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Left ventricular thrombus after acute myocardial infarction

Warren J Manning, MD
Neil J Weissman, MD
Section Editor
Scott Solomon, MD
Deputy Editor
Gordon M Saperia, MD, FACC


Left ventricular (LV) thrombus is one of the more common complications of myocardial infarction (MI). Thrombus development is important because it can lead to arterial embolic complications such as stroke. Patients with LV thrombus, or those at high risk, should receive anticoagulation for at least three months.

This topic will focus on the diagnosis of LV thrombus and the prevention of embolic complications. Other complications of MI such as arrhythmias, cardiogenic shock, and mechanical complications are discussed separately. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction" and "Supraventricular arrhythmias after myocardial infarction" and "Conduction abnormalities after myocardial infarction" and "Mechanical complications of acute myocardial infarction".)

Other causes of arterial emboli are presented elsewhere. (See "Overview of acute arterial occlusion of the extremities (acute limb ischemia)", section on 'Arterial emboli'.)


Formation — The likelihood of developing a left ventricular (LV) thrombus after an acute myocardial infarction (MI) varies with infarct location and size. LV thrombus is most often seen in patients with large anterior ST-elevation MI (STEMI) with anteroapical aneurysm formation; the incidence is lower with smaller infarctions and those involving other myocardial regions [1-11].

These anterior infarcts have large areas of poorly contracting LV muscle; adjacent intracavitary blood movement is sluggish compared to normal areas. This relative stasis of blood is thought to increase the risk of thrombus formation. An LV aneurysm and a mural thrombus have been identified in autopsy or surgery in more than 50 percent of these patients. Two factors contribute to clot formation in this setting: stasis of flow in the aneurysm cavity and contact of blood with the fibrous tissue in the aneurysm rather than normal endocardium. (See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction", section on 'Systemic embolization'.)


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Literature review current through: Jun 2016. | This topic last updated: Mar 24, 2014.
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