Background: Inflammation drives
atherosclerotic plaque rupture.
Not exact matches
As described in a scientific paper published earlier this year (Nature Genetics, 2004), this risk is probably the result of increased inflammation in
atherosclerotic plaques, contributing to
plaque rupture.
The tiny particles are 1,000 times smaller than the tip of a human hair, and are designed to latch on to
atherosclerotic plaques — hard deposits made from accumulated fat, cholesterol and calcium that build up on the walls of arteries and are prone to
rupture, producing dangerous clots.
This is most commonly due to occlusion (blockage) of a coronary artery following the
rupture of a vulnerable
atherosclerotic plaque, which is an unstable collection of lipids (cholesterol and fatty acids) and white blood cells (especially macrophages) in the wall of an artery.
Site of intimal
rupture or erosion of thrombosed coronary
atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant
plaque morphology.