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[Left ventricular mural thrombus in acute anterior myocardial infarct]
Insights
Left-ventricular thrombi occurred in 25% of patients with acute anterior infarction, particularly those with apical and septal dyskinesis. Anticoagulation is recommended due to embolic risk.
Area of Science:
- Cardiology
- Internal Medicine
Context:
- Acute anterior myocardial infarction is a common cardiovascular event.
- Left-ventricular thrombosis is a known complication, but its incidence and associated factors require further elucidation.
Purpose:
- To determine the incidence and complications of left-ventricular thrombosis in patients with acute anterior infarction.
- To identify factors associated with thrombus development and evaluate treatment efficacy.
Summary:
- Fifty-six patients with acute anterior infarction underwent two-dimensional echocardiography.
- Left-ventricular thrombus was detected in 14 patients (25%) between 25-54 days post-infarction.
- Apical and septal dyskinesis and Forrester's hemodynamic subset-III were significantly associated with thrombus formation (P<0.02).
- Heparin or aspirin/dipyridamole did not significantly prevent thrombus formation.
- Thrombus persisted in 6 patients with persistent dyskinesis.
- Three patients experienced cerebrovascular accidents, one from the thrombus group.
Impact:
- Apical and septal dyskinesis are strong predictors of mural thrombi in acute anterior infarction.
- The findings underscore the embolic risk associated with left-ventricular thrombi.
- Therapeutic anticoagulation should be considered in these high-risk patients to mitigate cerebrovascular events.
Abstract:
Fifty-six consecutive patients with acute anterior infarction were studied by two-dimensional echocardiography to determine the incidence and complications of left-ventricular thrombosis. Mean follow-up period was 4.4 months. Left-ventricular thrombus was demonstrated in 14 patients (25%) between 25 and 54 days after infarction (group A), in 42 patients (group B) it was not demonstrated. Apical and septal dyskinesis, and Forrester's hemodynamic subset-III were significantly (P less than 0.02) associated with thrombus development. Ten patients of group A received heparin (6.6 days mean); the remaining four patients received aspirin and dipyridamole. Thrombi formation were not significantly prevented with both treatments (chi 2 = 0.635). During follow-up period, thrombus persisted in 6 patients of group A, all of them with apical and septal dyskinesis. Three patients had a cerebrovascular accident (5.3%), one of them of group A; no heparin anticoagulation was administered in two. We conclude that apical and septal dyskinesis during acute anterior infarction is generally associated with mural thrombi development. Due to the embolic risk therapeutic anticoagulation must be considered in these patients.