# Right Atrial Appendage Thrombus as a Rare Source of Pulmonary Embolism: Multimodality Imaging and Clinical Implications

## TL;DR

A rare case of a right atrial appendage thrombus causing pulmonary embolism is described, highlighting the importance of advanced imaging and anticoagulation for effective treatment.

## Contribution

This case emphasizes the under-recognized role of right atrial appendage thrombi as a source of pulmonary embolism and the diagnostic value of multimodality imaging.

## Key findings

- Right atrial appendage thrombus was identified as the source of pulmonary embolism using transesophageal echocardiography and cardiac MRI.
- Anticoagulation therapy effectively resolved the thrombus and improved patient outcomes.
- The case suggests a multifactorial prothrombotic state involving brucellosis and lupus anticoagulant.

## Abstract

Right atrial appendage (RAA) thrombus is an uncommon but clinically significant source of pulmonary embolism (PE). Unlike left atrial appendage thrombi, which are well described, RAA thrombi remain under-recognized and may present with life-threatening embolic complications. Multimodality imaging plays a critical role in establishing the diagnosis and guiding management. We describe the case of a 32-year-old male soldier with a one-month history of fever, cough, and weight loss following recent dental infections. He presented as hemodynamically stable but with anemia, leukocytosis, and elevated inflammatory markers. Contrast-enhanced chest CT revealed bilateral pulmonary emboli. Transthoracic echocardiography (TTE) was unremarkable, but transesophageal echocardiography (TEE) demonstrated a large, mobile thrombus (20×17 mm) in the RAA. Cardiac magnetic resonance imaging (CMR) confirmed the mass as thrombus and documented marked regression with anticoagulation. Laboratory evaluation showed a positive lupus anticoagulant and strongly positive Brucella melitensis serology (>1:640). The patient was treated with intravenous heparin and transitioned to warfarin, alongside antibiotics targeting brucellosis. His symptoms resolved, and repeated imaging confirmed thrombus resolution. This case highlights the importance of suspecting RAA thrombus in patients with unexplained PE, especially when standard imaging such as transthoracic echocardiography is unrevealing. Multimodality imaging with TEE and CMR provided a definitive diagnosis and follow-up assessment. The coexistence of brucellosis and a positive lupus anticoagulant suggests a multifactorial prothrombotic state. Current evidence lacks consensus on the optimal management of right heart thrombi; however, anticoagulation was effective in this case. RAA thrombus is a rare but potentially fatal cause of pulmonary embolism. Prompt recognition, identification of underlying etiologies such as infection or antiphospholipid antibodies, and timely anticoagulation are essential to prevent recurrence and improve outcomes.