or ambulatory class IV HF symptoms with optimum recommended medical
Response to CRT
The success rate of transvenous placement of a LV lead has been ∼90% in major trials, and surgical implantation of the lead is required in the remaining patients.52 Approximately 70% of patients with successful transvenous lead placement show objective signs of improved cardiac function and hemodynamics. The patients who do not respond to CRT have been the subject of intense interest. The factors that have been associated with a favorable response to CRT include nonischemic cardiomyopathy,
Effect of LBBB on Stress Testing and Imaging
Stress electrocardiography alone has a poor diagnostic accuracy for detecting coronary artery disease in the presence of LBBB.60, 61 Hence, using an imaging modality is preferable according to the American College of Cardiology Appropriateness Criteria.62 The non-ST variables such as exercise time, work load, heart rate, and blood pressure responses remain useful in these patients as predictors of outcome, although not for detecting ischemia. Some of the studies60, 61, 63, 64, 65, 66, 67, 68
Disclosures
The authors have disclosed no conflicts of interest.
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2018, Journal of the American College of Cardiology
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