MORPHOLOGICAL CHANGES IN THE BLOOD VESSELS OF PLACENTAL TISSUE IN PREGNANT WOMEN WITH ECLAMPSIA
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Abstract
Eclampsia is a leading disease during pregnancy, occurring alongside the development of multiple organ failure. Studying its etiology and pathogenesis remains a pressing issue for many researchers. The complications of eclampsia in various diseases include obstetric hemorrhage, placental abruption, placental insufficiency, fetal growth restriction syndrome, HELLP syndrome, and severe cerebrovascular pathologies in women. The course of eclampsia and its complications reduces the quality of life for patients, which is related to the high prevalence of cardiovascular diseases. The development of this pathological process in the body of a pregnant woman leads to high maternal and perinatal morbidity and mortality rates. Modern statistical data confirm this: the proportion of eclampsia among pregnancy complications ranges from 10.1% to 20%, accounting for 21.3% of maternal mortality causes. In developing countries, eclampsia remains a leading cause of maternal deaths (40-80%).
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References
Morphometric indicators for supporting, intermediate, and terminal villi and their vessels in preeclampsia have been presented, showing negative dynamics correlated with changes in the main parameters of the vessel wall: thickening of the arteriolar wall and narrowing of the lumen (1.5-2.0 times compared to normal). The presence of obliterative angiopathy in supporting villi has been proven to be an integral component of fetal-placental insufficiency at various levels of eclampsia: hypertrophy of the muscle layer and obliteration of arteriolar lumens increased in accordance with the duration and severity of eclampsia.
Ongoing complex clinical-morphological studies indicate that concentric vascular remodeling occurs during the progression of preeclampsia, resulting in obliteration of the lumen, thickening of the vessel wall, and reduced geometric structure of capillaries in terminal villi. This leads to increased vascular resistance in circulation, decreased diffusion-exchange function of the placenta, and ultimately results in the development of placental insufficiency.