Abstract / Summary
Abstract Background Early structural valve deterioration (SVD) after transcatheter aortic valve replacement (TAVR) for aortic stenosis is uncommon, particularly within 5 years post-implantation. The impact of long-term corticosteroid therapy on transcatheter bioprosthetic valve durability remains poorly understood. Case Presentation An 80-year-old woman presented with severe calcific SVD 4.5 years after undergoing TAVR with a balloon-expandable transcatheter aortic valve, requiring surgical explantation and aortic valve replacement. She had received long-term corticosteroid therapy for bullous pemphigoid for over 9 years, complicated by steroid-induced diabetes mellitus and progressive chronic kidney disease. While post-procedural echocardiography initially confirmed favorable valve function (peak velocity 2.5 m/s, mean gradient 14.2 mmHg), follow-up echocardiography revealed Stage3 (severe) hemodynamic SVD, with a markedly reduced effective orifice area of 0.48 cm2 and an elevated peak/mean gradient of 139.2/80.1 mmHg (peak velocity 5.9 m/s). Computed tomography revealed marked leaflet calcification without evidence of hypoattenuated leaflet thickening or thrombosis. Pathological examination of the explanted valve confirmed advanced intrinsic and extrinsic calcific degeneration without active inflammation. Although moderate patient–prosthesis mismatch was present, these findings suggest that the patient’s systemic pro-calcific metabolic environment—driven by prolonged corticosteroid therapy and its associated metabolic comorbidities—might have played a key role in accelerating SVD. Discussion While hypothesis-generating, our findings suggest that long-term corticosteroid therapy and associated metabolic disorders might contribute to early transcatheter valve deterioration. Careful echocardiographic follow-up should be considered in post-TAVR patients with complex metabolic risk profiles.