fibrous cap


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Related to fibrous cap: atheroma, fibrous capsule, Foam cells

fibrous cap

A layer of connective tissue, including smooth muscle cells and macrophages, that forms on an atherosclerotic plaque. Rupturing of the cap into the underlying plaque is the cause of acute arterial obstruction during myocardial infarction.
See also: cap
References in periodicals archive ?
The Operation + HFD + Chronic Stress group exhibited significantly thinner fibrous caps than the Operation + HFD group ([73.
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).
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.
23) Recently, the role of microcalcifications embedded in the vulnerable fibrous cap in the development of acute ruptures has been highlighted.
Persistence of thin fibrous cap atheromas can be a cyclic process characterized by rupture of the fibrous cap, thrombosis, thrombus dissolution by fibrinolysis, repair/scarring, and subsequent rupture.
Furthermore, with a new developing VH scale IVUS system, we were able to analyze the histologic components of the ruptured plaque with a large lipid core and a thin fibrous cap.
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.
9) It is postulated that systemic inflammation causes the fibrous cap to be thinned, with decreased smooth muscle synthesis and increased collagen breakdown.
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).