Diagnosis
Echocardiography is the main diagnostic tool for LVT. A distinct mass is visible in the left ventricle. Computed Tomography and Magnetic Resonance Imaging are effective, but less common ways to detect LVT, due to their costs and risks. It is possible to assess whether a thrombus will become an embolus through echocardiography. Mobility and protrusion of the thrombus are two characteristics associated with increased embolic potential. Prevention
After an AMI, people should be treated to prevent LVT formation. Aspirin plus an oral anticoagulant such as warfarin are suggested for individuals at risk for thromboembolic events. Anticoagulants are also shown to reduce the risk of embolisms when a thrombus is already formed. Heparin, an injectable, fast-acting anticoagulant, is effective in high doses for preventing LVT formation after AMI. Treatment
Systemic anticoagulation is considered first-line medical therapy for LVT, as it reduces the risk of systemic embolism. There are also surgical procedures for removal of a thrombus (thrombectomy). Epidemiology
The rate of LVT formation after AMI is thought to be declining due to the use of better therapies and percutaneous coronary intervention used to treat myocardial infarction. In the modern era LVT formation after ST elevation MI treated with percutaneous coronary intervention is low, estimated at only 2.7%. However, incidence of LVT is considered higher in anterior wall AMI, compared with other types. References


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Benign hypertension or benign essential hypertension are historical terms that are considered misleading, as hypertension is never benign, and consequently they have fallen out of use (see history of hypertension). The terminology persisted in the International Classification of Disease (ICD9), but is not included in the current ICD10. == References ==