Fibrous intimal thickening and atheronecrosis of the thoracic aorta in coronary heart disease.

A series of 60 cases of coronary heart disease (CHD) deaths and 85 cases of Not-CHD deaths of a comparable age, race, and sex composition was assembled from a medicolegal service. Lateral walls of the thoracic aorta were sectioned, and measurements were made at 20 equally spaced points along the left and right sections, 40 points per case. At points having foci of atheronecrosis, the thickness of the necrotic focus and the fibroproliferative base and cap were measured. In points lacking atheronecrosis, full intimal thickness was measured. The sum of cap plus base is the total fibroproliferative tissue accompanying atheronecrosis. Aortas of CHD-death subjects had more necrotic points and more connective tissue associated with the necrosis. Aortas of CHD-death subjects also had proportionately less connective tissue in the cap rather than the base of necrotic lesions. These three variables contributed independently in a discriminant function, indicating that CHD-death status could in this set of cases best be predicted from the aortic condition by simultaneously considering the number of atheronecrotic foci, the bulk of connective tissue associated with those foci, and the relative thinness of the cap over the necrosis. One possible theory to explain these and other findings describes atherogenesis as the following two-phase process. In phase one, varying amounts of progressively increasing fibrous intimal thickening (preatheroma) are laid down. In phase two some loci develop atheronecrosis, a second set of loci develops accelerated fibroplasia, and a third set develops both features. The two features are each postulated to be increasingly likely to appear as intimal connective tissue increases. In this context the emergence of atheronecrosis, of accelerated fibroplasia, and of both together would be seen as greater in aortas of CHD-death subjects than in aortas of Not-CHD-death subjects.