1645 Unexpected aortic bioprosthetic valve thrombosis

Abstract

Abstract Introduction Prosthetic valve thrombosis (PVT) is a rare but feared complication of cardiac valve replacement which usually represents a difficult diagnostic challenge. Although PVT is not frequent in bioprosthetic valves, the advent of transcatheter heart valves and the advances in computed tomography, allowing the detection of subclinical thrombosis, have yielded growing interest in that field, specially taking into account that there is no consensus on optimal antithrombotic approach in these patients. Clinical Case A 74-year-old male with prior cardiac antecedents of aortic valve replacement (April 2010) with a bovine pericardial bioprosthesis (Mitroflow 25, Sorin group Inc.), ischemic dilated cardiomyopathy with moderately depressed left ventricle ejection fraction (33%) and carrier of VDD pacemaker due to third degree atrioventricular block was admitted to advanced heart failure unit. During routine follow-up echocardiograms, prosthetic valve presented no signs of dysfunction except slightly increased gradients (image C): max 38 mmHg (normal <36), med 23 mmHg (normal <20). Because of left ventricle dysfunction, high pacing rate (>95%) and dyspnea NYHA class III the patient was referred for upgrade to cardiac resynchronization therapy (CRT). Computed tomography to asses epicardial venous anatomy prior to CRT implant was performed. In addition to venous distribution, it was described a repletion defect in aortic bioprosthetic valve suggestive of leaflet thrombosis (image A). To complete the study the patient underwent a transesophageal echocardiography (TOE) revealing a swallow’s nest shaped hypoechoic occupation of non-coronary and left aortic leaflets (image B), and 3D effective orifice area of 0,9 cm2. Oral anticoagulation was started in association to previously taken acetylsalicylic acid (ASA). Control TOE was performed 3 months after diagnosis showing almost complete resolution of thrombi. During the follow-up a CRT-D was implanted, with significant response in systolic performance, reaching a LVEF of 45%. Interestingly, despite the increase in anterograde aortic flow, progressive decrease of aortic gradients (max 24 mmHg, med 15 mmHg) until normalization was found (image D). Clinical benefit was also patent, being the patient in NYHA class I at the moment. Discusion Valve thrombosis could be difficult to diagnose in the presence of left ventricle dysfunction as gradients shall remain low despite an important compromise in valve motion. We present a case of incidental diagnosis of non-obstructive leaflet thrombosis that was managed conservatively with oral anticoagulation and ASA. The descent in transaortic gradients, moreover taking into account the response to CRT increasing LVEF, indicates that gradients slightly increased or in the upper limit of normality should raise suspicion in valve dysfunction in the presence of decreased LVEF. Abstract 1645 Figure.