Neutrophil extracellular traps: a new source of tissue factor in atherothrombosis

This editorial refers to ‘Expression of functional tissue factor by neutrophil extracellular traps in the culprit artery of acute myocardial infarction’, by D.A. Stakos et al., on page doi:10.1093/eurheartj/ehv007. Atherosclerotic cardiovascular diseases are still major causes of morbidity and mortality worldwide. Sudden rupture of vulnerable atherosclerotic plaques expose to the flowing blood prothrombotic molecules that trigger platelet aggregates that grow in association with an increase in fibrin deposition and further entrapment of inflammatory and red blood cells.1 The resulting thrombus may lead to blood flow cessation and subsequent acute ST-elevation myocardial infarction (STEMI).2 Thrombus aspiration has offered a unique opportunity to characterize antemortem the culprit coronary thrombus. In this regard, within the last years several studies in coronary thrombectomy specimens extracted from occluded arteries have provided insights as to thrombus composition, reporting that platelets, erythrocytes, and activated neutrophils are major contributors of arterial thrombosis after plaque rupture.3–6Neutrophils are critical components of the innate immune system launching the first line of host defence against invading microorganisms. Seminal work by Brinkman and colleagues in 20047 revealed that, in addition to the well-established mechanism of phagocytosis, activated neutrophils fight microbes through the release of web-like filamentous structures of decondensed chromatin (so-called neutrophil extracellular traps, NETs). NETs are …