Background: Autopsies on COVID-19 deceased patients have many limitations due to necessary epidemiologic and preventative measures. The ongoing pandemic has caused a significant strain on healthcare systems and is being extensively studied around the world. Clinical data does not always corelate with post-mortem findings. The goal of our study was to find pathognomonic factors associated with COVID-19 mortality in 100 post-mortem full body autopsies.Materials and Methods: Following necessary safety protocol, we performed 100 autopsies on patients who were diagnosed with COVID-19 related death. The macroscopic and microscopic pathologies were evaluated along with clinical and laboratory findings.Results: Extensive coagulopathic changes are seen throughout the bodies of diseased patients. Diffuse alveolar damage is pathognomonic of COVID-19 viral pneumonia, and is the leading cause of lethal outcome in younger patients. Extrapulmonary pathology is predominantly seen in the liver and spleen. Intravascular thrombosis is often widespread and signs of septic shock are often present.Conclusion: The described pathological manifestations of COVID-19 in deceased patients are an insight into the main mechanisms of SARS-CoV-2 associated lethal outcome. The disease bears no obvious bias in severity, but seems to be more severe in some patients, hinting at genetic or epigenetic factors at play.

Purpose: The aim of our research was to study sex differences and the severity of inflammatory changes in target organs and the peculiarities of immunological disorders when low and high doses of lipopolysaccharide (LPS) were administered to rats. Methods: Male and female 2- to 3-month-old Wistar rats (200–250 g) were injected intraperitoneally with Escherichia coli LPS in one of two doses: 1.5 or 15 mg/kg. In a day after the LPS injection, we studied endotoxin, corticosterone, sex steroids, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activity levels in the serum; morphological disorders in the lung, liver, thymus, and spleen; ex vivo production of IL-2, IL-4, tumor necrosis factor (TNF), and interferon γ (IFNγ) by splenic cells activated by ConA; and relative amount of T- and B-lymphocytes in the peripheral blood. Results: After the injection of low-dose LPS, the serum endotoxin level increased only in males and was combined with a more pronounced inflammatory response in the lungs and thymus and an increase in ALT and AST activity levels without any changes in corticosterone level. After the injection of high-dose LPS, the inflammatory and pathological changes in the target organs manifested as severe endotoxemia and sex differences of pathological changes in the lungs and liver were not revealed. The level of production of IL-2, IL-4, IFNγ, and TNF by splenic cells and the number of T-lymphocytes, including cytotoxic cells, in the peripheral blood, decreased in males, which is an evidence of a pronounced suppression of the immune response. Conclusion: We have shown that the morphofunctional changes in the organs of the immune system in females and males, as well as the intensity of the sex differences of inflammation, depend on the severity of systemic inflammatory response, induced by different doses of LPS.

Дифференцированный подход в диагностике, формулировке диагноза, ведении больных и статистическом учете инфаркта миокарда 2 типа (согласованная позиция)

ПРОБЛЕМЫ ОЦЕНКИ ПОКАЗАТЕЛЕЙ СМЕРТНОСТИ ОТ ОТДЕЛЬНЫХ ПРИЧИН POSITION STATEMENT

The aim of this article is to represent the characterization of the clinical case of chemotherapy-related atrial fibrillation (AF) development in the young woman, elaborated as a result of multiple neoadjuvant and adjuvant modes of the intake of chemotherapy (both anthracycline based and non-anthracycline ones). In this case, the noted disturbances of heart rhythm should be recognized as a manifestation of cardiotoxicity. The latter implies the degree of detrimental effect of chemotherapeutical medication on the morphophynctional parameters of the cardiovascular system. Anthracycline drugs, being highly effective chemotherapytical agents, provide well-known toxic effects on the heart and vessels. Anthracycline mediated cardiotoxicity is a well- known veracity that dates back to the 60s of the last century, but up to now this medication sustains irreplaceable components of big volume of chemotherapy modes. Moreover, it should be noted that relatively newer drugs also posses certain cardiotoxicogenic potential.

Представлены данные литературы и собственные исследования о синдроме Такоцубо, относительно редкой патологии сердца, имеющей сходство с острым коронарным синдромом, но без существенного поражения коронарных артерий. Ведущим патогенетическим фактором является повреждающий эффект катехоламинов в условиях стресса с вовлечением в патогенез сосудов микроциркуляции. Имеется определенная недооценка синдрома Такоцубо как клиницистами, так и патологоанатомами, в связи с чем часть случаев синдрома Такоцубо ошибочно диагностируется как острый коронарный синдром. Морфологические проявления синдрома Такоцубо характеризуются выраженным отеком интерстициальной ткани миокарда с мукоидным компонентом, умеренно выраженной диффузно-очаговой лимфомакрофагальной инфильтрацией стромы и очаговыми повреждениями кардиомиоцитов.