BACKGROUND AND OBJECTIVE: Low-dose acetylsalicylic acid (ASA, aspirin) is a well-known and frequently studied drug for primary and secondary prevention of disease due to its anti-inflammatory and coagulopathic effects. COVID-19 complications are attributed to the role of thrombo-inflammation. Studies regarding the use of low-dose ASA in COVID-19 are limited. For this reason, we propose that the use of low-dose ASA may have protective effects in COVID-19-related thromboembolism and lung injury. This study was conducted to assess the efficacy of low-dose ASA compared with enoxaparin, an anticoagulant, for the prevention of thrombosis and mechanical ventilation. METHODS: We conducted a retrospective cohort study on COVID-19-confirmed hospitalized patients at the Mansoura University Quarantine Hospital, outpatients, and home-isolated patients from September to December 2020 in Mansoura governorate, Egypt. Binary logistic regression analysis was used to assess the effect of ASA compared with enoxaparin on thromboembolism, and mechanical ventilation needs. RESULTS: This study included 225 COVID-19 patients. Use of ASA-only (81-162 mg orally daily) was significantly associated with reduced thromboembolism (OR 0.163, p = 0.020), but both low-dose ASA and enoxaparin, and enoxaparin-only (0.5 mg/kg subcutaneously (SC) daily as prophylactic dose or 1 mg/kg SC every 12 hours as therapeutic dose) were more protective (odds ratio [OR] 0.010, OR 0.071, respectively, p < 0.001). Neither ASA-only nor enoxaparin-only were associated with a reduction in mechanical ventilation needs. Concomitant use of low-dose ASA and enoxaparin was associated with reduced mechanical ventilation (OR 0.032, 95% CI 0.004-0.226, p = 0.001). CONCLUSIONS: Low-dose ASA-only use may reduce the incidence of COVID-19-associated thromboembolism, but the reduction may be less than that of enoxaparin-only, and both ASA and enoxaparin. Concomitant use of ASA and enoxaparin demonstrates promising results with regard to the reduction of thrombotic events, and mechanical ventilation needs.
Subject(s)COVID-19 , Thrombosis , Anticoagulants/therapeutic use , Aspirin , Enoxaparin/therapeutic use , Humans , Respiration, Artificial , Retrospective Studies , SARS-CoV-2 , Thrombosis/prevention & control
OBJECTIVES: To review the pathophysiology of COVID-19 disease, potential aspirin targets on this pathogenesis and the potential role of aspirin in patients with COVID-19. DESIGN: Narrative review. SETTING: The online databases PubMed, OVID Medline and Cochrane Library were searched using relevant headlines from 1 January 2016 to 1 January 2021. International guidelines from relevant societies, journals and forums were also assessed for relevance. PARTICIPANTS: Not applicable. RESULTS: A review of the selected literature revealed that clinical deterioration in COVID-19 is attributed to the interplay between endothelial dysfunction, coagulopathy and dysregulated inflammation. Aspirin has anti-inflammatory effects, antiplatelet aggregation, anticoagulant properties as well as pleiotropic effects on endothelial function. During the COVID-19 pandemic, low-dose aspirin is used effectively in secondary prevention of atherosclerotic cardiovascular disease, prevention of venous thromboembolism after total hip or knee replacement, prevention of pre-eclampsia and postdischarge treatment for multisystem inflammatory syndrome in children. Prehospital low-dose aspirin therapy may reduce the risk of intensive care unit admission and mechanical ventilation in hospitalised patients with COVID-19, whereas aspirin association with mortality is still debatable. CONCLUSION: The authors recommend a low-dose aspirin regimen for primary prevention of arterial thromboembolism in patients aged 40-70 years who are at high atherosclerotic cardiovascular disease risk, or an intermediate risk with a risk-enhancer and have a low risk of bleeding. Aspirin's protective roles in COVID-19 associated with acute lung injury, vascular thrombosis without previous cardiovascular disease and mortality need further randomised controlled trials to establish causal conclusions.
Subject(s)Anti-Inflammatory Agents, Non-Steroidal , Aspirin , COVID-19 , Thromboembolism , Adult , Aged , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Aspirin/administration & dosage , Aspirin/adverse effects , Aspirin/therapeutic use , COVID-19/complications , COVID-19/physiopathology , COVID-19/therapy , Humans , Inflammation , Middle Aged , Practice Guidelines as Topic , Thromboembolism/drug therapy , Thromboembolism/etiology , Thromboembolism/prevention & control
INTRODUCTION: The role of systemic corticosteroid as a therapeutic agent for patients with COVID-19 pneumonia is controversial. OBJECTIVE: The purpose of this study was to evaluate the effect of corticosteroids in non-intensive care unit (ICU) patients with COVID-19 pneumonia complicated by acute hypoxemic respiratory failure (AHRF). METHODS: This was a single-center retrospective cohort study, from 16th March, 2020 to 30th April, 2020; final follow-up on 10th May, 2020. 265 patients consecutively admitted to the non-ICU wards with laboratory-confirmed COVID-19 pneumonia were screened for inclusion. 205 patients who developed AHRF (SpO2/FiO2 ≤ 440 or PaO2/FiO2 ≤ 300) were only included in the final study. Direct admission to the Intensive care unit (ICU), patients developing composite primary outcome within 24 hours of admission, and patients who never became hypoxic during their stay in the hospital were excluded. Patients were divided into two cohorts based on corticosteroid. The primary outcome was a composite of ICU transfer, intubation, or in-hospital mortality. Secondary outcomes were ICU transfer, intubation, in-hospital mortality, discharge, length of stay, and daily trend of SpO2/FiO2 (SF) ratio from the index date. Cox-proportional hazard regression was implemented to analyze the time to event outcomes. RESULT: Among 205 patients, 60 (29.27%) were treated with corticosteroid. The mean age was ~57 years, and ~75% were men. Thirteen patients (22.41%) developed a primary composite outcome in the corticosteroid cohort vs. 54 (37.5%) patients in the non-corticosteroid cohort (P = 0.039). The adjusted hazard ratio (HR) for the development of the composite primary outcome was 0.15 (95% CI, 0.07-0.33; P <0.001). The adjusted hazard ratio for ICU transfer was 0.16 (95% CI, 0.07 to 0.34; P < 0.001), intubation was 0.31 (95% CI, 0.14 to 0.70; P- 0.005), death was 0.53 (95% CI, 0.22 to 1.31; P- 0.172), composite of death or intubation was 0.31 (95% CI, 0.15 to 0.66; P- 0.002) and discharge was 3.65 (95% CI, 2.20 to 6.06; P<0.001). The corticosteroid cohort had increasing SpO2/FiO2 over time compared to the non-corticosteroid cohort who experience decreasing SpO2/FiO2 over time. CONCLUSION: Among non-ICU patients hospitalized with COVID-19 pneumonia complicated by AHRF, treatment with corticosteroid was associated with a significantly lower risk of the primary composite outcome of ICU transfer, intubation, or in-hospital death, composite of intubation or death and individual components of the primary outcome.
Subject(s)Adrenal Cortex Hormones/therapeutic use , Coronavirus Infections/drug therapy , Pneumonia, Viral/drug therapy , Adult , Aged , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/mortality , Coronavirus Infections/virology , Female , Hospital Mortality , Humans , Intensive Care Units , Kaplan-Meier Estimate , Male , Middle Aged , New York , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/virology , Proportional Hazards Models , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/etiology , Retrospective Studies , SARS-CoV-2 , Treatment Outcome
BACKGROUND Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the viral pathogen responsible for coronavirus disease 2019 (COVID-19), a pandemic respiratory illness. While many patients experience mild to moderate symptoms, severely affected patients often progress to acute respiratory distress syndrome (ARDS). Specific to COVID-19, abnormal coagulability appears to be a principal instigator in the progression of disease severity and mortality. In this report we summarize a case of COVID-19 in which extreme thrombophilia led to patient demise. CASE REPORT A 67-year-old man in New York presented to the hospital 14 days after testing positive for SARS-CoV-2 at an outpatient site. His initial presenting symptoms included sore throat, headache, fever, and diarrhea. He was brought in by his wife after developing sudden onset confusion and dysarthria. The patient's clinical picture, which was unstable on presentation, further deteriorated to involve significant desaturations, generalized seizure activity, and cardiac arrest requiring resuscitation. Upon return to spontaneous circulation, the patient required intensive care unit admission, mechanical ventilation, and vasopressor increases. Comprehensive workup uncovered coagulopathy with multiple thrombotic events involving the brain and lungs as well as radiographic evidence of severe lung disease. In the face of an unfavorable clinical picture, the family opted for comfort care measures. CONCLUSIONS In this case report on a 67-year-old-man with COVID-19, we present an account of extreme hypercoagulability that led to multiple thrombotic events eventually resulting in the man's demise. Abnormal coagulation 14 days from positive testing raises the question of whether outpatients with COVID-19 should be screened for hypercoagulability and treated with prophylactic anticoagulation/antiplatelet agents.