Clinical medicine (London, England)
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Comment Letter
A Bayesian strategy for the asymptomatic healthcare worker.
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Review
Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis.
The novel coronavirus infectious disease (COVID-19) has rapidly spread and poses a great challenge to researchers, both in elucidating its pathogenic mechanism and developing effective treatments. It has been recently proposed that COVID-19 is an endothelial disease. ⋯ Consequently, oxidative stress could prime these cells to acquire a pro-thrombotic and pro-inflammatory phenotype, predisposing patients to thromboembolic and vasculitic events and to disseminated intravascular coagulopathy (DIC). This implies a pivotal role played by oxygen in the pathogenetic mechanism of COVID-19 disease, in that its availability would tune the oxidant state and consequent damage.
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During the current SARS-CoV-2 pandemic the restructure of healthcare services to meet the huge increase in demand for hospital resource and capacity has led to the proposal that where necessary ST elevation myocardial infarction (STEMI) could be managed by intravenous thrombolysis in the first instance as a means of reducing the workforce requirements of a primary angioplasty service run at a heart attack centre. Our modelling, based on data from the UK, shows that contrary to reducing demand, the effect on both mortality and bed occupancy would be negative with 158 additional deaths per year for each 10% reduction in primary angioplasty and at a cost of ~8,000 additional bed days per year for the same reduction. Our analysis demonstrates that specialist services such as heart attack pathways should be protected during the COVID crisis to maximise the appropriate use of resource and prevent unnecessary mortality.