Plaque is composed of lipids (fats and cholesterol), calcium, white blood cells, muscle cells, and connective tissue. It is metabolically active and can be hotter than surrounding tissues. White blood cells enter and modify the plaque by becoming part of its structure and by secreting enzymes that degrade the fibrous cap that covers the plaque. Plaque formation starts in early adulthood and progresses at varying rates depending on many factors. Generally, as plaque grows, more calcium accumulates within the plaque structure.
Because cholesterol is a significant component of plaque, it became a major focus of drug research—to the detriment, I believe, of investigating other promoters of atherosclerosis. Though elevated cholesterol can accelerate atherosclerosis, it is not the only cause of the problem. Some people with high cholesterol never get heart disease, and others with normal cholesterol develop extensive atherosclerosis. The reason for this is that not all cholesterol is the same, and cholesterol is not the only factor to consider.
Plaque goes through many stages. Plaque usually progresses from being soft (and vulnerable to rupture) to a harder, relatively more stable stage. Because soft plaque is more unstable than hard plaque, it is more dangerous. Mixed plaque contains soft and hard forms and is also likelier to rupture than hard plaque. Total plaque burden and rate of plaque growth also predict plaque rupture and heart attack risk regardless of plaque type (Boudi 2006).
Plaque forms and becomes stable or unstable for complex reasons. The cells found in plaque—endothelial cells, smooth muscle cells, platelets (a fragment from a cell called a megakaryocyte), and white blood cells—interact with their environment, such as during expansion and contraction of the blood vessel. The health of the blood vessel wall, the state of activation of the blood clotting mechanism, and inflammation are other interrelated processes that contribute to plaque formation.