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Introduction. Pulmonary embolism is one of the most frequent cardiovascular diseases, potentially leading to death. There is no validated biomarker with both high specificity and sensitivity. Aim. The aim of the study was to define the diagnostic importance of platelet count (PLT), mean platelet volume (MPV) and platelet distribution width (PDW) on acute pulmonary embolism. Material and methods. We retrospectively reviewed the medical records of 145 patients with clinically suspected acute pulmonary embolism admitted to the Emergency Department. Demographic data and laboratory tests were collected on admission. All patients underwent computed tomography (CT) angiography. Results. The total data of 145 patients were analyzed, including 65 patients (67±17 years; 30 men/35 women) with acute pulmonary embolism confirmed with CT and 80 patients (67±19 years; 26 men/54 women) with negative CT. The MPV did not differ between the patients with acute PE and the control group (8.0 fL [IQR: 7.6-8.4] vs. 7.9 fL [IQR: 7.4-8.7], p=0.45). There were no significant differences in PLT (220x10³/mm³ [IQR: 172-274] vs. 243x10³/mm³ [IQR: 186-286], p=0.12) and PDW (59.0 ± 6.9% vs. 57.2 ± 7.3%, p=0.12). Conclusions. Our results suggest that platelet indexes (at a single time point) are not a reliable diagnostic biomarkers of acute pulmonary embolism.
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Introduction and aim. A small number of critically ill patients with coronavirus disease (COVID-19) develop thromboembolism (arterial or venous), both micro- and macrovascular complications such as deep vein thrombosis, pulmonary embolism, and pulmonary arterial thrombosis. The objective of the study is to describe the pathophysiology of venous thromboembolism in patients with COVID-19. Material and methods. In this article a narrative review regarding pathophysiology of thromboembolism in patients with COVID-19. Analysis of the literature. The development of coagulopathy is a consequence of the intense inflammatory response associated with hypercoagulability, platelet activation, and endothelial dysfunction. The pathophysiology that relates pulmonary thromboembolism (PTE) with COVID-19 is associated with a hypercoagulable state. PTE is suspected in hospitalized patients presenting dyspnea, decreased oxygen requirement, hemodynamic instability, and dissociation between hemodynamic and respiratory changes. In COVID-19-associated coagulopathy, initially, patients present with elevated levels of fibrinogen and D-dimer, with minimal changes in prothrombin time and platelet count. The main risk factor for the development of pulmonary embolism is the increase in D-dimer that is associated with the development of PTE. The administration of iodine-based contrast agent to patients with COVID-19 would affect P-creatinine and renal function, where Ultrasound is viewed as cost-effective and highly portable, can be performed at the bedside. Conclusion. Acute respiratory distress syndrome severity in patients with COVID-19 can explain PTE as a consequence of an exaggerated immune response.
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