B64-37 Chronic Thromboembolic Pulmonary Hypertension Secondary to Chronic Pacemaker Lead Infection Identified by Next-generation Sequencing

Abstract Introduction Chronic thromboembolic pulmonary hypertension (CTEPH), classified as Group 4 pulmonary hypertension, results from persistent pulmonary arterial obstruction despite adequate anticoagulation. Reported etiologies include coagulation abnormalities, malignancy, and cardiac disease. Pacemaker-related venous thrombosis occurs in approximately 1-3% of patients; however, progression to CTEPH secondary to chronic pacemaker lead infection has rarely been reported. We describe a rare case of CTEPH associated with chronic pacemaker lead infection, in which Staphylococcus epidermidis was identified by next-generation sequencing (NGS) after device extraction. Case Presentation A 54-year-old man with a permanent pacemaker (PPM) implanted at age 18 for sick sinus syndrome developed a PPM pocket infection in 2021, treated with antibiotics without device removal. In 2023, he presented with exertional dyspnea, fever, and pleuritic chest pain. Chest computed tomography revealed bilateral pulmonary artery thrombi, and echocardiography suggested pulmonary hypertension. Anticoagulation with apixaban was initiated. Recurrent pleuritis developed, and blood cultures yielded S. epidermidis, consistent with pacemaker lead infection and infective endocarditis. Fever subsided with oral cephalexin, and blood cultures became negative; however, dyspnea persisted. Right heart catheterization confirmed CTEPH (mean pulmonary arterial pressure mPAP 37 mmHg, pulmonary vascular resistance 9.9 Wood units). Riociguat and balloon pulmonary angioplasty (BPA) were initiated, resulting in transient hemodynamic improvement (mPAP 23 mmHg after four sessions). At the fifth BPA session, pulmonary pressures again increased with new thrombus formation, prompting a switch from apixaban to warfarin. Three months later, echocardiography revealed an 8 × 12 mm vegetation on the pacemaker lead (Panel A), and pulmonary angiography demonstrated fresh thrombi. Surgical device extraction was performed. Blood and vegetation cultures were negative, but histopathology showed granulation tissue with gram-positive cocci (Panels B and C). NGS identified S. epidermidis. Cefazolin was administered for 14 days, resulting in marked clinical improvement. Following device extraction and nine BPA sessions, mPAP decreased to 20 mmHg. Discussion This rare case demonstrates that chronic cardiac device-related infective endocarditis (CDRIE) can serve as a persistent source of septic pulmonary emboli, leading to CTEPH. Because antibiotic therapy alone is associated with high mortality, early and complete device removal should be considered when CDRIE is suspected. In this case, NGS provided a valuable diagnostic tool to identify the causative organism in culture-negative specimens, enabling targeted antimicrobial therapy. Conclusion Chronic pacemaker lead infection can act as a continuous source of embolic events, culminating in secondary CTEPH. Early recognition, device removal, and appropriate antimicrobial management are essential for optimal outcomes. This abstract is funded by: None