LAUSR

Acute deep vein thrombosis (DVT) and its most severe clinical complication pulmonary embolism (PE), is an important contributor to global cardiovascular mortality [1, 2]. VTE can be caused by several factors, including inflammation [3]. It is known since a long time that the cellular pathways of coagulation and inflammation are intrinsically coupled [4]. Patients diagnosed with a DVT or PE events might therefore benefit from targeted treatments of the underlying inflammatory state in order to improve thrombus resolution and prevent future recurrence. However, only few trials have been conducted for this purpose thus far, particularly because the cells and pathways involved in the interaction between inflammation and coagulation are not sufficiently elucidated. This article is protected by copyright. All rights reserved.