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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.

Sepsis is a global economic and health burden. Dipeptidyl peptidase 3 (DPP3) is elevated in the plasma of septic patients. The highest levels of circulating DPP3 (cDPP3) are found in non-survivor septic shock patients. The aim of this study was to evaluate the benefits of inhibiting cDPP3 by a specific antibody, Procizumab (PCZ), on cardiac function in an experimental model of sepsis, the caecal ligature and puncture (CLP) model. Rats were monitored by invasive blood pressure and echocardiography. Results are presented as mean ± SD, with p <0.05 considered significant. PCZ rapidly restored left ventricular shortening fraction (from 39 ± 4% to 51 ± 2% before and 30 min after PCZ administration (p = 0.004)). Cardiac output and stroke volume were higher in the CLP + PCZ group when compared to the CLP + PBS group (152 ± 33 mL/min vs 97 ± 25 mL/min (p = 0.0079), and 0.5 ± 0.1 mL vs 0.3 ± 1.0 mL (p = 0.009), respectively) with a markedly reduced plasma DPP3 activity (138 ± 70 U/L in CLP + PCZ group versus 735 ± 255 U/L (p = 0.048) in the CLP + PBS group). Of note, PCZ rapidly reduced oxidative stress in the heart of the CLP + PCZ group when compared to those of the CLP + PBS group (13.3 ± 8.2 vs 6.2 ± 2.5 UI, p = 0.005, 120 min after administration, respectively). Our study demonstrates that inhibition of cDPP3 by PCZ restored altered cardiac function during sepsis in rats.