The Operation + HFD + Chronic Stress group exhibited significantly thinner
fibrous caps than the Operation + HFD group ([73.974 [+ or -] 8.144] vs.
Plaque rupture is characterized by intraluminal thrombus on a disrupted thin
fibrous cap overlying a necrotic core with infiltration of macrophages whereas plaque erosion manifests as thrombus on an intact
fibrous cap with less or deep-seated necrotic core.
These examples highlight the need for a reliable imaging technique with suitable resolution to identify plaque at high resolution (for example, thickness of vulnerable
fibrous cap <<65 [micro]m).
The effects on the
fibrous cap and necrotic core were reversed by the autophagy inhibitor 3-MA.
Compared to non-O type, the O type subjects showed a thicker minimum
fibrous cap thickness (0.075 [+ or -] 0.033 versus 0.061 [+ or -] 0.024, p < 0.001).
Previous studies [24] have suggested that plaque stability depends upon the plaque composition and state of the
fibrous cap. The tensile strength of the intima increases as a rupture of the
fibrous cap occurs.
Ulcerated plaque and calcified plaque are stable, whereas the others are unstable.19 Unstable plaques are pathologically typified by large lipid cores and thin
fibrous caps, but stable plaques are mainly manifested as concentric stenosis, smooth boundary and free of filling defect.
The cross-section includes 5 parts: the arterial wall, the
fibrous cap, the lumen, the lipid pool, and the calcified inclusion.
MMP-14 positive macrophages/FCMs were found predominantly in the shoulder regions (SR) of atheromatous carotid plaques (Figures 2(a)-2(c)), whereas TIMP-3 positive macrophages/FCMs occurred predominantly within and around the
fibrous cap (FC) of fibrous atheromatous plaques (Figures 2(d)-2(e)).
Thrombosis occurs as a consequence of a ruptured
fibrous cap, and this catastrophic phenomenon is very frequent at the inflamed and thinned sites of the
fibrous cap in advanced lesions.
A major feature of this process is lipid accumulation, and the atheromatous plaque can become covered with a
fibrous cap over the focal necrotic area in the later stages of this process.
Previous research has suggested that arterial FDG uptake like that observed is due to macrophage accumulation at the interface between the lipid core and the
fibrous cap in atherosclerotic plaques (Circulation 2002;105:2708-11).
