Changes in components and structure of atherosclerotic lesions developing from childhood to middle age in coronary arteries.

The composition and structure of adaptive intimal thickening and of atherosclerotic lesions that can develop in human coronary arteries is described. Adaptive thickening occurs in defined locations from birth and represents a self-limited response of the intima to hemodynamic forces present within specific locations. Adaptive thickening does not indicate or presage an atherosclerotic lesion. However, some of the identical intima locations (progression-prone locations) accumulate more lipoprotein in persons exposed to risk factors of atherosclerosis and are first to develop advanced lesions if such lesions develop at all. Atherosclerotic disease can be resolved into eight (I-VIII) lesion types, each characteristic by its cells, matrix, architecture, or other specific features. The numerals I-VI represent the usual sequence in which lesions develop and progress from the initial accumulations of lipoproteins and macrophages to atheroma and fibroatheroma stages which are susceptible to thrombotic deposits and ischemic clinical episodes. The numerals VII and VIII represent morphological variants that may follow or precede Type VI. Types I-IV are the lesions most frequent in the first four decades of life. Type III is a lesion we identified in adolescents and young adults as morphologically intermediate between the small lesions of children (I and II) and the potentially symptom-producing Type IV lesion. Identification of Type III provides evidence that small lesions of children can develop into clinical ones. Because we know the age at which Type III lesions are present in our population, we also known the age when progression to advanced lesions generally begins and when preventive measures should already be in place.