page_title: Atheroma
section_title: Stenosis and closure
hierarchical_section_title: Atheroma / Mechanism / Stenosis and closure
caption_attribution_description: English: As atheroma enlarges, the arterial wall ruptures and releases blood clots that lead to narrowing of the artery.
context_page_description: An atheroma, or atheromatous plaque, is an abnormal accumulation of material in the inner layer of the wall of an artery.
  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 lumen of the artery, narrowing it and restricting blood flow. Atheroma is the pathological basis for the disease entity atherosclerosis, a subtype of arteriosclerosis.
context_section_description: 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 calibre 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 micrometres 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 larger than 200 micrometres, angiography after a cardiovascular event commonly does not reveal what happened.
caption: Narrowed arterial blood vessel blocked with an anteroma.
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