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Tertiary hyperparathyroidism-induced prosthetic valve obstruction: a complex clinical challenge
Session:
CASOS CLÍNICOS DE INTERVENÇÃO (PERCUTÂNEA E CIRÚRGICA)
Speaker:
Mariana Rodrigues Simões
Congress:
CPC 2025
Topic:
H. Interventional Cardiology and Cardiovascular Surgery
Theme:
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Subtheme:
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Session Type:
Sessão de Casos Clínicos
FP Number:
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Authors:
Mariana Rodrigues Simões; Rafaela Fernandes; Ana Luísa Silva; Gustavo Campos; Ana Vera Marinho; Joana Moura Ferreira; Carolina Lourenço; Susana Costa; Elisabete Jorge; Marco Costa; Fatima Franco; Lino Gonçalves
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Introduction: </span></strong><span style="font-family:"Calibri",sans-serif">Prosthetic valve dysfunction is a complex condition with various aetiologies, which can rapidly become a life-threating situation.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Case description:</span></strong><span style="font-family:"Calibri",sans-serif"> A 67-years-old male was admitted to the emergency room with lower gastrointestinal bleeding. Post-colonoscopy preparation, he develops acute pulmonary oedema. His previous medical history included end-stage kidney disease on haemodialysis, tertiary hyperparathyroidism, heart failure with mildly reduced left ventricle ejection fraction (LVEF), coronary artery disease treated percutaneously, and transcatheter aortic valve implantation (TAVI) for severe aortic stenosis, one year prior. Bedside transthoracic echocardiogram (TTE) revealed increased transprosthetic peak velocity (4.97m/s) and mean pressure gradient (64mmHg) and severe depression of LVEF. The patient was admitted to a Cardiology ward for study and clinical compensation. A transoesophageal echocardiogram confirmed an exuberant calcification of aortic prosthetic valve leaflets, causing a critic valve obstruction with an effective orifice area of 0.35cm2. The diagnosis of aortic prosthetic valve degeneration due to calcium deposition was confirmed by cardiac computed tomography angiography. On the 7<sup>th</sup> day of his hospital stay, the patient experienced clinical worsening and evolved into cardiogenic shock refractory to vasopressor and inotropic support. The case was discussed in Heart Team and due to his high surgical risk, he was deemed not operable. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support was initiated via the right femoral artery/vein route as a bridge to TAVI-in-TAVI. The procedure was successfully performed via the left femoral artery route, placing a 29mm<em> Navitor</em> self-expandable valve within a 26mm <em>Sapien S3</em> valve. VA- ECMO and v</span><span style="font-family:"Calibri",sans-serif">asopressor/inotropic support</span><span style="font-family:"Calibri",sans-serif"> were discontinued. Post TAVI-in-TAVI TTE showed a normally positioned aortic prosthetic valve with a peak velocity of 2.1 m/s and a mean pressure gradient of 8 mmHg.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-family:"Calibri",sans-serif">Conclusion:</span></strong> <span style="font-family:"Calibri",sans-serif"><span style="color:#111111">This case highlights tertiary hyperparathyroidism as a rare cause of rapid prosthetic valve degeneration and underscores the lifesaving role of VA-ECMO in rescuing and supporting the TAVI-in-TAVI procedure for high-risk patients.</span></span></span></span></p>
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