Background There have been reports of procoagulant activity in patients with COVID‐19. Whether there is an association between pulmonary embolism (PE) and COVID‐19 in the emergency department (ED) is unknown. The aim of this study was to assess whether COVID‐19 is associated with PE in ED patients who underwent a computed tomographic pulmonary angiogram (CTPA). Methods A retrospective study in 26 EDs from six countries. ED patients in whom a CTPA was performed for suspected PE during a 2‐month period covering the pandemic peak. The primary endpoint was the occurrence of a PE on CTPA. COVID‐19 was diagnosed in the ED either on CT or reverse transcriptase–polymerase chain reaction. A multivariable binary logistic regression was built to adjust with other variables known to be associated with PE. A sensitivity analysis was performed in patients included during the pandemic period. Results A total of 3,358 patients were included, of whom 105 were excluded because COVID‐19 status was unknown, leaving 3,253 for analysis. Among them, 974 (30%) were diagnosed with COVID‐19. Mean (±SD) age was 61 (±19) years and 52% were women. A PE was diagnosed on CTPA in 500 patients (15%). The risk of PE was similar between COVID‐19 patients and others (15% in both groups). In the multivariable binary logistic regression model, COVID‐19 was not associated with higher risk of PE (adjusted odds ratio = 0.98, 95% confidence interval = 0.76 to 1.26). There was no association when limited to patients in the pandemic period. Conclusion In ED patients who underwent CTPA for suspected PE, COVID‐19 was not associated with an increased probability of PE diagnosis. These results were also valid when limited to the pandemic period. However, these results may not apply to patients with suspected COVID‐19 in general.

Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10 days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice.