Type II injury follows type I and is characterized by the adhesion of platelets. Various growth factors and vasoactivators are released, resulting in a process that may contribute to the development of a fibrointimal lesion or a lipid lesion surrounded by a thin capsule. The lipid lesion can be easily disrupted, leading to a type III lesion, thrombus formation, and continued growth of the atherosclerotic plaque. Large thrombi can be occlusive and can cause unstable angina or myocardial infarction. Studies in animals indicate that blood flow to a coronary artery that is already partially narrowed by extrinsic compression can be periodically impaired by microscopic thrombi composed of platelets, erythrocytes, and leukocytes.
Endothelial damage occurs at the site of coronary artery narrowing.
Platelet aggregates may mechanically obstruct an artery or synthesize and release vasoactive agents, which can have vasoconstrictive properties. These cyclic variations in blood flow can be prevented by inhibitors of thromboxane synthetase, such as aspirin, or by antagonists of serotonin receptors, alpha 2 receptors, or thromboxane receptors. Leukotriene C4 released from leukocytes in intracoronary thrombi also reduces coronary blood flow. PGI 2 is also a vasodilator. A variety of vasoactive agents stimulate the endothelial production of a relaxing factor that inhibits smooth muscle contraction.