Resolution of Ascending Aorta and Pulmonary Vein Thrombi With Apixaban Therapy: A Case Study

This study aimed to investigate ascending aorta (AAo) thrombi and the effects of apixaban using transesophageal echocardiography (TEE) and cardiac computed tomography (CT).

Studies of thrombi retrieved from acute ischemic stroke (AIS) patients revealed that those thrombi contained collagen and calcifications, indicating that the thrombi were chronic or old. These patients had chronic thrombi before AIS occurred, and some of the thromboemboli could separate from chronic thrombi and cause AIS. Left atrial appendage (LAA) thrombi in atrial fibrillation (AF) patients are candidates for such chronic thrombi; however, patients without LAA thrombi may have an AIS. Where do those thrombi come from? In prior reports, we described several cases of pulmonary vein thrombi (PVTs), which can cause AIS and acute myocardial infarction (AMI) by separating large clots. We found other candidates in the AAo. We found that a reduced dose of apixaban partially resolved AAo thrombi.

A 73-year-old male with hypertension was examined using cardiac CT and TEE to detect AAo thrombi and PVTs. The patient was treated with apixaban.

TEE revealed white thrombi with surrounding dark thrombi on the right side in the AAo, and the white thrombi seemed to connect to white right upper pulmonary vein (RUPV) thrombi through line-like white thrombi. A reduced dose of apixaban (2.5 mg; twice daily) was used because the dose reduction weight criteria were met and resolved most AAo thrombi; however, the decreased dose of apixaban (2.5 mg; once a day) was not able to prevent AAo thrombi from regrowing.

TEE demonstrated that RUPV thrombi, seemingly contacting line-like white thrombi, and thrombi in the AAo were affected by apixaban. Line-like white thrombi looked to approach the wall of the AAo, and approaching areas looked like a mass; the wall of the AAo could not be clearly identified. How the wall was affected is unknown and could be associated with leukocytes such as monocytes, macrophages, and myofibroblasts present in white thrombi with shadows around the ostia of the RUPV.

White RUPV thrombi approached AAo thrombi through white line-like thrombi. These thrombi were partially resolved by treatment with a reduced dose of apixaban; however, the positive effect diminished with decreasing dose.