Background

• Post-MI LV thrombus is a complication of MI that is relatively common (up to 15% in the era of PCI)
• optimal antistrategies are uncertain given that newer evidence suggests that double therapy is better than triple therapy

Epidemiology

• LV thrombus incidence
  • in the era of thrombolysis, LV thrombus present in 17% of patients after acute MI, higher (up to 57% in anterior MI)
  • slightly decreased incidence with PCI - 15% in all STEMI patients and 25% in those with anterior MI
  • CMR has higher sensitivity and TTE may miss a significant number of LV thrombi
• Systemic embolism incidence
  • approx 9%
  • 33% RRR with anticoagulation

Pathogenesis

• Virchow triad post MI
  • LV dyskinesis/akinesis with blood stasis
  • subendothelial tissue injury leads to persistent hyperocoagulable state for ~6 months
• resultant LV thrombus is fibrin-rich, platelet-rich

Management

Diagnosis

Standard TTE is typically the screening modality of choice and should be performed within 24 hours of admission in those at high risk for apical LV thrombus (eg, those with large or anterior MI or those receiving delayed reperfusion). If (1) the LV apex is poorly visualized, (2) anterior or apical wall motion abnormalities are present, or (3) high apical wall motion scores are calculated (≥5 on noncontrast TTE), contrast TTE or CMR should be considered based on local availability and resources

• TTE is the most common diagnostic modality for LV thrombus
  • LV thrombus presents as echodense mass with distinct margins from endocardium
  • can be highly mobile, protruding into the ventricular cavity (new), or smooth cavitary surface and more static (older)
  • can develop calcification or central cavitation
  • suspect LV thrombus contiguous to LV wall akinesis/dyskinesis, especially with larger infarct size or reduced LVEF (<40%)
  • overall, TT has specificity 95-95% but sensitivity only 21-35%. Sensitivity improved to 64% with IV contrast.
• TEE has limited use in the diagnosis of LV thrombus because the apex is not often well visualized
• CMR is the most accurate modality for diagnosis of LV thrombus
  • sensitivity 82-88% and specificity 99-100%
• Pathways have been developed that use infarct size/RMWA scores to determine who would benefit from CMR, but these are not widely validated
• algorithm below:
  • (1) TTE
  • (2) if poor visualization of apex or (+) apical akinesis/dyskinesis then perform contrast TTE or CMR
  • (3) repeat imaging in 3 months if there is apical akinesis/dyskinesis

Prevention

• There are no dedicated RCTs addressing prevention of LV thrombus post-MI.
• Guidelines kind of discuss this:
  • 2013 ACC/AHA STEMI -- consider OAC in STEMI with anterior apical akinesis/dyskinesis
  • 2014 AHA/ASA -- consider OAC for 3/12 in acute anterior STEMI and ischemic stroke or TIA with anterior apical akinesis/dyskinesis
  • 2017 ESC STEMI -- no discussion on this topic
• Recent observational data suggest no benefit to anticoagulation in the prevention of LV thrombus.
• The COMMANDER-HF trial may provide more clarity on the prophylactic use of low-dose OAC in patients with severe LV dysfunction; however, until further data are available, the role of OAC, even at lower doses, in at-risk patients during this period of serial imaging is uncertain.

Treatment

In patients with a diagnosed LV thrombus, OAC should be started immediately. * No specific RCTs to address this. However, given similar pathophysiology to LAA thrombus in atrial fibrillation, similar considerations re: post-PCI AF thromboembolic ppx (dual therapy > triple therapy) can be argued for. Guidelines recommend the following:
* 2013 ACCF/AHA STEMI guidelines advise that it is reasonable to add OAC to dual antiplatelet therapy among patients with STEMI and asymptomatic LV thrombus for 3 months, targeting a lower international normalized ratio (INR) goal of 2.0-2.5. * AHA/American Stroke Association 2014 stroke prevention guidelines recommend a similar duration, targeting a higher INR of 2.5. * European Society of Cardiology 2017 STEMI guidelines advised that once an LV thrombus is diagnosed, OAC should be considered for up to 6 months, guided by repeated echocardiography and with consideration of bleeding risk and need for concomitant antiplatelet therapy. * Diagnosis of LV thrombus made? * Warfarin-based approach
* bridge with parenteral anticoagualant until therapeutic INR (2-3) is achieved for 24 hours * DOAC-based approach * dabigatran/edoxaban - bridge with 5 days of parenteral anticoagulation * apixaban/rivaroxaban - loading doses and then step down, similar to VTE Rx * Hepatin-based approach * used for large or highly mobile LV thrombi * consider dual therapy (OAC + P2Y12 inhibitor) over triple therapy (OAC + DAPT) based on studies in post-PCI + AF patients such as RE-DUAL PCI, AUGUSTUS, etc. * Duration of Antithrombotic Therapy * minimum of 3 months of double therapy * repeat imaging at 3 months * if LV thrombus resolved, then transition to DAPT for post-MI treatment * if lV thrombus not resolved, then the optimal duration is NOT known and should be individualized * Gastric Protection and Bleeding Reduction * unknown, pending COMPASS study results * reasonable to treat all patients with PPI therapy while on combination antithrombotic regimens

References

1. McCarthy CP, Vaduganathan M, McCarthy KJ, Januzzi JL Jr, Bhatt DL, McEvoy JW. Left Ventricular Thrombus After Acute Myocardial Infarction: Screening, Prevention, and Treatment. JAMA Cardiology. 2018;3(7):642-649. doi:10.1001/jamacardio.2018.1086