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Review: Mural thrombus after myocardial infarction increases risk for embolism and anticoagulant therapy is effective for reducing risks for thrombus and embolism

ACP J Club. 1994 Mar-April;120:34. doi:10.7326/ACPJC-1994-120-2-034

Source Citation

Vaitkus PT, Barnathan ES. Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol. 1993 Oct;22:1004-9.



To assess the risk for emboli associated with mural thrombus after anterior myocardial infarction (MI); the reduction in risk for emboli associated with mural thrombus after anticoagulation; and the effect of anticoagulation, thrombolytic therapy, and antiplatelet therapy for the prevention of mural thrombus formation.

Data sources

MEDLINE {(1980 to 1992) was searched using the key words myocardial infarction, thrombus, anticoagulation, stroke, and embolus}* and references of relevant studies were reviewed.

Study selection

English-language studies from peer-reviewed journals that included all patients or a subset of patients with an acute anterior Q-wave MI; used 2-dimensional echocardiography to identify left ventricular thrombus; and, for therapeutic trials, included a control group. Studies were excluded if they were published in abstract form or in books, had historical controls, or combined patients with anterior and inferior MIs.

Data extraction

Odds ratios (ORs) and event-rate differences for the association of emboli and mural thrombus, the reduction of emboli associated with mural thrombus after anticoagulation, and the reduction in rates of mural thrombus after anterior MI treated with anticoagulant therapy, thrombolytic therapy, and antiplatelet therapy.

Main results

11 studies with 856 patients evaluated the risk for emboli associated with mural thrombus. The pooled OR of increased risk for embolization was 5.45 (95% CI 3.02 to 9.83, event rate difference 0.09, CI 0.03 to 0.14), but there was heterogeneity in the results of the studies. 7 studies with 270 patients measured the reduction of risk for emboli associated with mural thrombi with anticoagulation therapy, showing a pooled OR of 0.14 (CI 0.04 to 0.52) and an event rate difference of -0.33 (CI -0.50 to -0.16). 4 studies with 307 patients showed that anticoagulation prevented mural thrombus formation (pooled OR 0.32, CI 0.20 to 0.52, event rate difference -0.19, CI -0.09 to -0.28). 6 studies with 390 patients showed that thrombolytic therapy prevented mural thrombus formation (pooled OR 0.48, CI 0.29 to 0.79, event rate difference -0.16, CI 0.10 to -0.42). 2 smaller studies with 112 patients did not show that antiplatelet therapy prevented mural thrombus formation.


Mural thrombus after acute, anterior Q-wave myocardial infarction increases the risk for embolism. The risk for embolism is reduced by anticoagulant therapy. Anticoagulation prevents mural thrombus formation, thrombolytic therapy may prevent mural thrombus formation, and evidence that antiplatelet therapy prevents mural thrombus formation is lacking.

Source of funding: Not stated.

For article reprint: Dr. P.T. Vaitkus, Cardiology Unit, Medical Center Hospital of Vermont, Burlington, VT 05401, USA. FAX 802-656-3637.

* Information supplied by author.


The meta-analysis by Vaitkus and Barnathan focuses on an important clinical question. Its strengths lie in reliance on 2-dimensional echocardiography to diagnose mural thrombi and in figures that effectively display the results of each study included in the analysis. Unfortunately, there was both clinical and statistical "heterogeneity" among the studies, which limits the confidence we can place in the odds ratios calculated from pooled data. The conclusions as stated, however, are reasonable.

This review helps us to come to several conclusions about clinical practice. First, because 11% of patients with anterior MI and mural thrombi had emboli compared with 2% of those without, and because systemic anticoagulation appears to prevent mural thrombi and emboli, there is evidence for using anticoagulation to prevent mural thrombus and, if a thrombus develops, to prevent embolization. Second, echocardiographic screening is not always accurate: 24% of emboli occur in patients without echocardiographically detectable thrombi.

Unfortunately, neither this review nor other sources provide enough information to support explicit guidelines for what to do. Clinicians must take many factors into account to decide whether and when to look for a mural thrombus and whether to begin or continue systemic anticoagulation. These factors include risk for thrombus formation and embolization (determined by factors such as extent and location of akinetic myocardium), response of myocardium to therapy (including thrombolysis and revascularization), risk for serious bleeding complications, and presence of other indications for anticoagulation (such as deep venous thrombosis, atrial fibrillation, or severe dilated cardiomyopathy).

Until reliable predictors of embolization are available, clinical judgment will have to suffice in the decisions about anticoagulation. If a decision is made to give anticoagulation for a mural thrombus or because of concern that one will form, full-dose heparin overlapping with warfarin (international normalized ratio goal of 2.0 to 3.0) for 3 months is a reasonable recommendation. It is not known whether adding low-dose aspirin as an antiplatelet agent confers more benefits than risks.

John T. Philbrick, MD
Ian J. Sarembock, MDUniversity of Virginia School of MedicineCharlottesville, Virginia, USA