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The effectiveness of anticoagulant therapy in the prevention and treatment of pulmonary artery thrombosis and the possibility of anti-inflammatory therapy in preventing this complication in clinical practice and experiments were assessed. Data from patients with a new coronavirus infection and those suffering from urgent noninfectious pathology with confirmed pulmonary artery thrombosis were retrospectively analyzed. The outcomes of anticoagulant therapy and anticoagulant therapy combined with glucocorticoid and/or anticytokine drugs were assessed. Histological preparations of the lung vessels of patients were examined. Using an experimental model of rats with induced thrombosis of the posterior vena cava, changes in the pulmonary artery branches were assessed in the main group administered with edible mussel (Mytilus edulis) hydrolyzate and the control group given a physiological solution. No statistically significant relationship was found between the therapeutic, intermediate, and preventive anticoagulant therapy regimens and mortality, changes in lung dynamics, and D-dimer levels in 313 patients with new coronavirus infection. No predominance of any anticoagulant therapy regimen used was found among deceased patients. Thirty-nine patients were treated with glucocorticoid and/or anticytokine drugs in the presence of anticoagulant therapy. No statistically significant relationship in the onset of thrombotic complications was found between the groups receiving therapy with glucocorticoid and anticytokine drugs. No differences were noted in the drug-induced pathomorphosis of the wall of the pulmonary artery branches in the group receiving anticoagulant therapy or in the group receiving a combination of anticoagulant therapy and glucocorticoid and/or anticytokine drugs. Pulmonary artery thrombosis developed in all 19 patients suffering from urgent noninfectious pathology, 11 of whom were under anticoagulant therapy. In 12 of 15 rats in the control group with thrombosis of the posterior vena cava, blood clots were found in the lumen of the pulmonary artery branches. In 14 rats of the main group administered M. edulis hydrolyzate, no blood clots were found in the pulmonary artery branches. Thus, the systemic effects of anticoagulant therapy were offset by the local prothrombotic effects of the vascular wall caused by inflammation. Glucocorticoid and anticytokine drugs did not affect inflammatory changes in the vascular wall and did not prevent pulmonary artery thrombosis. The introduction of M. edulis in the experiment prevented pulmonary artery thrombosis in the presence of posterior vena cava thrombosis, which indicates a promising direction in the search for pathogenetic prevention of this complication.
Accumulating evidence supports the need to consider pulmonary artery thrombosis the separate thrombotic complication, which requires its own treatment algorithms. The aim of the work is to demonstrate the pulmonary artery thrombosis clinical aspects and the effect of the standard thrombotic prophylactic algorithms with clinical examples. Clinical cases of patients with pulmonary artery thrombosis are presented. Pulmonary artery thrombosis is considered to be the thrombotic obstruction of the pulmonary artery branches in the absence of venous and cardiac chambers thrombosis. Patient S. with COVID-19 and 75% of lung involvement was treated in the accordance with the actual COVID-19 treatment recommendations. Enoxaparin sodium 6000 IE once a day followed by the increasing dosage of 8000 IE twice a day was used. To prevent exacerbation tocilizumab was infused, and systemic thrombolytic therapy was performed. On the 6th day after systemic thrombolytic therapy patient died. Examination revealed thrombi in the pulmonary artery branches. Patient P. with continued growth of cerebral left frontoparietal region glioblastoma was hospitalized. Surgical tumor removal was performed a year ago. Conservative therapy, dexamethasone injections and anticoagulant prophylaxis (enoxaparin sodium 4000 IE once a day) were prescribed. After the patient death thrombi were found in the pulmonary artery segmental branches. Outpatient D. had a history of four episodes of dyspnea during the acute respiratory diseases. Computed tomography performed at the time of the third and fourth episodes revealed thrombi in the pulmonary artery segmental branches. The fourth episode occured despite anticoagulant prophylaxis with rivaroxaban (10 mg once a day). Patient was recommended to switch to low molecular weight heparins in case of any disease. There have been no recurrent episodes over the past 8 months. Distinctive features of pulmonary artery thrombosis pathogenesis determine the development of the complication despite anticoagulant prophylaxis. Preventive effect of anti-inflammatory drugs on the pulmonary artery thrombosis development has not been demonstrated.
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