Atheroma

An atheroma, or atheromatous plaque ('plaque'), is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults.The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, narrowing it and restricting blood flow. Atheroma is the pathological basis for the disease entity atherosclerosis, a subtype of arteriosclerosis. An atheroma, or atheromatous plaque ('plaque'), is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults.The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The accumulated material forms a swelling in the artery wall, which may intrude into the channel of the artery, narrowing it and restricting blood flow. Atheroma is the pathological basis for the disease entity atherosclerosis, a subtype of arteriosclerosis. For most people, the first symptoms result from atheroma progression within the heart arteries, most commonly resulting in a heart attack and ensuing debility. However, the heart arteries, because (a) they are small (from about 5 mm down to microscopic), (b) they are hidden deep within the chest and (c) they never stop moving, have been a difficult target organ to track, especially clinically in individuals who are still asymptomatic. Additionally, all mass-applied clinical strategies focus on both (a) minimal cost and (b) the overall safety of the procedure. Therefore, existing diagnostic strategies for detecting atheroma and tracking response to treatment have been extremely limited. The methods most commonly relied upon, patient symptoms and cardiac stress testing, do not detect any symptoms of the problem until atheromatous disease is very advanced because arteries enlarge, not constrict in response to increasing atheroma. It is plaque ruptures, producing debris and clots which obstruct blood flow downstream, sometimes also locally (as seen on angiograms), which reduce/stop blood flow. Yet these events occur suddenly and are not revealed in advance by either stress testing, stress tests or angiograms. The healthy epicardial coronary artery consists of three layers, the intima, media, and adventitia. Atheroma 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. Over time, atheromata 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 caliber of the artery opening (lumen) remains unchanged until typically over 50% of the artery wall cross-sectional area consists of atheromatous tissue. If the muscular wall enlargement eventually fails to keep up with the enlargement of the atheroma 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 atheroma 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 atheroma from the blood in the lumen. If a rupture (see vulnerable plaque) of the endothelium and fibrous cap occurs, then both (a) a shower of debris from the plaque combined with (b) a platelet and clotting response (to both the debris and at the rupture site) occurs within fractions of a second. The rupture results in both (a) a shower of debris occluding smaller downstream vessels (debris larger than 5 microns are too large to pass through capillaries)) combined with (b) platelet and clot accumulation over the rupture (an injury/repair response) resulting in narrowing, sometimes closure, of the lumen. Downstream tissue damage occurs due to (a) closure of downstream microvascular and/or (b) closure of the lumen at the rupture, both resulting in loss of blood flow to downstream capillary microvasulature. 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 >>200 microns, angiography after a cardiovascular event commonly does not reveal what happened.