Left ventricular thrombus (LVT) is a frequent complication in patients with acute anterior myocardial infarction (MI) and in those with dilated cardiomyopathy (DCM). The clinical importance of LVT lies in its potential to embolize. The current treatment of patients with acute MI centers on reperfusion, and although controversial, the incidence of LVT complicating acute anterior MI is probably reduced when compared with historical controls. Nevertheless, stroke continues to be a clinically important complication of acute MI and is most common in patients with anterior MI, in part secondary to embolization of LVT. Therapeutic anticoagulation during acute MI reduces the incidence of LVT, and long-term anticoagulation has been associated with a reduction in recurrent infarction and ischemic stroke, but carries hemorrhagic risk. Primary treatment strategies for patients with acute MI center on reperfusion therapy followed by antiplatelet agents and pharmacologic blockade of abnormal neurohumoral mechanisms. Strategies to prevent stroke following infarction include risk stratification for development of LVT and embolism. For patients with anterior MI, particularly those with apical akinesis or dyskinesis, therapeutic anticoagulation reduces the number of LVT and cardioembolic strokes. However, the absolute number of ischemic strokes prevented with this strategy may only be marginal, given the anticoagulation risk, particularly if antiplatelet agents are used concurrently. An attractive alternative strategy is echocardiographic evaluation following anterior infarction with therapeutic anticoagulation reserved for those with demonstrable thrombus. The efficacy of this strategy, however, never has been proven in a clinical study. Primary prevention of cardioembolic stroke through therapeutic anticoagulation is controversial in patients with DCM; the greatest benefit would be expected for those with severe left ventricular dysfunction. If LVT is detected during the course of MI or DCM, therapeutic anticoagulation is usually indicated with the expectation that the majority of thrombi will resolve without clinical evidence of systemic embolism. Additional therapeutic intervention is rarely needed.
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