The bioprosthetic valve was thought to be superior to the conventional mechanical valve in terms of having low frequency of thrombosis previously . However, recent date suggest that bioprosthetic valve thrombosis is a more common complication than previously reported and the overall occurrence of thrombosis is 11.6% . Also, acute thrombosis after bioprosthetic valve replacement is a possible complication. There have been several case reports of bioprosthetic mitral valve thrombosis causing significant hemodynamic instability [2, 3, 5, 6]. In our case, we initially considered that the hemodynamic compromise might be slightly improved to eliminate pericardial hematoma and low cardiac function. Furthermore, poor TTE images under mechanical ventilation in the ICU masked the presence of thrombus adhering to the mitral valve. The removal of the hematoma and decreasing VA-ECMO flow rate on trial allowed us to inspect the mobility and configuration of the bioprosthetic valve under increased right ventricular output, which further elucidated the cause of mitral stenosis (MS) accompanied by a rapid increase in PAP and pulmonary edema.
To evaluate the bioprosthetic mitral valve, the following TEE examinations are recommended: confirm characterization of the valve morphology and leaflet movement by both two- and three-dimensional imagings and find transmitral inflow and regurgitation patterns by color flow Doppler, as well as pressure gradients (mean and peak) and estimates of mitral valve areas using either continuous or pulsed-wave Doppler.
Risk factors for prosthetic mitral valve thrombosis have been reported as atrial fibrillation, left atrial dilatation, low cardiac output syndrome, hypercoagulability such as heparin-induced thrombocytopenia, and lack of anticoagulation [2, 3, 5, 6]. In our patient, several risk factors for thrombosis were seen, such as a dilated left atrium, low cardiac function, and postoperative paroxysmal atrial fibrillation, in the ICU. We considered that the poor opening of both mitral and aortic valves due to low flow secondary to cardiogenic shock and retrograde perfusion by VA-ECMO synergistically induced bioprosthetic mitral valve thrombosis and valve failure while using proper anticoagulation therapy. VA-ECMO decreases left ventricular preload and increases afterload, leading to blood stasis in the left heart, and it can put the patient at potential risk for bioprosthetic valve thrombosis [2, 5]. The restoration of blood flow from the right ventricle to the left heart through the pulmonary artery after pericardial hematoma removal and decreasing ECMO pump flow provided clinical evidence of MS before LVAD implantation.