B52-39 When Treating Pulmonary Embolism Turns Catastrophic: A Case of Cardiac Tamponade Following Implantable Cardioverter-Defibrillator Placement Triggered by Anticoagulation for Pulmonary Embolism

Abstract Background Hemorrhagic cardiac tamponade is a life-threatening condition caused by accumulation of blood within the pericardial space, leading to impaired cardiac filling and hemodynamic collapse. Common etiologies include malignancy, myocardial infarction, coagulopathy, and trauma. Tamponade secondary to anticoagulation is exceedingly rare but may occur, particularly after cardiac device implantation. We present a case of silent right atrial perforation complicated by cardiac tamponade following initiation of Enoxaparin therapy for pulmonary embolism (PE) in a patient with implantable cardioverter-defibrillator(ICD) placement. Case Presentation 86-year-old male with history of Diabetes, Hypertension, Coronary artery disease, prior Myocardial infarction, and Heart failure, status post ICD placement one week prior to admission, presented with chest pain, shortness of breath, and near-syncope. A computed tomography angiogram of the chest demonstrated bilateral sub-segmental pulmonary emboli, and enoxaparin was initiated. The initial transthoracic echocardiogram(TTE) revealed mild pericardial effusion with ejection fraction of 40% and no evidence of tamponade physiology. On hospital day two, Patient developed hypotension(BP 60/40mmHg) and new-onset atrial fibrillation. Emergent TTE revealed moderate pericardial effusion with tamponade physiology and raised concern for right atrial lead perforation. Due to hemodynamic instability, anticoagulation was immediately discontinued. Patient was transferred to intensive care unit and initiated vasopressor support. Thoracic surgery was consulted, and patient underwent emergent pericardiocentesis, draining 500 mL of hemorrhagic fluid. Post-procedure TTE demonstrated trivial residual effusion with resolution of tamponade. Serial TTEs over the following days showed no recurrence ofeffusion. Anticoagulation was cautiously restarted with daily TTE monitoring for five-days, without evidence of reaccumulation. Patient was transitioned to apixaban and discharged in stable condition. Discussion Hemopericardium is an uncommon but potentially fatal complication of ICD implantation, particularly in patients receiving anticoagulation. The incidence of cardiac tamponade has been reported as approximately 0.8% in patients on anticoagulation and 0.3% in those with cardiac devices. In this case, patient developed delayed cardiac tamponade shortly after initiation of Enoxaparin. Initial TTE showed a small, stable effusion, but after anticoagulation, hemodynamic deterioration occurred, revealing tamponade physiology and suspected right atrial lead perforation. It is hypothesized that the ICD lead may have partially penetrated the atrial wall during implantation, initially sealed by clot. Subsequent anticoagulation likely dissolved the seal, precipitating bleeding into thepericardial space and resulting in tamponade. This case underscores the importance of careful risk assessment before initiating anticoagulation in patients who have recent cardiac device implantation. Early recognition of clinical deterioration, prompt imaging, and multidisciplinary intervention are crucial for successful outcomes. This abstract is funded by: None