Comparative Assessment of Survival and Clinical Outcome Between Two Commercial Vitrification Kits with Different Warming Protocols After Blastocyst Culture: Potential Perspectives Toward Simplified Warming Procedures.

This study investigates whether there is an effect on laboratory results and clinical outcome using commercial kits with similar vitrification but different warming procedures for blastocysts vitrified on day 5 or day 6. A single-center retrospective cohort study was performed between 2011 and 2020. A change from a stage-specific kit (Kit 1) to a universal kit (Kit 2) was undertaken in 2017. A total of 1845 untested blastocysts were warmed for single vitrified-warmed blastocyst transfers (SVBT). Eight hundred and twenty-five blastocysts were vitrified with Kit 1 and 1020 with Kit 2. Blastocyst survival was not different (96.1% versus 97.3%). Seven hundred seventy-seven SVBT were performed from Kit 1 and 981 from Kit 2. Overall clinical pregnancy and live birth rates were not different (35.4% versus 34.1% and 30.9% versus 30.5% for Kit 1 and 2, respectively). Subgroup analysis for live birth rates in relation to the day of blastocyst vitrification showed no differences (36.1% and 36.1% for day 5 and 25.4% and 23.5% for day 6 blastocysts, respectively). For both kits, the mean gestational age was not different (38.8 ± 2.5 weeks versus 38.8 ± 2.0 weeks) with a singleton birth weight of 3413 ± 571 g and 3410 ± 528 g for Kit 1 and Kit 2, respectively. Differences in warming procedures do not affect laboratory performance or clinical outcome after blastocyst vitrification. The plasticity of a human blastocyst may allow for further investigation on simplification of blastocyst warming procedures.

Haplotyping-based preimplantation genetic testing reveals parent-of-origin specific mechanisms of aneuploidy formation.

Chromosome instability is inherent to human IVF embryos, but the full spectrum and developmental fate of chromosome anomalies remain uncharacterized. Using haplotyping-based preimplantation genetic testing for monogenic diseases (PGT-M), we mapped the parental and mechanistic origin of common and rare genomic abnormalities in 2300 cleavage stage and 361 trophectoderm biopsies. We show that while single whole chromosome aneuploidy arises due to chromosome-specific meiotic errors in the oocyte, segmental imbalances predominantly affect paternal chromosomes, implicating sperm DNA damage in segmental aneuploidy formation. We also show that postzygotic aneuploidy affects multiple chromosomes across the genome and does not discriminate between parental homologs. In addition, 6% of cleavage stage embryos demonstrated signatures of tripolar cell division with excessive chromosome loss, however hypodiploid blastomeres can be excluded from further embryo development. This observation supports the selective-pressure hypothesis in embryos. Finally, considering that ploidy violations may constitute a significant proportion of non-viable embryos, using haplotyping-based approach to map these events might further improve IVF success rate.