Anatomical characteristics of the placental cotyledon bloodstream in women with exacerbation of cytomegalovirus infection during the second trimester of gestation

Abstract

   Aim. To give an anatomical description of the placental cotyledon bloodstream in women who had an exacerbation of cytomegalovirus infection (CMVI) in the second trimester of gestation.   Materials and methods. A study was conducted on 117 placentas, of which 101 were from women with full-term pregnancy and 16 from women with premature birth. In all cases, CMVI led to the development of chronic compensated (CCPI), subcompensated (CSPI) and decompensated placental insufficiency (CDPI). 5 groups were identified: the first group consisted of 30 placentas from women with full-term pregnancy seronegative for cytomegalovirus (CMV); the second – 27 placentas from patients who had an acute phase of chronic CMVI, initiating the development of CCPI; the third – 23 placentas from women with exacerbation of CMVI, leading to the formation of CSPI; the fourth – 21 placentas from patients with an exacerbation of CMVI, which caused the development of CDPI and prolongation of pregnancy to the term of delivery; the fifth – 16 placentas from women with an acute phase of chronic CMVI, initiating the formation of CDPI and miscarriage. The assessment of the bloodstream of cotyledons of the placenta was carried out by injection of contrast (red lead-paint on dryingoil) through the vein of the umbilical cord. To obtain X-ray phlebograms, the apparatus RUM-20M “Sapphire” was used.   Results. It was shown that the total number of cotyledons did not differ in the studied groups. In the first group, anatomical forms with a well-contrasted bloodstream were 21.4±2.17, with weakly contrasted vessels – 9.3±0.47, and with no contrast in the veins, arteries and capillaries of the villi – 2.9±0.22. In the placentas of the second group, in comparison with the first one, no differences were found in the number of cotyledons, in which blood vessels were clearly visualized and not detected. However, the number of anatomical forms with poorly contrasted vessels increased by 1.51 times (p<0.05). The placentas of the third group in comparison with the second one were characterized by a decrease by 1.97 times (p < 0.001) in the proportion of cotyledons with a clear contouring of the vascular network and an increase in anatomical forms with a poorly contrasted bloodstream by 2.34 times (p<0.001). In the fourth group, in comparison with the third group, the number of cotyledons with clear visualization of vessels decreased by 2.05 times (p<0.001), and the number of anatomical forms increased by 1.44 times (p<0.01), in which X-ray phlebography did not determine the vasculature. In the fifth group compared to the fourth one, cotyledons with a well-contrasted bloodstream were found 2.83 times less frequently (p < 0.01).   Conclusion. With an exacerbation of CMVI in the second trimester of gestation, leading to the formation of CDPI, in comparison with CCPI and CSPI in the placenta, a reduction of blood flow in cotyledons is more often detected as a result of direct endotheliotropic and mediated effects of CMV. This is the anatomical basis of placental ischemia and one of the pathogenetic mechanisms for the development of miscarriage.