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

@entity1 @entity63 @entity75 @entity797 @entity1442 @entity1856 @entity731 @entity715
The composition and structure of adaptive intimal thickening and of @entity731 that can develop in @entity1 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 @entity731 . However, some of the identical intima locations (progression-prone locations) accumulate more lipoprotein in @entity1 exposed to risk factors of @entity731 and are first to develop @entity1442 if such lesions develop at all. @entity731 can be resolved into eight (I- @entity797 ) 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 @entity1856 and @entity1856 stages which are susceptible to @entity715 and @entity63 clinical episodes. The numerals VII and @entity797 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 @entity1 (I and II) and the potentially symptom-producing Type IV lesion. Identification of Type III provides evidence that small lesions of @entity1 can develop into clinical ones. Because we know the age at which @entity75 are present in our population, we also known the age when progression to @entity1442 generally begins and when preventive measures should already be in place.
