A vulnerable plaque is a kind of atheromatous plaque – a collection of white blood cells (primarily macrophages) and lipids (including cholesterol) in the wall of an artery – that is particularly unstable and prone to produce sudden major problems such as a heart attack or stroke. The defining characteristics of a vulnerable plaque include but are not limited to: a thin fibrous cap, large lipid-rich necrotic core, increased plaque inflammation, positive vascular remodeling, increased vasa-vasorum neovascularization, and intra-plaque hemorrhage. These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture. Increased hemodynamic stress, e.g. increased blood pressure, especially pulse pressure (systolic blood pressure vs. diastolic blood pressure difference), correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels the individual does routinely. Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen. Tearing of the cover is called plaque rupture. However, a repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, that creates artery stenosis. Formation Researchers have found that accumulation of white blood cells, especially macrophages, termed inflammation, in the walls of the arteries leads to the development of "soft" or vulnerable plaque, which when released aggressively promotes blood clotting. Researchers now think that vulnerable plaque, (see atherosclerosis) is formed in the following way: Hyperlipidemia, hypertension, smoking, homocysteine, hemodynamic factors, toxins, viruses, and/or immune reactions results in chronic endothelial injury, dysfunction, and increased permeability. Lipoprotein LDL particles, which carry fats (including the fat cholesterol made by every human cell) within the water/plasma portion of the blood stream, are absorbed into the intima, past the endothelium lining, some of the LDL-lipoprotein particles become oxidized and this attracts macrophages that uptake the particles. This process typically starts in childhood. To be specific: oxidized lipoprotein particles in the artery wall are an irritant which causes the release of proteins (called cytokines) which attract monocyte white blood cells (white blood cells are the inflammatory cells within the body). The cytokines induce the endothelial cells lining the artery wall to display adhesion molecules that attract immune-system white blood cells (to be specific, monocytes). The monocytes squeeze into the artery wall. Once inside, they transform