The healthy epicardial coronary artery consists of three layers, the tunica intima, media, and adventitia.<unk>  and changes in the artery wall usually result in small aneurysms (enlargements) just large enough to compensate for the extra wall thickness with no change in the lumen diameter. However, eventually, typically as a result of rupture of vulnerable plaques and clots within the lumen over the plaque, stenosis (narrowing) of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual. Stenosis and closure Over time,<unk> ta usually progress in size and thickness and induce the surrounding muscular central region (the media) of the artery to stretch out, termed remodeling, typically just enough to compensate for their size such that the calibre of the artery opening (lumen) remains unchanged until typically over 50% of the artery wall cross-sectional area consists of<unk> tous tissue. Narrowed arterial blood vessel blocked with an<unk> . If the muscular wall enlargement eventually fails to keep up with the enlargement of the<unk>  volume, or a clot forms and organizes over the plaque, then the lumen of the artery becomes narrowed as a result of repeated ruptures, clots & fibrosis over the tissues separating the<unk>  from the blood stream. This narrowing becomes more common after decades of living, increasingly more common after people are in their 30s to 40s. The endothelium (the cell monolayer on the inside of the vessel) and covering tissue, termed fibrous cap, separate<unk>  from the blood in the lumen. If a rupture (see vulnerable plaque) of the endothelium and fibrous cap occurs, then both a shower of debris from the plaque (debris larger than 5 micrometres are too large to pass through capillaries)) combined with a platelet and clotting response (an injury/repair response to both the debris and at the rupture site) begins within fractions of a second, eventually resulting in narrowing or sometimes closure of the lumen. Eventually downstream tissue damage occurs due to closure or obstruction of downstream microvessels and/or closure of the lumen at the rupture, both resulting in loss of blood flow to downstream tissues. This is the principal mechanism of myocardial infarction, stroke or other related cardiovascular disease problems. While clots at the rupture site typically shrink in volume over time, some of the clot may become organized into fibrotic tissue resulting in narrowing of the artery lumen; the narrowings sometimes seen on angiography examinations, if severe enough. Since angiography methods can only reveal larger lumens, typically larger than 200 micrometres, angiography after a cardiovascular event commonly does not reveal what happened. Artery enlargement If the muscular wall enlargement is overdone over time, then a gross enlargement of the artery results, usually over decades of living. This is a less common outcome.<unk>  within aneurysmal enlargement (vessel bulging) can also rupture and shower debris of<unk>  and clot downstream. If the arterial enlargement continues to 2 to 3 times the usual diameter, the walls often become weak enough that with just the stress of the pulse, a loss of wall integrity may occur leading to sudden hemorrhage (bleeding), major symptoms and debility; often rapid death. The main stimulus for aneurysm formation is pressure atrophy of the structural support of the muscle layers. The main structural proteins are collagen and elastin. This causes thinning and the wall balloons allowing gross enlargement to occur, as is common in the abdominal region of the aorta.
Atheroma
Askin's tumor
Lymphangioma
Hemangioma
Nuchal fibroma
Chorangioma
Ganglion cyst
Baker's cyst