Management of Patients With LBB and Suspected MI
Management of Patients With LBB and Suspected MI
The intraventricular conduction system of the left ventricle is composed of fibers of the bundle of His that become the main left bundle branch and then divide into anterior and posterior fascicles, further branching to become the distal conduction system. In contrast to the right bundle branch, which is a discrete structure that can be injured acutely with a small focal insult, the left bundle branch is a large and diffuse structure that typically requires a large insult to lead to acute injury. When a new LBBB is caused by AMI, the site of infarction usually is anterior or anteroseptal, with the infarction involving a large myocardial territory. Inferior or posterior infarctions uncommonly may result in a new LBBB from involvement of the more proximal portion of the conduction system supplied by the atrioventricular nodal artery. However, most cases of LBBB in AMI are not a result of focal infarctions, because either a discrete lesion just distal to the bundle of His or extensive myocardial damage involving a large portion of the distal conduction system including both fascicles would be required to cause LBBB (Figure 1).
(Enlarge Image)
Figure 1.
Anatomy of the Left Bundle Branch
The left bundle branch comprises the main left bundle and distal anterior and posterior fascicles. Left bundle branch block (LBBB) resulting from an incident myocardial infarction requires a lesion just distal to the bundle of His (1) or extensive myocardial damage involving a large portion of the distal conduction system, including both fascicles (2 and 3).
Although LBBB can occur de novo in AMI, it is more often a pre-existing marker of underlying structural heart disease, and thus reflective of the patient's baseline cardiovascular risk. In these cases, LBBB may be the result of an aging or fibrotic conduction system, or both; chronic ischemic heart disease; left ventricular hypertrophy (most commonly from long-standing hypertension); adverse ventricular remodeling resulting from congestive heart failure; or valvular heart disease. It is not possible to determine the chronicity of LBBB without reviewing previous ECG tracings, because the onset of LBBB usually is asymptomatic. LBBB in AMI may be transient or permanent, although early accounts note that most cases of permanent LBBB were not the result of an acute transmural infarction, because true AMI-associated LBBB was associated with very high mortality.
Pathophysiology of LBBB in AMI
The intraventricular conduction system of the left ventricle is composed of fibers of the bundle of His that become the main left bundle branch and then divide into anterior and posterior fascicles, further branching to become the distal conduction system. In contrast to the right bundle branch, which is a discrete structure that can be injured acutely with a small focal insult, the left bundle branch is a large and diffuse structure that typically requires a large insult to lead to acute injury. When a new LBBB is caused by AMI, the site of infarction usually is anterior or anteroseptal, with the infarction involving a large myocardial territory. Inferior or posterior infarctions uncommonly may result in a new LBBB from involvement of the more proximal portion of the conduction system supplied by the atrioventricular nodal artery. However, most cases of LBBB in AMI are not a result of focal infarctions, because either a discrete lesion just distal to the bundle of His or extensive myocardial damage involving a large portion of the distal conduction system including both fascicles would be required to cause LBBB (Figure 1).
(Enlarge Image)
Figure 1.
Anatomy of the Left Bundle Branch
The left bundle branch comprises the main left bundle and distal anterior and posterior fascicles. Left bundle branch block (LBBB) resulting from an incident myocardial infarction requires a lesion just distal to the bundle of His (1) or extensive myocardial damage involving a large portion of the distal conduction system, including both fascicles (2 and 3).
Although LBBB can occur de novo in AMI, it is more often a pre-existing marker of underlying structural heart disease, and thus reflective of the patient's baseline cardiovascular risk. In these cases, LBBB may be the result of an aging or fibrotic conduction system, or both; chronic ischemic heart disease; left ventricular hypertrophy (most commonly from long-standing hypertension); adverse ventricular remodeling resulting from congestive heart failure; or valvular heart disease. It is not possible to determine the chronicity of LBBB without reviewing previous ECG tracings, because the onset of LBBB usually is asymptomatic. LBBB in AMI may be transient or permanent, although early accounts note that most cases of permanent LBBB were not the result of an acute transmural infarction, because true AMI-associated LBBB was associated with very high mortality.
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