Marked changes in bioprosthetic valve thrombosis by anticoagulation therapy

摘要

A 74-year-old woman presented to our hospital with dyspnoea on exertion. She underwent mitral valve replacement (MVR) with a 27-mm-stented porcine valve and coronary artery bypass surgery for ruptured mitral chordae tendineae following inferior acute myocardial infarction 2?years ago. Postoperatively, she had been treated with vitamin K antagonist (VKA) and aspirin for 3?months, and VKA was discontinued thereafter. Even though serial transthoracic echocardiography examination demonstrated a gradual increase in the mitral transvalvular gradient and the inferior wall motion abnormality, she did not have any symptoms and both ventricular function was preserved. Upon admission, transoesophageal echocardiography (TOE) revealed thickened mitral leaflets with restricted motion and low echoic mass extended to the left atrial septal wall (Figure 1C and 1D, Supplementary material online, Video S1). The peak mitral velocity and mean transmitral gradient increased to 2.5?m/s and 17?mmHg, respectively (Figure 1B). Additionally, the mitral valve area calculated by the continuity equation was 0.53 cm2. The bioprosthetic valve thrombosis (BPVT) was suspected because it occurs mostly within 2?years after valve replacement,1 VKA was initiated instead of surgery or thrombolysis because she was hemodynamically stable without thromboembolic event.2,3 Three months later, follow-up TOE demonstrated normal leaflet thickness and opening (Figure 2C and D, Supplementary material online, Video S2). The peak mitral velocity and mean transmitral gradient markedly decreased to 1.4?m/s and 2?mmHg, respectively (Figure 2B). The mitral valve area calculated by continuity equation recovered to 1.18 cm2. Bioprosthetic valve thrombosis is not uncommon, with an incidence of 0.74%.1 Haemodynamic, haemostatic, and surface factors are considered as potential mechanisms of BPVT. She did not have laboratory findings of thrombotic disorders, maintained cardiac function and sinus rhythm throughout the clinical course. As we currently lack a precise understanding of the mechanism leading to BPVT, she was ultimately diagnosed with unprovoked BPVT. Careful follow-up is necessary even in the chronic phase after bioprosthetic valve replacement.