Breakthrough pulmonary embolism occurred in an 81-year-old male despite chronic DOAC and concurrent therapeutic unfractionated heparin, resolving completely at 1-month follow-up on apixaban.
Case Report (n=1)
This case highlights the rare occurrence of breakthrough pulmonary embolism despite therapeutic anticoagulation with DOAC and unfractionated heparin, emphasizing the need to investigate resistance mechanisms and secondary prothrombotic conditions.
Abstract Background Pulmonary embolism (PE) is a potentially life-threatening condition most commonly arising from thromboembolic obstruction of the pulmonary arteries. Anticoagulation remains the cornerstone of treatment and prevention. The occurrence of PE despite both chronic direct oral anticoagulation (DOAC) and concurrent therapeutic unfractionated heparin (UFH) infusion is exceedingly rare and presents unique diagnostic and management challenges. Case Presentation An 81-year-old male with a complex medical history, including atrial fibrillation status post Watchman device placement (previously on rivaroxaban), prior deep vein thrombosis, coronary artery disease post-transcatheter aortic valve replacement, chronic obstructive pulmonary disease, hypertension, and cutaneous polyarteritis nodosa, presented with acute abdominal pain radiating to the chest. Vital signs revealed mild tachycardia and borderline hypotension. Initial CTA (computed tomography angiography) of the chest identified a right lower lobe pulmonary artery filling defect consistent with acute pulmonary embolism (PE). Rivaroxaban was held, and a continuous unfractionated heparin infusion was initiated within five hours. The patient maintained therapeutic anticoagulation by aPTT monitoring. Due to concerns brought by the team and for clarification purposes on the initial study, a repeat CTA with PE protocol was obtained the following morning, confirming new right upper lobe pulmonary artery emboli (figure 1). No evidence of deep vein thrombosis was found on duplex ultrasound. Abdominal imaging revealed cholelithiasis with mild gallbladder wall thickening but no signs of active infection. Given the underlying polyarteritis nodosa and potential hypercoagulable contribution, rheumatology and pulmonology were consulted for further evaluation. The patient remained hemodynamically stable throughout hospitalization and was transitioned to apixaban prior to discharge. At one-month follow-up, CT imaging demonstrated complete resolution of pulmonary emboli. Discussion This case highlights the rare phenomenon of “breakthrough” PE despite dual anticoagulation exposure, initially with a DOAC and subsequently with therapeutic UFH. Possible mechanisms include heparin resistance, assay discordance between aPTT and anti-factor Xa monitoring, or a hypercoagulable state associated with systemic vasculitis. Evaluation of antithrombin activity, acute-phase reactants, and anti-Xa levels is essential when UFH resistance is suspected. Underlying autoimmune or inflammatory thrombophilias, including those associated with polyarteritis nodosa, should also be considered. Conclusion PE occurring during therapeutic anticoagulation with both a DOAC and UFH is exceptionally uncommon and underscores the importance of confirming true therapeutic exposure, identifying resistance mechanisms, and investigating secondary prothrombotic conditions. Multidisciplinary management is critical to guide safe and effective long-term anticoagulation strategies. This abstract is funded by: none
Nasato et al. (Fri,) conducted a case report in Pulmonary embolism (n=1). Continuous unfractionated heparin infusion was evaluated on Resolution of pulmonary emboli. Breakthrough pulmonary embolism occurred in an 81-year-old male despite chronic DOAC and concurrent therapeutic unfractionated heparin, resolving completely at 1-month follow-up on apixaban.