15th European Lupus Meeting, Lisbon, Portekiz, 4 - 07 Mart 2026, cilt.13, sa.1, ss.126, (Özet Bildiri)
Abstract
Objectives We aimed to characterize the clinical features and long-term prognosis of valvular heart disease (VHD) in patients with SLE and/or APS and to identify associated factors.
Methods Data of 1,791 patients from our SLE/APS cohort were retrospectively reviewed. The analysis included 72 (10 PAPS, 21 SLE+APS, 8 aPL+ SLE, 33 aPL- SLE) patients who were diagnosed with VHD by transthoracic/transesophageal echocardiography (TTE/TEE) between 2017-2024 and underwent follow-up TTE/TEE at least 6 months later. VHD was defined as valvular thickening and/or vegetation and/or moderate–severe regurgitation/stenosis. The composite adverse outcomes (CAO) comprised valve replacement, heart failure, infective endocarditis (IE), or death. Post-VHD cranial MRI scans were evaluated for ischemic lesions. Associations of thrombosis, aPL positivity, SLEDAI-2K, and post-VHD treatments with the composite outcome were assessed by univariate regression analysis.
Results Main features and valvular lesions are summarized in table 1 and 2, respectively. Over a mean follow-up of 38 months, valvular dysfunction worsened in 15 (20.8%), improved in 18 (25%), and remained stable in 54.2%. CAO occurred in 14 (19.4%) patients (mechanical aortic valve replacement in 5, heart failure in 9, IE in 2, and death in 3). Median time to CAO was 8.5 months (range, 1–45; figure 1). Prior to VHD, 88.9% of patients were receiving antithrombotic and/or immunosuppressive therapy; post-VHD treatments were aspirin (48.6%), anticoagulants (50%), hydroxychloroquine (86.1%), glucocorticoids (84.7%), cyclophosphamide/mycophenolate mofetil/azathioprine (68.1%), and rituximab (23.6%). Baseline SLEDAI-2K scores (SLE patients), were not associated with CAO and decreased at follow-up (median 12.5 vs. 4; P<0.0001). In regression analysis, only prior vascular thrombosis was associated with CAO (OR 4.01; 95% CI 1.11–14.57; P=0.035). Cranial MRI revealed ischemic lesions in 25 patients (34.7%), of whom 6 had neurological manifestations. Valvular thickening was associated with cranial ischemic lesions (OR 3.16; 95% CI 1.13–8.78; P=0.027). Conclusions In the long term, one in five SLE/APS patients with VHD experienced CAO. Prior thrombotic events strongly predicted CAO whereas, no significant beneficial effect of antithrombotic/immunosuppressive therapy on the development of CAO was observed. Valvular thickening was associated with cranial ischemic lesions, supporting the need for long-term neurologic surveillance in these patients.