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Background: In patients hospitalised with COVID-19, an increased incidence of thromboembolic events, such as pulmonary embolism, deep vein thrombosis and stroke, has been reported. It is unknown whether anticoagulation can prevent these complications and improve outcome. Methods: A systematic literature search was performed to answer the question: What is the effect of (prophylactic and therapeutic dose) anticoagulation therapy in COVID-19 patients on cardiovascular and thromboembolic complications and clinical outcome? Relevant outcome measures were mortality (crucial), hospital admission, length of stay, thromboembolic complications (pulmonary embolism, stroke, transient ischaemic attack), need for mechanical ventilation, acute kidney injury and use of renal replacement therapy. Medline and Embase databases were searched with relevant search terms until 17 July 2020. After systematic analysis, eight studies were included. Analysis was stratified for the start of anticoagulation before or during hospital admission. Results: There was insufficient evidence that therapeutic anticoagulation could improve the outcome in patients hospitalised with COVID-19. None of the studies demonstrated improved mortality, except for one very small Italian study. Furthermore, none of the studies showed a positive effect of anticoagulation on other outcome measures in COVID-19, such as ICU admission, length of hospital stay, thromboembolic complications, need for mechanical ventilation, acute kidney failure or need for renal replacement therapy, except for two studies demonstrating an association between anticoagulation and a lower incidence of pulmonary embolism. However, the level of evidence of all studies varied from 'low' to 'very low', according to the GRADE methodology. Conclusion: Analysis of the literature showed that there was insufficient evidence to answer our objective on the effect of anticoagulation on outcome in COVID-19 patients, especially due to the low scientific quality of the described studies. Randomised controlled studies are needed to answer this question. [ABSTRACT FROM AUTHOR]

Background: There has been debate on the use of angiotensin-converting enzyme‑2 (ACE2) expression mediating pharmacotherapy in COVID-19 infected patients. Although it has been suggested that these drugs might lead to a higher susceptibility and severity of COVID-19 infection, experimental data suggest these agents may reduce acute lung injury via blocking angiotensin-II-mediated pulmonary permeability, inflammation and fibrosis. Methods: A systematic literature search was performed to answer the question: What is the effect of medications that influence ACE2 expression (ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), nonsteroidal anti-inflammatory drugs (NSAIDs) and thiazolidinediones) on the outcomes of COVID-19? Relevant outcome measures were mortality (crucial), hospital admission, length of stay, thromboembolic complications (pulmonary embolism, stroke, transient ischaemic attack), need for mechanical ventilation, acute kidney injury and use of renal replacement therapy. Medline and Embase databases were searched with relevant search terms until 24 June 2020. After systematic analysis, nine studies were included. Results: The results were described for two different groups, an overall group in which all users were compared with non-users and a group in which only hypertensive patients were included. Within each group a distinction was made between results for ACEI/ARB use, ACEI use, ARB use, NSAID use and thiazolidinedione use. None of the studies demonstrated increased mortality in the two groups. Furthermore, none of the studies showed an effect on other outcome measures in COVID-19, such as ICU admission, length of hospital stay, thromboembolic complications, need for mechanical ventilation, acute kidney failure or need for renal replacement therapy. However, the level of evidence of all studies varied from 'moderate' to 'very low', according to the GRADE methodology. Conclusion: Analysis of the literature demonstrated that there was insufficient evidence to answer our objective on the effect of ACE2 expression mediating pharmacotherapy on outcome in COVID-19 patients, especially due to the low scientific quality of the described studies. Randomised controlled studies are needed to answer this question. [ABSTRACT FROM AUTHOR]

Background: COVID-19 can cause myocardial injury in a significant proportion of patients admitted to the hospital and seems to be associated with worse prognosis. The aim of this review was to study how often and to what extent COVID-19 causes myocardial injury and whether this is an important contributor to outcome with implications for management. Methods: A literature search was performed in Medline and Embase. Myocardial injury was defined as elevated cardiac troponin (cTn) levels with at least one value > 99th percentile of the upper reference limit. The primary outcome measure was mortality, whereas secondary outcome measures were intensive care unit (ICU) admission and length of hospital stay. Results: Four studies and one review were included. The presence of myocardial injury varied between 9.6 and 46.3%. Myocardial injury was associated with a higher mortality rate (risk ratio (RR) 5.54, 95% confidence interval (CI) 3.48–8.80) and more ICU admissions (RR 3.78, 95% CI 2.07–6.89). The results regarding length of hospital stay were inconclusive. Conclusion: Patients with myocardial injury might be classified as high-risk patients, with probably a higher mortality rate and a larger need for ICU admission. cTn levels can be used in risk stratification models and can indicate which patients potentially benefit from early medication administration. We recommend measuring cTn levels in all COVID-19 patients admitted to the hospital or who deteriorate during admission. [ABSTRACT FROM AUTHOR]