Severe acute respiratory syndrome coronavirus 2 has been causing the pandemic of coronavirus disease 2019 (COVID-19) that has so far resulted in over 450 million infections and six million deaths. This respiratory virus uses angiotensin-converting enzyme 2 as a receptor to enter host cells and affects various tissues in addition to the lungs. The present study reports that the placental arteries of women who gave birth to live full-term newborns while developing COVID-19 during pregnancy exhibit severe vascular wall thickening and the occlusion of the vascular lumen. A morphometric analysis of the placental arteries stained with hematoxylin and eosin suggests a 2-fold increase in wall thickness and a 5-fold decrease in the lumen area. Placental vascular remodeling was found to occur in all of SARS-CoV-2-positive mothers as defined by RT-PCR. Immunohistochemistry with α-smooth muscle actin and the Kv11.1 channel as well as Masson’s trichrome staining showed that such placental vascular remodeling in COVID-19 is associated with smooth muscle proliferation and fibrosis. Placental vascular remodeling may represent a response mechanism to the clinical problems associated with childbirth in COVID-19 patients.

Hypoplastic left heart syndrome (HLHS) is one of the most complicated congenital heart defects which leads to the inevitable fatal outcome in the natural course of the disease. Currently, Norwood procedure and fetal aortic valvuloplasty are considered the major approaches for surgical treatment of HLHS. However, the prognosis of such surgeries is often unpredictable. The aim. To study morphological variations of the left ventricle (LV) in HLHS and evaluate the prognostic significance of each of them in the choice of surgical approach. Materials. The main group included 63 hearts of newborns with HLHS, the comparison group included 53 hearts of newborns without cardiac pathology. Methods. The methods used were survey microscopy, as well as macro- and micromorphometry of various parameters of the heart, calculation of the ratio of their absolute values (indices) with subsequent statistical data processing. Results. Five types of LV were identified in HLHS patients based on the size and shape of the cavity, wall thickness, presence or absence of fibroelastosis: slit-like hypoplastic (Type I) (n = 10; 15.9%); slit-like hypertrophic (Type II) (n = 19; 30.2%); cylindrical (Type III) (n = 22; 34.9%); lacunar (Type IV) (n = 6; 9.5% ); lacunar-cylindrical (Type V) (n = 6; 9.5%). In Type I left ventricles, the interventricular index (IVI) (the ratio of the areas of the free walls of the left and right ventricles on the cross sections of the heart) was the smallest: 0.13 ± 0.03 units versus normal 1.96 ± 0.31 units. In Type II left ventricles, the value was equal to 1.69 ± 0.23 units; in Type III it was 1.59 ± 0.64 units; in Type IV it was 1.31 ± 0.03 units; in Type V it was 1.05 ± 0.52 units. The index of the working area of the right ventricular myocardium (RVI) (the ratio of the area of the free wall of the right ventricle to the sum of the areas of the free wall and interventricular septum) in Type I LV was the highest: 81.3 ± 5.7% versus normal 57.1 ± 2.02%; in Type II it was 49.7 ± 6.4%; in Type III it was 39.8 ± 2.9%; in Type IV it was 69.7 ± 16.1%; in Type V it was 41.3 ± 24.4%.Type III–V LVs have always been associated with fibroelastosis, in contrast to Type I and II LVs. Conclusions. In HLHS, Type I hearts are the most eligible for the Norwood procedure, since the LV, due to its minimal size, is not an excess ballast for the working right ventricle. Type II LV is optimal for the fetal aortic valvuloplasty, since during the II-III trimesters of gestation they can join the circulatory system due to remodeling. HLHS with LV fibroelastosis (Types III, IV, V) seem to be the least favorable for both pre- and postnatal surgery, especially in the presence of fibroelastosis of the right ventricle.

Severe acute respiratory syndrome coronavirus 2 has been causing the pandemic of coronavirus disease 2019 (COVID-19) that has so far resulted in over 180 million infections and nearly 4 million deaths. This respiratory virus uses angiotensin-converting enzyme 2 as a receptor to enter host cells, exhibiting a unique feature that affects various tissues in addition to the lungs. The present study reports that the placental arteries from women who gave birth to live full-term newborns while developing of COVID-19 during pregnancy exhibit severe vascular wall thickening and the occlusion of the vascular lumen. A morphometric analysis of the placental arteries stained with hematoxylin and eosin suggest a 2-fold increase in wall thickness and a 5-fold decrease in the lumen area. Immunohistochemistry with alpha-smooth muscle actin and Masson's trichrome staining showed that such placental vascular remodeling in COVID-19 is associated with smooth muscle proliferation and fibrosis. Placental vascular remodeling may represent a mechanism of the clinical problems associated with childbirth in COVID-19 patients.

The objective: to determine the pathomorphological changes in the placenta by antenatal asphyxia of the fetus associated with the coronavirus disease (COVID-19) in pregnant women.Materials and methods. 21 placentas by fetal antenatal asphyxia which occurred at different terms of pregnancy in women with COVID-19 were examined. COVID-19 was diagnosed by a positive PCR test – detection of SARS-CoV-2 RNA. The study groups were defined depending on the duration of the post-covid interval (time from the diagnosis of COVID-19 to delivery). I group (n=12) included placentas of women with antenatal fetal asphyxia, in whom the postpartum interval was 1–4 weeks; II group (n=9) – placentas of women with fetal death, in whom the postpartum interval was 5–14 weeks.In the I group, antenatal asphyxia of the fetus occurred in the term from the 13th to 36th weeks of gestation, in the II group – in period from the 29th to the 41st week. Macroscopic, organometric, microscopic methods of placenta research and a statistical method were applied. Fetal-placental index (FPI) was calculatedResults. In the studied cases, antenatal fetal death occurred in different terms of pregnancy, namely, from the 14th to the 41st week of gestation (median is 32 weeks). Pregnant women had COVID-19 from the 13th to the 35th week of gestation (median is 25 weeks); when the mother was diagnosed with COVID-19 after the 35th week, there was no case of antenatal fetal death. The severity of the course of the coronavirus disease was mild in 7 pregnant women, moderate – 12 persons, and a severe course with pneumonia was diagnosed in 2 women. The severity of morphological changes in the placenta did not depend on the severity of the course of COVID-19 in the pregnant woman (chorioamnionitis, p=1.0; intervillositis, p=0.63; obliteration of arterioles, p=0.32).In the I group, a slight increase in FPI was found up to 0.19 [0.12; 0.34], in the II group – a similar indicator was 0.16 [0.13; 0.24]. However, the absolute values of the weight of the fetus and placenta in both groups were lower than those for the given gestational age.The I group of placentas there were the pronounced inflammatory changes – placentitis: chorioamnionitis – 100% (95%CI: 85.4–100) and basal deciduitis – 91.7% (95%CI: 67.1–100). In the II group the inflammatory changes of the chorioamniotic membranes and basal plate were focal and were found in 6 placentas – 66.7% (95% CI: 29.2–94.8). Intervillositis was detected in 11 placentas – 91.7% (95%CI: 67.1–100) in the I group versus 2 placentas – 22.2% (95%CI: 1.1–58.9; p=0.006) in the II group.Villositis in the I group was determined in 8 cases – 66.7% (95%CI: 35.4–91.4) and in only one placenta in the II group – 11.1% (95%CI: 0.0–43.91; p=0.034). In the placentas of both groups the fibrinoid necrosis of the arteriole wall, proliferative changes in the vessel wall and necrosis of the endothelium were detected – 100% (95%CI: 85.4–100), dyscirculatory disorders (stasis, thrombosis, hemorrhages) were found in 75% (95% CI: 44.4–95.8) of cases in the I group and in 66.7% (95% CI: 29.2–94.8) – in the II group. An increased number of syncytial nodules was observed as a manifestation of compensatory mechanisms: in the I group – 83.3% (95%CI: 54.7–98.9), in the II group – 88.9% (95%CI: 56.1–100).All studied cases in the II group were accompanied by obliteration of the lumen of the arterioles of trunk and semi-trunk villi – 100% (95%CI: 80.9–100; p=0.0006), versus the I group – 16.7% (95%CI: 1.1–45.3). At the same time, in 6 cases in the II group the morphological manifestations of restoration of the lumen (revascularization) were detected – the formation of intravascular septa – 66.7% (95% CI: 29.2–94.8), which were not found in the I group (р=0.0093). In 100% (95%CI: 80.9–100) of placentas of the II group and in 66.7% (95%CI: 35.4–91.4) of the I group the stroma fibrosis of stem and semi-stem villi, obliteration intervillous space, and hypoplasia of terminal villi were determined.Conclusions. Statistically significant differences of placentas in antenatal asphyxia of the fetus depended on the length of the postcovid interval: in the postcovid interval of 1–4 weeks (I group) the inflammatory changes prevailed – placentitis: chorioamnionitis – 100% (95%CI: 85.4–100), intervillositis – 91.7% (95% CI: 67.1–100), p=0.006; villositis – 66.7% (95%CI: 35.4–91.4), p=0.034. When the duration of the postcovid interval increased to 5–14 weeks (II group), arteriosclerosis prevailed – 100% (95% CI: 80.9–100); p=0.0006.The cause of antenatal fetal death in the women with COVID-19 in the I group is acute placental insufficiency associated with the exudative phase of inflammation (chorioamnionitis, villositis, intervillositis). In the II group, the cause of antenatal fetal asphyxia is the formation of chronic placental dysfunction caused by the proliferation phase, which was manifested by proliferative changes in the muscular layer of arterioles and their subsequent fibrosis with obliteration of the lumen of arterioles (arteriosclerosis).