Abstract Introduction Severe COVID-19 is associated with a profound hypercoagulable state, with venous thromboembolic disease (VTE) in up to one-third of critically ill patients. VTE is a life-threatening manifestation of COVID-19-associated coagulopathy, and right-atrial (RA) thrombi are a rare manifestation of this. We present a case of recurrent massive right atrial thrombosis within 24 hours of successful transesophageal echocardiographic (TEE) guided suction thrombectomy, highlighting the thrombotic potential of this condition and the uncertainty surrounding optimal prophylactic anticoagulation strategies in severe COVID-19 infection. Case Presentation 73-year-old man was admitted with acute hypoxemic respiratory failure secondary to severe COVID-19 pneumonia, requiring mechanical ventilation. On the fifth day of mechanical ventilation, persistent hypoxemia despite improved pulmonary infiltrates prompted further imaging with computed-tomography angiography (CTA) of the chest, which revealed acute pulmonary emboli involving the right upper, right lower, and left lower lobar pulmonary arteries. Anticoagulation was escalated from prophylactic to therapeutic dosing. Transthoracic echocardiography (TTE) demonstrated a large, mobile RA thrombus measuring 6.8 x 1.5 cm, protruding into the right ventricle Figure 1. Emergent TEE-guided suction thrombectomy achieved complete thrombus removal with visualization. One day later, repeat TTE demonstrated a recurrent massive RA thrombus. Duplex venous ultrasound revealed extensive thrombi in the right internal jugular, femoral, and external iliac veins. Given the refractory thrombotic disease, the patient’s family elected to transition to a comfort-oriented approach, and the patient passed shortly thereafter. Discussion This case demonstrates fulminant COVID-19-related coagulopathy characterized by rapid thrombus reformation despite suction thrombectomy and therapeutic anticoagulation. Management of mobile RA thrombi has shifted toward percutaneous suction thrombectomy as the preferred invasive approach, given its high success rate and reduced morbidity compared with surgical embolectomy or systemic thrombolysis. However, recurrence may occur when the underlying prothrombotic process persists; in this case, reflecting ongoing endothelial injury, inflammation, and coagulation cascade activation, theorized as the pathogenic mechanisms driving COVID-19 hypercoagulability. Efforts to mitigate this thrombotic drive have focused on optimizing prophylactic anticoagulation intensity during hospitalization. Several randomized trials investigated higher-dose heparin regimens to reduce the risk of VTE associated with COVID-19, with improved outcomes in non-critically ill patients, and no benefit among the critically ill. Current guidelines recommend standard or intermediate-dose prophylaxis in critically ill patients. However, this case highlights the limitations of current thrombophylactic strategies in the critically ill, and underscores the need for predictive markers to improve risk-stratification and identification of high-risk patients and guide personalized anticoagulation strategies in COVID-19-associated coagulopathy. This abstract is funded by: None
Ali et al. (Fri,) studied this question.