If the atherosclerotic process continues and other risk factors are involved, the lipid core of the plaque grows and pushes the arterial wall out. Eventually, enzymes called myeloperoxidases and metalloproteinases can degrade the cellular matrix, thinning the fibrous cap making it capable of tearing. If this cap tears it will unmask collagen and lipids, which can allow rapid formation of a platelet plug. Once this aggregation and coagulation cascade begins, a thrombi or blood clot becomes part of the plaque and further occludes the artery. Plaque growth and or platelet aggregation will lead to blockage of the artery and then necrosis of the tissue it feeds. Varying degrees of pain, cerebral or pulmonary infarction, and/or ischemic heart disease result when this occlusion happens.
