Is placental haemostasis relevant to recurrent implantation failure?

Abstract

Successful pregnancy requires the implantation of a developmentally competent embryo into a receptive endometrium. In many species, pregnancy is readily achieved and maintained. In contrast in humans, monthly fecundity rates compared to other mammalian species is relatively low at approximately 20% [1]. In addition to this relative subfertility the incidence of embryo wastage and pregnancy loss is extraordinarily high in humans, estimated to be at least 30% prior to spontaneous conception, a further 30% before 6 weeks gestation and 10% of clinical pregnancies, mostly prior to 12 weeks gestation [1]. Even in assisted conception cycles, where embryos are created and transferred a potentially even greater proportion of IVF cycles result in implantation failure. Notably the clinical pregnancy rates (CPRs) per embryo transfer in Europe for the year 2006 were 32.4% [2], meaning that 67.6% of embryos failed to implant adequately. Similarly the respective report of the Centers for Disease Control and Prevention (CDC), demonstrated an average live-birth rate per embryo transfer in the United States of America for the year 2006 of 35%. Furthermore the percentage distribution of women with a history of one or more previous failures undergoing a new IVF cycle was 34.3, 44.8, 49.6, 53.3, and 58.1% for the age groups 42 years, respectively, reflecting the emerging problem of repeated implantation failures (RIFs). Unfortunately there is no clear consensus regarding the definition of recurrent implantation failure. For some groups it is an unsuccessful patient with more than ten good quality embryos transferred in subsequent cycles [4]. This definition may seem too loose, according to the actual method of practice. Thus, we can consider that if a patient has undergone three good quality embryos if she is <37 years old, or two good quality embryo transfer if she is ≥37, extended investigation is required (Table 1). Consequently although numerous anatomical, endocrine, immunological, thrombophilic and genetic perturbations have been