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According to a widespread theory, thrombotic masses are not formed in the pulmonary artery (PA) but result from migration of blood clots from the venous system. This concept has prevailed in clinical practice for more than a century. However, a new technologic era has brought forth more diagnostic possibilities, and it has been shown that thrombotic masses in the PA could, in many cases, be found without any obvious source of emboli. Chronic obstructive pulmonary disease, asthma, sickle cell anemia, emergency and elective surgery, viral pneumonia, and other conditions could be complicated by PA thrombosis development without concomitant deep vein thrombosis (DVT). Different pathologies have different causes for local PA thrombotic process. As evidenced by experimental results and clinical observations, endothelial and platelet activation are the crucial mechanisms of this process. Endothelial dysfunction can impair antithrombotic function of the arterial wall through downregulation of endothelial nitric oxide synthase (eNOS) or via stimulation of adhesion receptor expression. Hypoxia, proinflammatory cytokines, or genetic mutations may underlie the procoagulant phenotype of the PA endothelium. Both endotheliocytes and platelets could be activated by protease mediated receptor (PAR)- and receptors for advanced glycation end (RAGE)-dependent mechanisms. Hypoxia, in particular induced by high altitudes, could play a role in thrombotic complications as a trigger of platelet activity. In this review, we discuss potential mechanisms of PA thrombosis in situ.

Background Venous thromboembolism (VTE) with the prevalence of pulmonary microcirculatory thrombosis is considered a common complication of novel coronavirus disease (COVID-19) that develops despite anticoagulation. Methods The clinical course of the disease and the autopsy findings of seven deceased patients with verified COVID-19 were analyzed. The chest computed tomography (CT) scan was routinely performed while CT pulmonary angiography and a duplex ultrasound scan (DUS) of the lower limbs were used in cases of suspected VTE. The VTE prophylaxis was administered to all patients with intermediate or therapeutic doses of low-molecular-weight heparin. The histological examination of the lung tissue and other organs was performed with particular attention paid to the pulmonary vasculature. Results Venous thromboembolism, including deep vein thrombosis in one patient and pulmonary artery thrombosis in two patients, was confirmed by imaging tests despite anticoagulation. Systemic thrombolysis was performed in two patients with putative and confirmed pulmonary embolism. An autopsy revealed the signs of acute respiratory distress syndrome in all seven patients. Abnormalities of lung vessels were found in all cases and were represented by dystrophy and necrosis in the endothelium and muscle fibers, and by infiltration by plasmatic cells, neutrophils, and lymphocytes. Multiple clots of variable maturity were observed. All those changes developed despite anticoagulation and were preserved after systemic thrombolysis. Conclusion Inflammatory and prothrombotic changes in the arterial wall in parallel with the lack of lung perfusion may cause diffuse arterial thrombosis in the lungs. This background may be responsible for the low response to systemic anticoagulation and thrombolysis in severe forms of COVID-19.

Goal Presentation of the first Russian computer program ( www.carotidscore.ru ) for risk stratification of postoperative complications of carotid endarterectomy (CEE). Material and methods The present study is based on the analysis of a multicenter Russian database that includes 25,812 patients after CEE operated on from 01/01/2010 to 04/01/2022. The following types of CEE were implemented: 6814 classical CEE with plastic reconstruction of the reconstruction zone with a patch; 18,998 eversion CEE. Results In the hospital postoperative period, 0.18% developed a lethal outcome, 0.14%—myocardial infarction, 0.35%—stroke. The combined endpoint was 0.68%. For each factor present in patients, a predictive coefficient was calculated. The prognostic coefficient was a numerical indicator reflecting the strength of the influence of each factor on the development of postoperative complications. Based on this formula, predictive coefficients were calculated for each factor present in patients in our study. The total contribution of these factors was reflected in “%” and denoted the risk of postoperative complications with a minimum value of 0% and a maximum of 100%. On the basis of the obtained calculations, a computer program CarotidSCORE was created. Its graphical interface is based on the QT framework ( https://www.qt.io ), which has established itself as one of the best solutions for desktop applications. It is possible not only to calculate the probability of developing a complication, but also to save all data about the patient in JSON format (for the patient’s personal card and his anamnesis). The CarotidSCORE program contains 47 patient parameters, including clinical-demographic, anamnestic and angiographic characteristics. It allows you to choose one of the four types of CEE, which will provide an accurate stratification of the risk of complications for each of them in person. Conclusion CarotidSCORE ( www.carotidscore.ru ) is able to determine the likelihood of postoperative complications in patients undergoing CEE.

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