Progrediente Dyspnoe nach Implantation einer Edwards-Sapien-3-Bioprothese

Valve thrombosis of THV is a rare event. An 80 year old woman had undergone transfemoral aortic valve implantation (26-mm Edwards Sapien prosthesis). Exercise capacity improved dramatically, but dyspnea (NYHA III) returned 7 month after the procedure. Echocardiography showed an increase of mean gradient (48 mmHg versus 13 mmHg after implantation). TEE revealed a sessile mass at the bottom of the right aortic cusp preventing it from opening properly. Laboratory test results showed slightly elevated values for d dimers, but no signs for infection. Numerous blood culture tests remained sterile. Assuming valve thrombosis, the patient received unfractionated heparin (aPTT 60–70 s) for 7 days prior to admission to our hospital. Heparin treatment proofed ineffective and was terminated since the patient developed heparin induced thrombopenia. We continued anticoagulation with argatroban (aPTT 70–80 s) for another 8 days. Treatment had to be stopped because the patient developed severe anemia without an obvious source of bleeding. The patient is a Jehovah`s Witness and refused blood transfusions. Echocardiographic controls showed a steady decline of the transvalvular mean gradient, most surprisingly even after argatroban treatment had been stopped. After 19 days, a TEE study showed that the formation had disappeared. To our knowledge, this is the first case of a cusp thrombosis of a THV that has been successfully treated with argatroban as an anticoagulant agent. No thrombembolic complications were noticed. Argatroban has been shown to have a much better clot dissolving capacity than heparin.The patient had a number of predisposing factors for thrombus formation. She tested positive for a heterozygote mutation of the prothrombin gene which is associated with a 3 to 4 fold higher risk for thrombosis. This risk is further increased by conditions like hyperhomocysteinemia. The patient was diagnosed with several factors known to promote hyperhomocysteinemia including chronic renal failure, folic acid deficiency and a compound mutation of the methylene-tetrahydrofolate reductase gene. When valve thrombosis has occurred, lifelong oral anticoagulation needs to be considered.