Left ventricular thrombus after acute myocardial infarction
- Gregory YH Lip, MD, FRCPE, FESC, FACC
Gregory YH Lip, MD, FRCPE, FESC, FACC
- Professor of Cardiovascular Medicine
- The University of Birmingham, UK
- Warren J Manning, MD
Warren J Manning, MD
- Section Editor — Noninvasive Cardiac Imaging and Stress Testing
- Professor of Medicine and Radiology
- Harvard Medical School
- Neil J Weissman, MD
Neil J Weissman, MD
- Professor of Medicine
- Georgetown University School of Medicine
The development of left ventricular (LV) thrombus is an important complication of myocardial infarction and occurs most often with ST-elevation myocardial infarction. However, the use of reperfusion therapies, including percutaneous coronary intervention or fibrinolysis, has significantly reduced the risk. LV thrombus can lead to arterial embolic complications such as stroke. Patients found to have an LV thrombus, or those at high risk, should receive warfarin anticoagulation for at least three months.
This topic will discuss LV thrombus in detail. Other potential causes of arterial emboli originating in the heart are presented elsewhere. (See "Overview of acute arterial occlusion of the extremities (acute limb ischemia)", section on 'Arterial emboli' and "Secondary prevention for specific causes of ischemic stroke and transient ischemic attack", section on 'Cardiogenic embolism'.)
Left ventricular (LV) thrombus is most often seen in patients with large anterior ST-elevation myocardial infarction with anteroapical aneurysm formation. In most cases, these infarcts occur in the distribution of the left anterior descending coronary artery . These anterior infarcts have large areas of poorly contracting LV muscle; adjacent intracavitary blood movement is sluggish (stasis) compared with normal areas. This relative stasis of blood is thought to increase the risk of thrombus formation. Many, but not all, of these patients will have an LV apical aneurysm with akinesis or dyskinesis. In most cases, thrombus is located within or adjacent to the LV apex  but can also occur with large inferolateral infarctions/aneurysms. Contact of blood with the fibrous tissue in the aneurysm rather than normal endocardium is also thought to trigger clot formation. (See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction", section on 'Systemic embolization'.)
Based on the pathophysiology of the development of left ventricular (LV) thrombus, the following are clinical risk factors:
●Anterior ST-elevation myocardial infarction by electrocardiographic criteria. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Anterior, lateral, and apical MI'.)
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