Review on LV Thrombus Following MI

 The following are key points to remember from this state-of-the-art review on left ventricular (LV) thrombus following myocardial infarction (MI):

1. LV thrombus after acute MI (AMI) has declined significantly since the introduction of reperfusion therapy. The current estimate is that LV thrombus occurs in up to 6.3% of patients with ST-segment elevation MI (STEMI) and 19.2% of patients with anterior wall STEMI complicated by LV ejection fraction <50%.
2. The imaging modality to detect LV thrombus greatly impacts the frequency of detection. Transthoracic echocardiogram (TTE) is inferior to cardiac magnetic resonance (CMR) imaging for detecting small, laminar LV mural thrombus. In fact, the sensitivity of TTE is only 29%, while the specificity is 98% as compared to CMR.
3. CMR is the optimal imaging modality for diagnosis of LV thrombus. It maintains a sensitivity of 82-88% and specificity approaching 100% compared to surgical and/or pathological confirmation. Use of late gadolinium enhancement improves thrombus detection over cine CMR.
4. Thromboembolic events caused by LV thrombi can be devastating. The risk of thromboembolism is most closely related to thrombus mobility and protrusion as described on imaging. The rate of thromboembolism varied between 3% in patients with consistently therapeutic anticoagulation and 19% in patients with poorly controlled anticoagulation.
5. Most LV thrombi can be detected by imaging within 2 weeks of AMI. High-risk patients without LV thrombus on early imaging (e.g., within 48 hours after AMI) should be reimaged 2 weeks after the acute event.
6. Virchow’s triad, which outlines the pathophysiology of thrombosis formation, applies to LV thrombus following AMI. Blood stasis from LV dysfunction and apical/anterior aneurysms is complicated by a hypercoagulable state from inflammation, elevated fibrinogen and neutrophils, platelet aggregation, and clotting cascade activation. This is further potentiated by tissue injury impacting the subendothelial tissue and exposing collagen.
7. Therapies to prevent and treat LV thrombus following AMI also target Virchow’s triad. Guideline-directed medical therapy addresses issues of blood stasis, while anticoagulation addresses hypercoagulability and reperfusion therapy ± anti-inflammatory therapy addresses tissue injury.
8. Prophylactic anticoagulation may be considered for patients with STEMI and anterior apical akinesis or dyskinesis. The 2013 American College of Cardiology/American Heart Association STEMI guidelines recommend use of a vitamin K antagonist (VKA) with a lower international normalized ratio (INR) target of 2.0-2.5. However, no prospective trial has examined the role of anticoagulation plus antiplatelet therapy in the modern percutaneous coronary intervention era.
9. For patients who have been diagnosed with LV thrombus following AMI, studies have produced conflicting results regarding the safety and efficacy of VKA versus direct oral anticoagulants (DOACs). The authors recommend the use of VKA with goal INR 2-3. DOAC should be used if VKA cannot be tolerated.
10. The authors recommend that repeat imaging be obtained after 3 months of therapy. If the LV thrombus has resolved, anticoagulation can be discontinued and dual antiplatelet therapy continued per management of AMI. If the LV thrombus is persistent, anticoagulation should continue with repeat imaging every 3 months. Once anticoagulation has been discontinued, repeat imaging 3 months later is advised.

Geoffrey D. Barnes, MD, MSc, FACC

10 March 2022