Mitrosz Maciej, Chlabicz Malgorzata, Hapaniuk Katarzyna, Kaminski Karol A, Sobkowicz Bozena, Piszcz Jaroslaw, Dobrzycki Slawomir, Musial Wlodzimierz J, Hirnle Tomasz, Tycinska Agnieszka M
Department of Cardiac Surgery, Poland.
Department of Cardiology, Poland.
Adv Med Sci. 2017 Sep;62(2):378-382. doi: 10.1016/j.advms.2017.04.003. Epub 2017 May 25.
Thrombocytopenia (TP) following transcatheter aortic valve implantation (TAVI) procedure is a common phenomenon but the underlying mechanisms are neither well known nor described. Postinterventional severe TP is related to worse early and late outcome. Moreover, the statement of enhanced platelet and coagulation activation might justify even stronger antiplatelet and anticoagulation therapy following TAVI procedure. Thus, the examination of the pathomechanisms responsible for TP post TAVI seems to be crucial. Several hypotheses have been raised. TP can be caused by insufficient production or impaired platelet renewal. On the other hand, increased platelet activation, consumption and destruction might also be responsible for TP. These findings, mostly related to the procedure alone, need further investigation. Here, we summarize the potential multifactorial causes of post TAVI thrombocytopenia.
