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Updated: Jul 22, 2025

A Porcine Model of Acute Autologous Pulmonary Embolism
Published on: September 6, 2024
Pulmonary Embolism of COVID-19: A Year of Reflection
Margarida Agudo1, Pedro Moura2, Francisca Santos1
1Internal Medicine, Centro Hospitalar de Setúbal, Setúbal, PRT.
Abstract:
Introduction The coronavirus disease 2019 (COVID-19) pandemic has brought about significant changes in the medical field. While primarily characterized as a respiratory syndrome, COVID-19 is also associated with vascular events, particularly thrombotic complications. These events can manifest as initial presentations or develop as complications during the course of the disease, predominantly driven by immune-mediated mechanisms. Methods Patients with thrombotic complications followed in the post-COVID-19 thrombosis consult of 2021 were retrospectively analyzed and assessed for predisposing factors for pulmonary embolism (PE), including thrombophilias. Patients underwent reassessments over a minimum six-month period following diagnosis to evaluate vascular reperfusion and the potential discontinuation of anticoagulant therapy. Results All patients with PE exhibited segmental or subsegmental PE. Pulmonary CT angiography revealed that only one patient did not show complete reperfusion after six months of anticoagulant therapy alone. There were no instances of recurrent thrombotic events observed during this observation period. Among the studied patients, hypertension, diabetes, and obesity were identified as the most prevalent predisposing factors. No patients were diagnosed with thrombophilias or other relevant factors. Despite extensive research on the predisposing mechanisms of this complication in recent years, limited data exist regarding patients with this specific complication. Discussion and conclusion Continued research into COVID-19 patients and their complications is crucial for understanding the pathophysiological mechanisms and risk factors associated with these complications. The findings of this study support the existence of a multifactorial mechanism, with a significant pro-inflammatory component exacerbated by pre-existing risk factors, rather than a purely prothrombotic mechanism.
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