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Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by
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Patients with anterior myocardial infarction and severe apical wall motion abnormalities face a high risk of left-ventricular thrombosis. Early identification of this risk group is possible through echocardiography.
Area of Science:
- Cardiology
- Medical Imaging
Background:
- Left-ventricular thrombosis is a potential complication following myocardial infarction.
- Transmural myocardial infarction can lead to significant cardiac wall motion abnormalities.
Purpose of the Study:
- To determine the incidence of left-ventricular thrombosis after transmural myocardial infarction.
- To identify patient subgroups at high risk for developing left-ventricular thrombi.
Main Methods:
- Serial two-dimensional echocardiography was performed in 70 consecutive patients post-myocardial infarction.
- Echocardiographic findings, including wall-motion abnormalities, were correlated with the presence of left-ventricular thrombi.
Main Results:
- Left-ventricular thrombi were observed in 12 of 35 patients (34%) with anterior-wall infarction, but none in 35 patients with inferior-wall infarction.
- All patients with left-ventricular thrombi exhibited severe apical-wall-motion abnormalities (akinesis or dyskinesis).
- Among anterior infarction patients with severe apical akinesis/dyskinesis, 46% developed left-ventricular thrombi.
Conclusions:
- Severe apical-wall-motion abnormalities during acute transmural anterior myocardial infarction indicate a high risk for left-ventricular thrombosis.
- This high-risk group can be identified prospectively using echocardiography.
- Patients with inferior infarction or anterior infarction without severe apical dysfunction are at low risk.
Abstract:
To study the incidence of left-ventricular thrombosis after transmural myocardial infarction, we performed serial two-dimensional echocardiography in 70 consecutive patients. Thirty-five patients had inferior-wall infarction: none had a left-ventricular thrombus. The other 35 had anterior-wall infarction: 12 had left-ventricular thrombi. Thrombi were diagnosed an average of five days after the infarction (range, one to 11 days). All patients with left-ventricular thrombi had severe apical-wall-motion abnormalities (akinesis or dyskinesis). Twenty-six of the 35 patients with anterior infarctions had apical akinesis or dyskinesis on echocardiography; left-ventricular thrombi developed in 12 of these 26 (46 per cent). We conclude that patients with severe apical-wall-motion abnormalities during acute transmural anterior myocardial infarction are at high risk for left-ventricular thrombosis. This high-risk group can be identified before the development of left-ventricular thrombi. Patients with inferior infarction or anterior infarction without a severe apical-wall-motion abnormality are at low risk.