Acute myocardial infarction—Part IIBMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7343.963 (Published 20 April 2002) Cite this as: BMJ 2002;324:963
- June Edhouse,
- William J Brady,
- Francis Morris
This article describes the association of bundle branch block with acute myocardial infarction and the differential diagnosis of ST segment elevation.
Bundle branch block
Acute myocardial infarction in the presence of bundle branch block carries a much worse prognosis than acute myocardial infarction with normal ventricular conduction. This is true both for patients whose bundle branch block precedes the infarction and for those in whom bundle branch block develops as a result of the acute event. Thrombolytic treatment produces dramatic reductions in mortality in these patients, and the greatest benefits are seen in those treated early. It is therefore essential that the electrocardiographic identification of acute myocardial infarction in patients with bundle branch block is both timely and accurate.
Left bundle branch block
Left bundle branch block is most commonly seen in patients with coronary artery disease, hypertension, or dilated cardiomyopathy. The left bundle branch usually receives blood from the left anterior descending branch of the left coronary artery and from the right coronary artery. When new left bundle branch block occurs in the context of an acute myocardial infarction the infarct is usually anterior and mortality is extremely high.
The electrocardiographic changes of acute myocardial infarction can be difficult to recognise when left bundle branch block is present, and many of the conventional diagnostic criteria are not applicable.
Abnormal ventricular depolarisation in left bundle branch block leads to secondary alteration in the recovery process (see earlier article about bradycardias and atrioventricular conduction block). This appears on the electrocardiogram as repolarisation changes in a direction opposite to that of the main QRS deflection—that is, “appropriate discordance” between the QRS complex and the ST segment.
Thus leads with a predominantly negative QRS complex show ST segment elevation with positive T waves (an appearance similar to that of acute anterior myocardial infarction).
Recognition of acute ischaemia
Many different electrocardiographic criteria have been proposed for identifying acute infarction in left bundle branch block, but none has yet proved sufficiently sensitive to be useful in the acute setting. However, some features are specific indicators of acute ischaemia.
ST segment elevation in association with a positive QRS complex, or ST segment depression in leads V1, V2, or V3 (which have predominantly negative QRS complexes), is not expected in uncomplicated left bundle branch block and is termed “inappropriate concordance.”
Inappropriate concordance strongly indicates acute ischaemia. Extreme ST segment elevation (5 mm) in leads V1 and V2 also suggests acute ischaemia. If doubt persists, serial electrocardiograms may show evolving changes.
Right bundle branch block
Right bundle branch block is most commonly seen in association with coronary artery disease, but in many cases no organic heart disease is present. Uncomplicated right bundle branch block usually causes little ST segment displacement and neither causes nor masks Q waves. Thus it does not generally interfere with the diagnosis of acute myocardial infarction, though it may mask a posterior myocardial infarction.
The Brugada syndrome, which is familial, occurs particularly in young men and is characterised by right bundle branch block and ST segment elevation in the right precordial leads. There is a high incidence of death as a result of ventricular tachyarrhythmias
Differential diagnosis of ST segment elevation
ST segment elevation has numerous possible causes. It may be a variant of normal or be due to cardiac or non-cardiac disease. A correct diagnosis has obvious advantages for the patient but is also particularly important before the use of thrombolytic treatment so that unnecessary exposure to the risks of thrombolytic drugs can be avoided.
Causes of ST segment elevation
Acute myocardial infarction
Benign early repolarisation
Left bundle branch block
Left ventricular hypertrophy
Coronary vasospasm/Printzmetal's angina
The interpretation of ST segment elevation should always be made in the light of the clinical history and examination findings. There are often clues in the electrocardiogram to differentiate the ST segment elevation of acute ischaemia from other causes; for example, reciprocal changes (see last week's article) may be present, which strongly indicate acute ischaemia. Serial electrocardiography or continuous ST segment monitoring is also useful as ischaemic ST segment elevation evolves over time. Old electrocardiograms are also useful for comparison.
Care is required when interpreting ST segment elevation in right sided chest leads as the ST segments, particularly in leads V2 and V3, tend to be upsloping rather than flat. Isolated ST segment elevation in these leads should be interpreted with caution. (For more information on “high take-off” see the second article in this series.)
Benign early repolarisation
A degree of ST segment elevation is often present in healthy individuals, especially in young adults and in people of African descent. This ST segment elevation is most commonly seen in the precordial leads and is often most marked in lead V4. It is usually subtle but can sometimes be pronounced and can easily be mistaken for pathological ST segment elevation.
Benign early repolarisation can be recognised by its characteristic electrocardiographic features: elevation of the J point above the isoelectric line, with high take-off of the ST segment; a distinct notch at the junction of the R wave and S wave, the J point; an upward concavity of the ST segment; and symmetrical, upright T waves, often of large amplitude.
Antecedent myocardial infarction
The ST segment elevation associated with acute infarction usually resolves within two weeks of the acute event, but it may persist indefinitely, especially when associated with anterior myocardial infarction. In these patients a diagnosis of left ventricular aneurysm should be considered. Care should be taken when interpreting the electrocardiogram within two weeks of an acute event, and comparison with old electrocardiograms may be useful.
Acute pericarditis is commonly mistaken for acute myocardial infarction as both cause chest pain and ST segment elevation. In pericarditis, however, the ST segment elevation is diffuse rather than localised, often being present in all leads except aVR and V1. The elevated ST segments are concave upwards, rather than convex upwards as seen in acute infarction. Depression of the PR segment may also be seen.
ST segment elevation in pericarditis is thought to be due to the associated subepicardial myocarditis. The zone of injured tissue causes abnormal ST vectors; the end result is that leads facing the epicardial surface record ST segment elevation, whereas those facing the ventricular cavity (leads aVR and V1) record ST segment depression. The absence of widespread reciprocal change, the presence of PR segment depression, and absence of Q waves may be helpful in distinguishing pericarditis from acute myocardial infarction.
Other causes of ST segment elevation
The characteristic features of left ventricular hypertrophy are also often misinterpreted as being caused by acute ischaemia. ST segment elevation in the precordial leads is a feature of left ventricular hypertrophy and is due to secondary repolarisation abnormalities.
ST segment abnormalities are seen in association with intracranial (particularly subarachnoid) haemorrhage. ST segment elevation or depression may be seen; a putative explanation is that altered autonomic tone affects the duration of ventricular repolarisation, producing these changes.
Printzmetal's angina (vasospastic angina) is associated with ST segment elevation. As the changes are due to coronary artery spasm rather than acute infarction, they may be completely reversible if treated promptly. ST segment abnormalities may be seen in association with cocaine use and are probably due to a combination of vasospasm and thrombosis.
The ABC of clinical electrocardiography is edited by Francis Morris, consultant in emergency medicine at the Northern General Hospital, Sheffield; June Edhouse, consultant in emergency medicine, Stepping Hill Hospital, Stockport; William J Brady, associate professor, programme director, and vice chair, department of emergency medicine, University of Virginia, Charlottesville, VA, USA; and John Camm, professor of clinical cardiology, St George's Hospital Medical School, London. The series will be published as a book in the summer.