778 Acute clinical valve thrombosis after transcatheter mitral valve-in-valve replacement
Authors: Calvi Emiliano , Bernardi Nicola , Milidoni Antonino , Cimino Giuliana , Cersosimo Angelica , Amore Ludovica , Vizzardi Enrico 
Published: December 2021

Aims

Transcatheter heart valve (THV) thrombosis is a frequent and potentially life-threatening complication of transcatheter mitral valve replacement (TMVR), occurring in approximately 12% of patients (mainly within the first 3 months after the procedure). The majority of THV thromboses is non-obstructive and subclinical, and remains undetected until a routine echocardiogram is performed.

Methods

A 65 years old male was suffering from post-ischaemic dilated cardiomyopathy and severe left ventricle systolic dysfunction (LVEF 28%), secondary to a previous STEMI in 2010 treated with primary PCI on proximal LAD; after the STEMI he developed a left ventricle aneurysm and a subsequent severe secondary mitral regurgitation. In late 2020 he underwent a surgical valve replacement with a biologic valve (Perimount Magna Mitral Ease n. 27), alongside a left ventricle reshaping (Dor procedure). After a few months, the patient developed worsening dyspnoea and severe exercise intolerance; a transesophageal echocardiogram (TEE) showed an extensive valve degeneration with diffuse leaflet thickening determining severe valve stenosis and regurgitation.

The patient was then admitted to the Cardiology department. A coronary angiography was performed, showing good result of previous PCI and excluding other critical stenoses. The patient then underwent a transcatheter valve-in-valve replacement with a Sapien S3 n. 29 in mitral position. The patient was already in chronic therapy with acetilsalicilic acid (ASA), and after the procedure anticoagulant therapy with Warfarin was started.

In the post-procedural period the patient developed an acute worsening of the LVEF with severe hypotension, likely due to after-load mismatch; hence, supportive inotropic therapy with Adrenalin and Enoximone was required. A TEE performed 7 days after the procedure showed absence of diastolic excursion of posterior and lateral cusps and leaflet thickening with a 4 mm thrombotic apposition on the ventricular side, determining severe valve stenosis with markedly increased transvalvular gradients (peak gradient 20 mmHg, mean gradient 11 mmHg). A CT scan of the heart confirmed the valve thrombosis on the inferior and lateral leaflets.

Results

Unfractioned heparin (UFH) was then added to ASA and Warfarin (INR target of 3.0). After 11 days of aggressive antithrombotic therapy a new TEE was performed, showing marked reduction in transvalvular gradients (peak gradient 10 mmHg, mean gradient 5 mmHg) due to partial dissolution of the thrombotic formation. Warfarin was then stopped, and after switching from UFH to Enoxaparin the patient was discharged asymptomatic and in good general conditions, with indication of follow-up with TEE at 1 month.

Conclusions

Valve-in-valve TMVR is a relatively new and still infrequent procedure, therefore few evidences about its complications are currently available. Thrombosis on these valves is not rare (12%), but usually develops on the atrial side of the leaflets; interestingly, in this patient the thrombosis was on the ventricular side, likely due to an acute reduction in flow velocity caused by the after-load mismatch and the subsequent cardiogenic shock.