No Epicardial Fat, No Plaque Rupture.

the vasa vasorum (VV). In this ex vivo study, LADs from 10 fresh cadavers of patients who had died of noncardiovascular causes were evaluated. The levels of inflammatory molecules from the adjacent EAT trimmed from the coronary artery were measured and the density of VV in the coronary artery was pathologically evaluated. The degree of inflammation in adjacent EAT was significantly higher in lipid-rich lesions than in lipid-poor lesions. In addition, adventitial VV was more prominent in the lipid-rich lesions compared with lipid-poor lesions, suggesting that EAT, together with inflammatory cells via VV, may play an important role in coronary plaque progression. Previous pathologic studies have demonstrated that the greatest amount of EAT is seen over the lateral right ventricular wall, followed by the anterior wall.6 Although EAT in the LCA is abundant in the proximal segment relative to the distal part, the RCA is deeply embedded in EAT from the P laque rupture is the primary mechanism of coronary thrombosis causing myocardial infarction and sudden cardiac death. The pathology of a ruptured plaque consists of a necrotic core with an overlying disrupted thin fibrous cap.1 Previous pathologic and clinical studies have consistently shown that plaque rupture occurs mainly in the proximal site of a coronary artery, especially in the left anterior descending artery (LAD).2 Structural stress of plaque in the proximal site of the coronary artery was believed to be one of the reasons for the nonuniform distribution of plaque rupture, because higher levels of structural stress could disrupt the fibrous cap.3 However, there may be other mechanisms because the “plaque structural stress” hypothesis cannot fully explain why plaque rupture in the right coronary artery (RCA) is most common in not only the proximal but also the mid segment.2,4 In this issue of the Journal, Ito et al5 shed light on the mechanism of nonuniform distribution of plaque rupture, showing an association of local inflammation in epicardial adipose tissue (EAT) and coronary plaque progression via Article p ????

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