Untreatable Severe Structural Degeneration of a Transcathete
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A 67-year-old female patient with a background of chronic obstructive pulmonary disease and relapsing polychondritis initially presented to the cardiology outpatient department in 2010 with progressively worsening exertional dyspnea. Echocardiography demonstrated severe aortic stenosis and normal left ventricular systolic function, whereas coronary angiography showed normal coronary arteries. She was considered for surgical aortic valve replacement (SAVR) but was deemed to be at extreme risk because of her comorbidities; in particular, the requirement for long-term immunosuppressive therapy with prednisolone and azathioprine for treatment of her relapsing polychondritis raised concerns regarding post-surgical wound healing.

Transcatheter aortic valve implantation (TAVI) was performed with deployment of a 29-mm CoreValve (Medtronic, Minneapolis, Minnesota), with a good procedural result. She was asymptomatic following the TAVI and remained so until 2017, when she presented to the emergency department with dyspnea on minimal exertion, orthopnea, and paroxysmal nocturnal dyspnea. Clinical examination demonstrated features of pulmonary edema, with bilateral lower zone crepitations audible on auscultation of her lungs, hypoxia, and tachycardia. Auscultation of her heart sounds elicited ejection systolic and early diastolic murmurs. Her jugular venous pressure was not elevated, and there was no peripheral edema.

A chest radiograph confirmed the presence of pulmonary edema, with bilateral pleural effusions and central pulmonary vascular congestion. Blood tests demonstrated a significant rise in N-terminal pro–B-type natriuretic peptide, but results were otherwise unremarkable. Her electrocardiogram showed sinus rhythm with mild left ventricular hypertrophy.

Source: https://www.sciencedirect.com/science/article/pii/S2666084920301352
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