An Interesting Case of COVID-19 Induced Hypercoagulability Manifesting as Pulmonary Embolism and Apical Left Ventricular Thrombus

Introduction: Recent data demonstrates a strong correlation between COVID-19 and hypercoagulability with the spectrum of thromboembolic manifestations, including deep vein thrombosis and pulmonary embolism (PE). Here we present a unique case of COVID-19 associated hypercoagulability manifesting as both PE and apical left ventricular (LV) thrombosis in the absence of underlying coronary artery disease (CAD). Case: A 71-year-old female with a diagnosis of mild COVID-19 pneumonia presented with worsening fatigue, cough, shortness of breath, and chest heaviness on the thirteenth day of her illness. The patient was hypoxic on presentation requiring 3 L supplemental oxygen. Laboratory analysis showed an extremely high D-dimer level (greater than 20,000 ng/mL). Hence, computed tomography angiography of the chest was performed, showing evidence of right lower lobe segmental and subsegmental PE along with bilateral multifocal consolidation. Incidentally, the imaging demonstrated a filling defect within the apex of LV, transcending into further cardiac workup. Initial troponin was elevated at 0.04 ng/mL, and electrocardiogram showed sinus rhythm without any acute ST-T wave changes. Transthoracic echocardiography confirmed the presence of large, sessile, mobile, 1.3 x 2.1 cm LV thrombus but normal LV systolic function, ejection fraction, and no evidence of regional wall motion abnormalities. However, due to ongoing chest heaviness, the decision was made to perform a diagnostic left heart catheterization, which showed insignificant CAD. The patient received treatment with convalescent plasma, Remdesivir, and dexamethasone as per our institutional protocol and started on unfractionated heparin for anticoagulation. She was discharged on enoxaparin as per the patient's preference on a stable condition with close cardiology follow up. DiscussionLV thrombosis is a well-known complication of LV dysfunction associated with ischemic cardiomyopathy. While PE is an established phenomenon of COVID- 19 induced hypercoagulability, thrombus formation within the cardiac chamber is rarely reported. As cardiovascular complications such as acute myocardial injury, myocarditis, and cardiomyopathy are substantially reported in COVID-19, through this case report, we highlight the rare presentation of COVID 19 hypercoagulability with LV thrombus in the absence of predisposing cardiac conditions such as myocardial infarction or atrial fibrillation. Although the mechanism remains unclear, endothelial dysfunction eliciting local myocardial inflammation and blood stasis is a plausible explanation. Early recognition of LV thrombus and treatment with anticoagulation is of paramount importance to reducing stroke risk and systemic embolization. The detection of LV thrombus mandates anticoagulation with warfarin or heparin due to insufficient evidence to support the use of direct oral anticoagulants.