LAUSR

The exploration of the steps that lead to coronary thrombi needs another chapter. Decades ago, it was found that the majority (≈3 of 4) of lesions underlying lethal thrombi featured a necrotic core into which blood had entered through a severed fibrous cap.1 Sometimes, bits of core material were embedded in the thrombus linking cap rupture and thrombosis closely in time. Like watching a crashed car or a broken plate, it took modest imagination to understand what must have happened. A thin fibrous cap had ruptured, ripping open the lesion, and exposing the thrombogenic core to the hemostatic system. The lack of a credible alternative mechanism that could explain the observed has made it less of a problem that re-enactment of plaque rupture in model systems or formal proof for the sequence of events in humans have been difficult to achieve. Article, see p 31 For the remainder of thrombi that are not formed on ruptured plaques, it is a completely different game. These cases give few signs away about what caused them. Endothelial cells (ECs) at the plaque-thrombus interface are generally absent, leading to the term plaque erosion, and macrophages are rarely conspicuous.2 More notably, neutrophils are often present.3 But, autopsies cannot tell for sure whether the missing endothelium and neutrophil accumulation were the cause or result of thrombosis. This is not an academic question. EC sloughing and neutrophil invasion occur secondarily to stasis-induced venous thrombosis,4 and thrombi precipitated by plaque rupture can produce the appearance of plaque erosion in neighboring segments.2 The idea that erosions are preceded by plaques deprived of large regions of its endothelial lining may thus be far too …