MORPHOFUNCTIONAL DEVELOPMENT OF THE FETAL HEART DURING PRENATAL ONTOGENESIS UNDER MATERNAL HYPOTHYROIDISM

Abstract

Maternal hypothyroidism is recognized as a significant pathogenic factor adversely affecting fetal organogenesis. Thyroid insufficiency is detected in 5–10% of women of reproductive age, with many cases remaining undiagnosed during pregnancy (WHO, 2022). Thyroid hormones regulate cell proliferation, differentiation, and tissue maturation from the earliest stages of embryogenesis (Forhead & Fowden, 2021). The fetal heart undergoes its critical morphogenetic period during weeks 3–8 of gestation. Studies have linked maternal hypothyroidism with impaired cardiac septation, endocardial cushion hypoplasia, and valvular dysplasia (Ahmed et al., 2022; Li et al., 2023). However, morphological changes across defined stages of prenatal ontogenesis remain insufficiently characterized. In Uzbekistan, iodine deficiency-related hypothyroidism is prevalent among pregnant women, yet systematic endocrine screening is not consistently applied, amplifying perinatal cardiovascular risk.