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Diagnosis: Left Ventricular Aneurysm

Brady, William J. MD; Harrigan, Richard A. MD; Chan, Theodore MD

Cases in Electrocardiography

Dr. Brady is an associate professor and the program director in the department of emergency medicine at the University of Virginia School of Medicine in Charlottesville, Dr. Harrigan is an associate professor of emergency medicine and the associate research director in the department of emergency medicine at Temple University Hospital and School of Medicine in Philadelphia, Dr. Chan is an associate professor of clinical medicine, emergency medicine, the director of CQI, and the associate medical director of the department of emergency medicine at the University of California, San Diego.

Left ventricular (LV) aneurysms are a not infrequent complication of large, anterior wall ST segment elevation myocardial infarction. LV aneurysm is defined by a dyskinetic segment of the left ventricle with persistent outward bulging of the segment during the entire cardiac cycle, both systole and diastole. Patients who develop LV aneurysm include those with completed, large myocardial infarction, particularly in individuals with resultant LV dysfunction manifested by ejection fractions less than 50%. In fact, approximately 60 percent of patients with completed myocardial infarction who manifest persistent ST segment abnormality will demonstrate ventricular aneurysm at cardiac catheterization or echocardiography.

The incidence of LV aneurysm depends on the diagnostic investigation used for diagnosis. At coronary angiography, LV aneurysm is seen in approximately eight percent of post-MI patients. Autopsy examination demonstrates an incidence of three percent to 15 percent of myocardial infarction patients who do not survive the initial event. (Am J Cardiol 1982;50:157.) The vast majority of LV aneurysms result from myocardial infarction although other etiologies are encountered, including blunt chest injury with myocardial contusion, Chagas disease, and cardiac sarcoidosis. Pathologically, the aneurysm is characterized by transmural fibrosis, clearly delineated from and markedly thinner than the adjacent myocardium. (Hurst's The Heart. New York, McGraw-Hill, 1998.) Associated post-mortem cardiopulmonary findings include significant multi-vessel coronary artery disease, scarred papillary muscle, pulmonary edema, pericardial thickening, and mural thrombi.

The electrocardiographic characteristics of LV aneurysm include ST segment elevation, T wave abnormality, and Q waves. LV aneurysm is characterized electrocardiographically by persistent ST segment elevation for days to weeks after MI. In fact, the majority of post-MI cases of persistent ST segment elevation are due to ventricular aneurysm. The ST segment elevation varies in magnitude and morphology. Typically, the magnitude of the elevation ranges from 1 to 3 mV; less often, elevations greater than 3 mV are encountered. The morphology of the elevated ST segment varies from concave to nonconcave with both convex and obliquely straight varieties. The ST segment elevation itself ranges in appearance from the benign, minimally displaced, concave elevation to more ominous, pronounced, convex ST segment elevation (Figures 2 and 3). Among ED patients with ST segment elevation, LV aneurysm is an uncommon cause of the ST segment abnormality, accounting for only three percent to four percent of all patients with ST segment elevation seen in the ED population. (Am J Emerg Med 2001;19:25; Acad Emerg Med 2001;8:961.)

The T wave is usually diminished in height, flattened, or inverted, all findings of a past myocardial infarction (Figures 2 and 3). Of course, prominent Q waves also are seen in the same anatomic distribution. Most often, QS complexes (Figures 2 and 3) are seen, though other QRS complex morphologies are possible, including QR complexes. The relationship of the T wave to the QRS complex has recently been described by Smith who noted a T wave to QRS complex ratio less than 0.36 in patients with LV aneurysm (Figures 2, 3, and 4). (Smith SW. T-wave amplitude to QRS amplitude ratio best distinguishes the ST elevation of anterior LV aneurysm from anterior acute myocardial infarction. Presented at the 2003 Society for Academic Emergency Medicine meeting.) This ratio is an important finding because it shows the first and so far only objective electrocardiographic description of LV aneurysm. This ratio makes use of the appearance of the prominent T wave seen in early ST segment elevation AMI presentations. The T wave is relatively larger compared with the QRS complex while in completed infarction with resulting aneurysm, the T wave is diminished, thereby reducing the ratio (Figure 4).

Fig. 3

Fig. 3

Fig. 4

Fig. 4

While ST segment elevation, diminished T waves, and prominent QS complexes are the most frequent electrocardiographic findings of LV aneurysm, ST segment depression also are seen. ST segment depression can be seen in lead aVl in the patient with inferior wall LV aneurysm, but caution is advised in attributing this ST segment depression as reciprocal change of ST segment elevation AMI in inferior ST segment elevation.

The anatomic location of the electrocardiographic change in LV aneurysm is most frequently anterior or anterolateral, and as such, ST segment elevation is usually seen in leads V1 to V6. Inferior, lateral, and posterior LV aneurysm also are encountered with ST segment elevation in leads II, III, and aVf, leads I, aVl, V5, and V6, and leads V8 and V9, respectively. The magnitude of the ST segment elevation is usually greatest in the precordial leads and least in the limb leads. Approximately three-quarters of LV aneurysms involve the anterior wall. (Heart Disease. Philadelphia, W.B. Saunders Co., 1997.) Inferior and posterior wall aneurysms are seen yet are much less common.

The electrocardiographic findings of LV aneurysm are static. These changes will not change over time compared with the often dynamic abnormalities of acute coronary syndrome. The clinician therefore can use serial ECGs or ST segment trend monitoring for the continued surveillance of the elevated ST segment.

The ECG is of limited value in establishing the diagnosis of LV aneurysm. Rather, the diagnosis is most appropriately made by an analysis of the history (past MI) and physical examination (evidence of congestive heart failure). The results of imaging studies, such as echocardiography or coronary angiography, are of more use in this situation. These studies can demonstrate the anatomic and functional features of LV aneurysm. For example, echocardiography has a sensitivity and specificity of 93% and 94%, respectively, for detecting LV aneurysm, representing the most frequent and easily applied test for such an anatomic abnormality. Coronary angiography, however, remains the gold standard for the diagnosis.

With continued therapy, the patient's pain resolved. The ECG did not reveal any change with the pain-free status. An ECG from a past visit revealed no change, including the ST segment changes in the anterior leads. The ECG analysis, including the current findings, serial ECG analysis, and past comparisons, suggested a non-STEMI cause of the ST segment elevation, likely a left ventricular aneurysm. Cardiology consultation was requested. An echocardiogram demonstrated an aneurysm of the anterolateral wall; no other wall motion abnormalities were found. No significant coronary lesions were seen at cardiac catheterization. Serial cardiac serum markers were not elevated. The patient was ultimately discharged with the diagnoses of unstable angina and past left ventricular aneurysm.

© 2006 Lippincott Williams & Wilkins, Inc.