Introduction:

Acute myocardial infarction (MI) and non-ischemic cardiomyopathy may lead to the occurrence of left ventricular thrombus (LVT). The incidence of LVT is decreasing due to early reperfusion techniques. The more extensive the myocardial injury is, the higher the risk of developing LVT. Furthermore, patients with STEMI are more likely to have LVT(43%) compared to non-STEMI patients (5%). We report a rare case of LVT after non-STEMI.

Case presentation:

A 71-year-old female with a medical history of hypertension presented to the emergency department with typical chest pain. Vitals signs included regular tachycardia of 108beats/minute, blood pressure of 140/60 mmHg, respiratory rate of 18 breaths/minute, and oxygen saturation of 97% on room air. Physical exam revealed regular rate and rhythm without murmurs, gallops, and rubs. Jugular venous distention was not observed. An electrocardiogram showed ST depressions in the lateral leads. Troponin I was 2.1(positive > 0.1ng/ml). Transthoracic Echocardiogram (TEE) demonstrated apical hypokinesis and a large mobile irregular mass on the septal wall highly suspicious for left ventricular thrombus. A Transesophageal Echocardiogram demonstrated apical thrombus, diffuse hypokinesis, and an estimated ejection fraction of 35%. A new diagnosis of LVT related to non-STEMI was made. Systemic anticoagulation was initiated, followed by weight-based enoxaparin to achieve the goal of an international normalized ratio of 2.0 to 3.0 The patient was discharged with a scheduled outpatient follow-up to assess the elimination of LVT.

Discussion:

Myocardial infarction can lead to a unbalance of Virchow’s triad factors due to reduced ventricular motion, local myocardial injury, and hypercoagulability. Transthoracic and transesophageal echocardiograms have high specificity but low sensitivity in detecting LVT, however, cardiac magnetic resonance has the highest diagnostic accuracy. Current guidelines suggest management with vitamin K antagonist (VKA) for 3 to 6 months and are initially coadministered with parenteral anticoagulation due to its prothrombotic effect. However, the high risk of the embolic event remains after the resolution of LVT and potentially may lead to stroke, other cardiovascular events, and death. Direct oral anticoagulants can potentially be a safe and efficient alternative to VKA. However, there are no randomized controlled trials to confirm this.

Conclusion: LVT is a rare condition in reperfusion era. Although not expected, it can occur in patients with non-STEMI. This case highlights the existing lack of randomized trials to determine the type and duration of anticoagulant therapy for managing LVT.

References

1. Cruz Rodriguez JB, Okajima K, Greenberg BH. Management of left ventricular thrombus: a narrative review. Ann Transl Med. 2021 Mar;9(6):520.
2. Habash F, Vallurupalli S. Challenges in the management of left ventricular thrombus. TherAdv Cardiovasc Dis. 2017 Aug;11(8):203–13.
3. LV Thrombus After Acute MI [Internet]. American College of Cardiology. [cited 2022Mar 8]. Available from: https://www.acc.org/latest-in-cardiology//2018/05/15/15/45/left-ventricular-thrombus-after-acute-myocardial-infarction