Left ventricular (LV) thrombus is typically a result of stasis from myocardial hypokinesis/akinesis. A segment of myocardium stops moving, blood lingers in the cul-de-sac of an akinetic apex, and the endocardial surface becomes a scaffold for clot. Large anterior infarctions, end-stage heart failure, and dilated ventricles can set the stage for stasis, injury, and time to promote thrombus formation.
An LV thrombus may be asymptomatic until it starts showering emboli to the periphery, causing strokes, acute limb ischemia, renal infarction, etc. Standard transthoracic echocardiography can struggle to visualize the true apex of the LV (especially when it is heavily trabeculated), so contrast echo often provides the necessary clarity by demonstrating a filling defect (see the asterisk labeled in the video). Cardiac MRI remains the most reliable option when imaging is ambiguous.
Treatment is centered around anticoagulation stratified to bleeding risk and guided by follow-up imaging. Coumadin has the longest track record (especially in post-infarct thrombus), but direct oral anticoagulants are increasingly used when the patient profile makes them attractive and the tradeoffs are acceptable. A practical target is three to six months with repeat imaging to confirm resolution, and longer if the thrombus persists or the ventricle remains severely dysfunctional.
Here are some PubMed IDs to review the data: 36106537, 25913472, 21757159, 34387565, 33517885
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