Unexpected bioprosthetic mitral valve thrombus during left ventricular assist device implantation

Written informed consent was obtained from the patient for the publication of this report. A 61-year-old man (height, 160 cm; weight, 64 kg) with symptomatic functional mitral regurgitation underwent on-pump beating-heart mitral valve replacement (MVR) with a 27-mm Epic stented tissue valve (St. Jude Medical, St. Paul, MN, USA). He had a history of dilated-phase hypertrophic cardiomyopathy, with a decreased left ventricular ejection fraction of 16% and a severely dilated left atrium (LA) (61 × 61 mm, left atrial volume index of 72 mL/m²); he was registered as a candidate for transplantation before MVR. He was weaned off cardiopulmonary bypass (CPB) with intra-aortic balloon pumping support and was transferred to the intensive care unit (ICU). In the ICU, heparin therapy was started after achieving hemostasis and controlled to prolong the activated partial thromboplastin time to approximately twice that of the control value over days. On postoperative day (POD) 2, he experienced atrial fibrillation and ventricular tachycardia storm and required venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. He was dependent on VA-ECMO (pump speed of 3300 revolutions/min with a blood flow rate of 4.2 L/min) because of extremely low cardiac output. Transthoracic echocardiography (TTE) examination in the ICU revealed pericardial hematoma, decreased cardiac contractility, and poor opening of the aortic valve, but it could not point out the abnormality of the bioprosthetic mitral valve due to poor echocardiographic images. His clinical status did not improve, and he was scheduled for surgical treatment of pericardial hematoma and DuraHeart (Terumo Heart, Inc., Ann Arbor, Michigan, USA) LVAD implantation as bridge to transplantation to prevent multi-organ dysfunction on POD 9. Transesophageal echocardiography (TEE) before surgical incision revealed right ventricular collapse. Our initial analysis indicated that the hematoma was a part of the cause of the persistent hemodynamic instability (Fig. 1). After removing the hematoma with a median sternotomy, central venous pressure decreased from 17 to 12 mmHg, and the VA-ECMO flow rate decreased incrementally to evaluate cardiac function; pulmonary artery pressure (PAP) drastically increased to 55/35 mmHg. In addition, a large amount of pink blood-stained secretions were expectorated through the endotracheal tube. Additional TEE examination revealed a poor opening of aortic valve, spontaneous echo contrast in the LA, immobilization of the bioprosthetic mitral valve in diastole (Fig. 2a), and abnormal transmitral inflow by color flow Doppler study (Fig. 2b). Continuous-wave Doppler study estimated a mean mitral pressure gradient of 20 mmHg (Fig. 3a). After consultation with surgeons about the possibility of mitral valve thrombus, it was decided that an unscheduled left atriotomy should be performed after CPB initiation, followed by aortic cross-clamp. Direct inspection through the LA revealed an organized thrombus attached to the bioprosthetic valve, which was the cause of valve immobilization (Fig. 3b). After removal of the thrombus, an LVAD was implanted and a temporary right ventricular assist device (RVAD) with a membrane oxygenator was also inserted because of severe pulmonary edema and possible right heart failure after LVAD implantation. CPB was weaned off using dobutamine (5 μg/kg/min), adrenaline (0.05 μg/kg/min), milrinone (0.2 μg/kg/min), and nitric oxide inhalation (20 ppm) support. TEE before weaning off CPB confirmed normal opening of the bioprosthetic mitral valve, and pulsed-wave Doppler examination revealed a mitral pressure gradient of 3 mmHg. The patient was successfully weaned off temporary RVAD 4 days later without an episode of severe right ventricular failure and is waiting for a heart transplant.