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1.
Preprint in English | medRxiv | ID: ppmedrxiv-22278392

ABSTRACT

Background/ObjectivesCoronavirus disease 2019 (COVID-19) is associated with a hypercoagulable state and increased thrombotic risk in infected individuals. Several complex and varied coagulation abnormalities were proposed for this association1. Acetylsalicylic acid(ASA, aspirin) is known to have inflammatory, antithrombotic properties and its use was reported as having potency to reduce RNA synthesis and replication of some types of coronaviruses including human coronavirus-299E (CoV-229E) and Middle East Respiratory Syndrome (MERS)-CoV 2,3. We hypothesized that chronic low dose aspirin use may decrease COVID-19 mortality relative to ASA non-users. MethodsThis is a retrospective, observational cohort analysis of residents residing at Veterans Affairs Community Living Centers from December 13, 2020, to September 18, 2021, with a positive SARS-CoV-2 PCR test. Low dose aspirin users had low dose (81mg) therapy (10 of 14 days) prior to the positive COVID date and were compared to aspirin non-users (no ASA in prior 14 days). The primary outcome was mortality at 30 and 56 days post positive test and hospitalization. ResultsWe identified 1.823 residents who had SARS-CoV-2 infection and 1,687 residents were eligible for the study. Aspirin use was independently associated with a reduced risk of 30 days of mortality (adjusted HR, 0.60, 95% CI, 0.40-0.90) and 56 days of mortality (adjusted HR, 0.67, 95% CI, 0.47-0.95) ConclusionChronic low dose aspirin use for primary or secondary prevention of cardiovascular events is associated with lower COVID-19 mortality. Although additional randomized controlled trials are required to understand these associations and the potential implications more fully for improving care, aspirin remains a medication with known side effects and clinical practice should not change based on these findings.

2.
Preprint in English | medRxiv | ID: ppmedrxiv-21260676

ABSTRACT

ObjectivesCOVID-19 has had a severe impact on morbidity and mortality among nursing home (NH) residents. Earlier detection of SARS-CoV-2 may position us to better mitigate risk of spread. Both asymptomatic or pre-symptomatic transmission are common in outbreaks, and threshold temperatures, such as 38C, for screening for infection could miss timely detection in the majority. DesignRetrospective cohort study using electronic health records MethodsWe hypothesized that in long-term care residents, temperature trends with SARS-CoV-2 infection could identify infection in pre-symptomatic and asymptomatic individuals earlier. We collected information about age and other demographics, baseline temperature, and specific comorbidities. We created standardized definitions, and an alternative hypothetical model to test measures of temperature variation and compare outcomes to the VA reality. Settings and participantsOur subjects were 6,176 residents of the VA NHs who underwent SARS-CoV-2 trigger testing. ResultsWe showed that a change from baseline of >0.4C identifies 47% of the SARS-CoV-2 positive NH residents early, and achieves earlier detection by 42.2 hours. Range improves early detection to 55% when paired with a 37.2C cutoff, and achieves earlier detection by 44.4 hours. Temperature elevation >0.4C from baseline, when combined with a 0.7C range, would detect 52% early, leading to earlier detection by more than 3 days in 22% of the residents. This earlier detection comes at the expense of triggering 57,793 tests, as compared to the number of trigger tests ordered in the VA system of 40,691. Conclusion and implicationsOur model suggests that current clinical screening for SARS-CoV-2 in NHs can be substantially improved upon by triggering testing using a patient-derived baseline temperature with a 0.4C degree relative elevation or temperature variability of 0.7C trigger threshold for SARS-CoV2 testing. Such triggers could be automated in facilities that track temperatures in their electronic records.

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