In our current study, chronic stress increased plaque vulnerability to rupture, characterized with thinner
fibrous caps, larger lipid cores, more macrophages and new vessels but less SMCs and elastic fibers.
(a, b, c) Plaque erosion: adjacent thrombus (yellow arrows) overlying an intact
fibrous cap.
Besides that, calcifications locating in the middle area (small [alpha]) of
fibrous cap are seemly influenced more than those in the shoulder area (large [alpha]).
(30) Recently, a combination of multi-vessel IVUS and near-infrared spectroscopy techniques has exhibited promising efficacy in the detection of the development of inflamed fibroatheromas with thinner
fibrous caps, greater plaques, and necrotic core areas possessing the characteristics of increased plaque instability.
More mature plaques (stable plaques) have a thick
fibrous cap, which is less likely to rupture.
As the LRNC of the lesion enlarges, macrophages and lymphocytes infiltrate the
fibrous cap, causing it to thin.
Vulnerable plaque is characterized by a thin
fibrous cap, large lipid core, and increased inflammatory cell penetration in the shoulder regions.
Plaques with large lipid cores and thin
fibrous caps are vulnerable to rupture, resulting in thrombus formation and possible arterial occlusion.
Macrophages are capable of degrading extracellular matrix by phagocytosis or by secreting proteolytic enzymes such as plasminogen activators and a family of matrix metalloproteinases (collagenases, gelatinases and stromeolysins) which may weaken the
fibrous cap, predisposing it to rupture.
Vulnerable plaques which are thought to be the precursors of ACS have thin
fibrous cap, large lipid core, more inflammatory cells and less collagen (13,14).
Early studies reported evidence of local activation of inflammatory cells in the shoulder region of coronary plaques, with release of proteolytic enzymes (metalloproteinases) that degrade the extracellular matrix and contribute to the
fibrous cap weakening and plaque instability (1-3).