Two Cases of Acute Bioprosthetic Mitral Valve Thrombosis Immediately After Mitral Valve Replacement
Prosthetic valve thrombosis (PVT) is a rare complication, and most of PVT occurs in patients with mechanical valves. We present 2 extremely rare cases of acute bioprosthetic mitral valve thrombosis immediately after mitral valve replacement under veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and anticoagulant therapy.
In Case 1, a 75-year-old woman underwent aortic valve replacement and mitral valve replacement with 23- and 29-mm bioprosthetic valves, respectively. On postoperative day 2, VA-ECMO was started because of hemodynamic compromise. At the initiation of VA-ECMO, transthoracic echocardiography indicated normal bioprosthesis function (Figure 1; see Movie I in the online-only Data Supplement). On postoperative day 9, transesophageal echocardiography revealed severely stenotic bioprosthetic mitral valve, but the bioprosthetic aortic valve was normal (Figure 2; see Movies II and III in the online-only Data Supplement). Emergent percutaneous mitral valvuloplasty was performed, resulting in partial improvement of hemodynamic state. On postoperative day 17, re-mitral valve replacement was performed. The left atrial side of the retrieved bioprosthetic valve leaflet was covered with thrombus, resulting in leaflet fusion (Figure 3).
In Case 2, a 70-year-old man underwent emergent mitral valve replacement with a 27-mm bioprosthetic valve attributable to acute myocardial infarction with rupture of a papillary muscle. During the procedure, VA-ECMO was started and continued. Two days later, transesophageal echocardiography revealed that the bioprosthetic valve was thickened and its opening was restricted (Figure 4; see Movies IV and V in the online-only Data Supplement). Intravenous infusion of urokinase at a dose of 10 000 U/h was started and continued for 3 days. After thrombolysis, transesophageal echocardiography showed that the thickening of the valve ameliorated and its opening improved (Figure 5; see Movies VI and VII in the online-only Data Supplement). His hemodynamic state improved, and he could be weaned off VA-ECMO.
In Case 1, histological examination revealed thrombus formation on the bioprosthetic valve. In Case 2, echocardiographic and clinical findings strongly implicated that thrombosis caused prosthetic valve stenosis. In both cases, PVT developed despite the use of intravenous heparin to maintain the ACT above 150 seconds.
Risk factors for PVT have been reported as left atrial dilatation, atrial fibrillation, hypercoagulability, and low cardiac output.1 In our cases, low cardiac output was 1 possible cause of PVT. Recently, cases with left ventricular or bioprosthetic valve thrombosis during VA-ECMO were reported.2,3 VA-ECMO is a device that provides circulatory and pulmonary support with draining blood from the inferior vena cava and sending the blood to the femoral artery. Because it increases left ventricular afterload and decreases preload, cardiac output from the native heart is reduced or completely abandoned, and thereby it may increase the risk of thrombosis in the left heart.3 PVT in our cases may also be developed as a result of decreased blood flow through the prosthetic valves. Adequate device adjustment, or keeping low flow of VA-ECMO using intra-aortic balloon pumping or percutaneous left ventricular assist device, would be useful to prevent thrombosis. In a patient with prosthetic valve under VA-ECMO, more aggressive anticoagulant therapy would also reduce the risk of thrombosis.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.113.005583/-/DC1.
- © 2014 American Heart Association, Inc.