The concept of the Great Obstetrical Syndromes was introduced to explain the unique nature of obstetrical disease, which differs fundamentally from disorders in other areas of medicine. These syndromes, including preeclampsia, fetal growth restriction, fetal death, and spontaneous preterm birth, represent clinical endpoints rather than single diseases and share defining characteristics: they arise from multiple etiologies, have a prolonged subclinical phase, involve the fetus as an active participant, are adaptive in nature, and result from complex genetic and environmental interactions between the mother and fetus. Among the diverse mechanisms leading to these syndromes, abnormalities of the maternal supply line to the placenta constitute one major etiology and are often caused by vascular disorders affecting the maternal cardiovascular system and uterine spiral arteries, resulting in placental lesions of maternal vascular malperfusion. The most severe spiral artery lesion is atherosis, which closely resembles atherosclerosis and links obstetrical syndromes to maternal vascular disease. Disorders of deep placentation associated with maternal vascular malperfusion are accompanied by characteristic alterations in angiogenic balance, and the ratio of placental growth factor to soluble fms-like tyrosine kinase-1 in the maternal circulation serves as a biomarker of this pathophysiologic process. Importantly, each obstetrical syndrome is associated with a stereotypic temporal pattern of angiogenic imbalance that reflects differences in disease burden, timing, and clinical expression. While substantial progress has been made in the prediction and prevention of preeclampsia, these concepts extend to other obstetrical syndromes, including fetal growth restriction, fetal death, and spontaneous preterm labor, supporting a unified biologic framework for early risk assessment and personalized prevention.
Leipold et al. (Thu,) studied this question.