Abstract
BACKGROUND: AMH is a dependable indicator of ovarian reserve function and assessment of ovarian responsiveness. The relationship between reduced ovarian reserve and pregnancy loss remains poorly understood and requires further investigation. Currently, it has not been systematically evaluated in populations with PGT which could exclude the influence of embryonic chromosomal abnormalities on the outcomes. METHODS: This study enrolled 1982 non-PCOS patients who underwent PGT and had their first frozen-thawed embryo euploidy blastocyst transfer between January 2016 and August 2023. Primary outcomes included early pregnancy loss rates (defined as spontaneous miscarriage during the early first trimester) with secondary outcomes encompassing clinical pregnancy rates and live birth rates. The cohort was divided into three subgroups using quintile-based categorization of AMH levels: low (≤ 1.872 ng/mL, n = 260); medium (1.873-5.276 ng/mL, n = 779); high (≥ 5.277 ng/mL, n = 258). After propensity score matching, 143 patients in each group were ultimately included in the current research. RESULTS: The matched data revealed a higher rate of EPL in the low AMH level group and a lower rate of clinical pregnancy and live births (P < 0.05). Compared to the medium AMH level group, the low AMH group had a considerably higher risk of EPL, with an unadjusted OR of 1.76 (95% CI, 1.10-2.82) and an adjusted OR of 1.85 (95% CI, 1.13-3.04). A significant association between low AMH levels and EPL was also found in the < 35 subgroup. Moreover, there was no discernible non-linear relationship between AMH levels and EPL rates in the restricted cubic spline (P-non-linear = 0.356). Subgroup analyses demonstrated the effect of AMH levels on EPL was more significant in younger patients, those with primary infertility, AFC ≥ 10, and transferred with D6 blastocysts. CONCLUSION: In non-PCOS women < 35 years undergoing euploid blastocyst transfer, low AMH (≤ 1.8 ng/mL) independently predicts EPL risk. AMH could as a biomarker of oocyte competence beyond chromosomal integrity. Future research should focus on mechanistic studies to elucidate non-chromosomal pathways linking AMH to pregnancy loss. CLINICAL TRIAL NUMBER: Not applicable.