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Updated: Aug 18, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction
Insights
Anterior wall myocardial infarction significantly increases the risk of left ventricular thrombosis, a condition linked to cerebrovascular accidents. Early diagnosis via echocardiography is crucial for managing this complication.
Area of Science:
- Cardiology
- Internal Medicine
Background:
- Left ventricular thrombosis is a known complication of myocardial infarction.
- Anterior wall myocardial infarction is associated with a higher risk of complications.
Purpose of the Study:
- To investigate the incidence and risk factors of left ventricular thrombosis in patients with acute myocardial infarction.
- To determine the association between left ventricular thrombosis and cerebrovascular accidents.
Main Methods:
- Prospective study of 90 consecutive patients with acute myocardial infarction.
- Cross-sectional echocardiography used to diagnose left ventricular thrombosis.
- Analysis of patient history, cardiac imaging, and clinical outcomes.
Main Results:
- Left ventricular thrombosis occurred in 28.3% of patients with anterior wall infarction, but none with inferior infarction.
- Four of five patients experiencing cerebrovascular accidents had pre-existing left ventricular thrombosis.
- Apical akinesis was present in all patients with left ventricular thrombosis.
Conclusions:
- Large anterior wall myocardial infarction with apical akinesis identifies patients at high risk for left ventricular thrombosis.
- Left ventricular thrombosis is a potential source of peripheral emboli, including cerebrovascular accidents.
- Left ventricular thrombosis is rare in myocardial infarctions located elsewhere.
Abstract:
In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations.
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