Vulnerable plaque

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. 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. Repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, that creates artery stenosis. 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: When this inflammation is combined with other stresses, such as high blood pressure (increased mechanical stretching and contraction of the arteries with each heart beat), it can cause the thin covering over the plaque to split, spilling the contents of the vulnerable plaque into the bloodstream. Recent studies have shown cholesterol crystals within the plaque play a key role in splitting the plaque and also inducing inflammation. The sticky cytokines on the artery wall capture blood cells (mainly platelets) that accumulate at the site of injury. When these cells clump together, they form a thrombus, sometimes large enough to block the artery. The most frequent cause of a cardiac event following rupture of a vulnerable plaque is blood clotting on top of the site of the ruptured plaque that blocks the lumen of the artery, thereby stopping blood flow to the tissues the artery supplies. Upon rupture, atheroma tissue debris may spill into the blood stream; this debris has cholesterol crystals and other material which is often too large (over 5 micrometers) to pass on through the capillaries downstream. In this, the usual situation, the debris obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply to, and death of, the previously supplied tissues. A severe case of this can be seen during angioplasty in the slow clearance of injected contrast down the artery lumen. This situation is often termed non-reflow.