After the introduction of the criteria for the definition of vulnerable plaque, 60 studies published in the past 7 years focused on histopathologic findings of culprit plaques from the coronary or carotid vessel walls (Appendix Table 3). Twenty-eight studies evaluated coronary artery samples, derived from living persons during coronary atherectomy or from autopsy specimens. Among the hallmark histopathologic features of vulnerability, macrophage infiltration of the plaque was the most commonly examined but only in 4 studies. Most of the studies analyzed the tissue expression of molecules or cells proposed to be involved in the pathophysiologic processes of the disease (such as C-reactive protein, matrix metalloproteinases, and lipoprotein-associated phospholipase A2) as potential pathology markers. In 19 studies, the histopathology features were examined in association with clinical outcomes, most commonly acute coronary syndrome (ACS), whereas in the remaining studies, experimental pathology markers (that is, inflammatory molecules expressed in the plaque tissue) were compared with reference histopathologic features, such as cap thickness, large lipid core, and inflammatory cells. Thirty-two studies evaluated carotid artery samples, almost exclusively taken from living persons (n = 31), given the easier availability of carotid artery samples after carotid endarterectomy, compared with coronary tree samples. Macrophage infiltration was again the most commonly evaluated hallmark feature of vulnerability but only in 3 studies; other studies evaluated the tissue expression of molecules, such as matrix metalloproteinases and vascular endothelial growth factor. Study outcomes included either clinical disease (that is, symptomatic carotid disease) in 18 studies or other histopathologic features in the remaining 14 studies.