ABSTRACT
Background and aims: Clinicians and researchers have addressed concerns about the negative impact of COVID-19 outbreaks on the ability of health care systems to provide timely assessment and acute therapies to patients with stroke. The aims of this study are to describe stroke care during the first wave of the COVID-19 pandemic compared to the same period the year before at a large acute care hospital in Sweden. Methods: In this cohort study data were collected from March 1st to August 31st in 2019 and 2020 on all patients diagnosed with stroke and TIA and registered at Danderyd Hospital in the national quality registry (Riksstroke). Data were completed with information from the medical record. Sweden had no lockdown during 2020. The number of patients with COVID-19 the same period 2020 treated at Danderyd Hospital were collected. Results: In year 2019 there were 472 registered stroke patients at Danderyd Hospital, compared to 481 registered stroke patients the same period during 2020. The number of minor stroke and TIA during the period in 2019 compared to 2020 were 424 versus 410 respectively (-3.3%). During the study period 2020 1428 patients with a COVID-19 diagnosis were treated. There was an increased delay from onset to arrival to the ED and door-to needle time. The rate of admission to Stroke Unit care and the rate of thrombolysis was maintained. Conclusions: There were no difference in the number of patients diagnosed with stroke and TIA during the first wave of the COVID-19 pandemic.
ABSTRACT
Background : Angiotensin-converting enzyme 2 (ACE2) is the main entry receptor for SARS-CoV-2, but how virus-receptor interactions affect the RAS-balance and COVID-19 pathology is largely unknown. Aims : To measure soluble ACE2 (sACE2) and sACE during and after COVID-19 and investigate associations with risk factors for severe COVID-19, outcome and markers of thromboinflammation. Methods : Plasma sACE2 and sACE were measured by ELISA in 114 hospital-treated patients with COVID-19 and 10 healthy controls. Follow-up samples after four months were available for 58/114 patients. Markers of inflammation and endothelial dysfunction during COVID-19 were available from routine testing or had been previously determined (VWF, factor VIII, D-dimer, IL-6, TNFa and PAI-1). Results : Levels of sACE2 were higher in COVID-19 patients than in healthy controls, median 5.0 (interquartile range 2.8-11.8) ng/ml versus 1.4 (1.1-1.6) ng/ml, P < 0.0001. sACE2 was higher in men than women, but was not affected by other risk factors for severe COVID-19. sACE2 decreased to 2.3 (1.6-3.9) ng/ml at follow-up, P < 0.0001, but remained higher than in healthy controls, P = 0.012. Follow-up sACE2 was associated with several risk factors for severe COVID-19 and treatment with RAS-inhibition. sACE was marginally lower during COVID-19 compared with four months later 57 (45-70) ng/ml versus 72 (52-87) ng/ ml, P = 0.008. Levels of sACE2 and sACE were not associated with survival or disease severity (care level, respiratory support). sACE2 during COVID-19 correlated positively with monocyte count and platelet count, while sACE was negatively correlated with both. sACE2 correlated with VWF, fVIII and D-dimer, while sACE correlated with IL-6, TNFα and PAI-1. Conclusions : Shedding of ACE2 is increased and shedding of ACE is marginally decreased in COVID-19. sACE2 and sACE differ distinctly in correlations with markers of thromboinflammation, which may suggest different types of underlying endothelial injury, alternatively release from different cell types or vascular beds.