Chapter 54 - Coronary Atherosclerosis and Restenosis

Abstract

This chapter reviews the current concepts regarding the pathogenesis of atherosclerosis with special emphasis on plaque composition, the pathogenesis of plaque rupture, and the development of stable and unstable coronary syndromes. It also summarized current concepts concerning the pathogenesis of restenosis after balloon angioplasty with emphasis on the role of neointimal proliferation and vascular wall remodeling. Atherosclerosis is the form of arteriosclerosis that involves generally the larger and medium-sized arteries and it is the entity that forms the pathogenetic basis underlying most forms of ischemic heart disease. Atherosclerosis has been referred to primarily as a disease of the intima. The changes are also found in the media, which include medial thinning, calcific deposits, phenotypic changes of the smooth muscle cells, and even foam cell accumulation, which may depend on the degree of vascular injury, age of the lesion, and lipoprotein levels in the blood. The adventitia is also intimately involved, with changes including increased fibrous tissue deposition, inflammatory cell infiltrates, and increased vascularization. Fibrous plaques have been generally considered to be the characteristic lesion of well-developed atherosclerosis. Lesions in the coronary vessels occur generally later than in the aorta and occur earlier, as a rule, in men than in women. Macroscopically, fibrous plaques are white in appearance and protrude to varying degrees into the vascular lumen accounting for the term raised lesions. Rupture of the vulnerable plaque leads to various degrees of thrombus formation. The extent of thrombosis, the diameter of the artery, the degree of flow in the artery, and the amount of collateral blood vessels determine the severity of the clinical consequences following plaque rupture.