COVID-19 first appeared in Wuhan, Hubei Province, China, in December 2019. Thought to be of zoonotic origin, it has been named SARS-CoV-2 (COVID-19) and has spread rapidly. As of April 20, 2020, there have been >2.4 million cases recorded worldwide. The inflammatory process, cytokine storm, and lung injury that are associated with COVID-19 can put patients at an increased risk of thrombosis. The total incidence of thrombotic events in COVID-19 patients is currently uncertain. Those with more severe disease and with other risk factors, including increasing age, male sex, obesity, cancer, comorbidities, and intensive care unit admission, are at higher risk of these events. However, there is little international guidance on managing these risks in COVID-19 patients. In this paper, we explore the current evidence and theories surrounding thrombosis in these unique patients and reflect on experience from our center.
Coronavirus disease (COVID‐19) first presented in Wuhan, Hubei province, China in December 2019. Since then, it has rapidly spread across the world, and is now formally considered a pandemic. The disease does not discriminate but increasing age and the presence of comorbidities are associated with severe form of the disease and poor outcomes. Although the prevalence of COVID‐19 in patients with cardiovascular disease is under‐reported, there is evidence that pre‐existing cardiac disease can render individuals vulnerable. It is thought that COVID‐19 may have both a direct and indirect effect on the cardiovascular system; however, the primary mechanism of underlying cardiovascular involvement is still uncertain. Of particular interest is the role of angiotensin‐converting enzyme 2, which is well known for its cardiovascular effects and is also considered to be important in the pathogenesis of COVID‐19. With a range of different drug candidates being suggested, effective anti‐virals and vaccines are an area of on‐going research. While our knowledge of COVID‐19 continues to rapidly expand, this review highlights recent advances in our understanding of the interaction between COVID‐19 and the cardiovascular system.
Electronic nicotine delivery systems, or e.cigarettes utilise a liquid solution that normally contains propylene glycol (PG) and vegetable glycerine (VG) to generate vapour and act as a carrier for nicotine and flavourings. Evidence indicated these 'carriers' reduced growth and survival of epithelial cells including those of the airway. We hypothesised that 3% PG or PG mixed with VG (3% PG:VG, 55:45) inhibited glucose uptake in human airway epithelial cells as a first step to reducing airway cell survival. Exposure of H441 or human bronchiolar epithelial cells (HBEC) to PG and PG/VG (30-60 minutes) inhibited glucose uptake and mitochondrial ATP synthesis. PG/VG inhibited glycolysis. PG/VG and mannitol reduced cell volume and height of air-liquid interface cultures. Mannitol but not PG/VG increased phosphorylation of p38 MAPK. PG/VG reduced TEER which was associated with increased transepithelial solute permeability. PG/VG decreased FRAP of GFP linked glucose transporters GLUT1 and GLUT10 indicating that glucose transport function was compromised. Puffing PG/VG vapour onto the apical surface of primary HBEC for 10 mins to mimic the effect of e.cigarette smoking also reduced glucose transport. In conclusion, short term exposure to PG/VG, key components of e.cigarettes, decreased glucose transport and metabolism in airway cells. We propose that this was a result of PG/VG reduced cell volume and membrane fluidity, with further consequences on epithelial barrier function. Taken together, we suggest these factors contribute to reduced defensive properties of the epithelium. We propose that repeated/chronic exposure to these agents are likely to contribute to airway damage in e-cigarette users.
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