The relationship between diffuse intimal thickening, medial enzyme failure and intimal lipid deposition in various human arteries.

Summary The relationship between diffuse intimal thickening and zonal loss of medial enzyme activity was studied in 23 human aortas, from the 1st to the 10th decade of life, by means of the NADH-tetrazolium reductase-Van Gieson histoenzymic method. This relationship, together with the relationship to lipid accumulation, was examined with the histoenzymic NADH-TR and ATPase-Oil Red 0 methods in the aorta, coronary, internal carotid, middle cerebral, femoral, popliteal, axillary and brachial arteries in a fuither 8 subjects. At a critical intimal thickness of 0.15 mm the aortic media showed enzymic loss in its middle zone. In the other arteries examined this critical intimal thickness for medial enzyme loss varied from 0.2–0.45 mm. Intracellular lipid (the "fatty streak") was noted in some relatively unthickened intimas, where the tunica media showed no enzyme loss. Extracellular diffuse intimal lipid was only observed where enzyme activity was impaired in the tunica media. In a few cases diffuse intimal thickening and medial enzyme loss were seen in the absence of intimal lipid accumulation. These results support the hypothesis that progressive diffuse intimal thickening over-extends nutritional perfusion from the lumen to the inner and middle zones of the tunica media. The resulting failure of energy-producing metabolism in the media would impair the local synthesis of lipotrophic agents (phospholipid and protein) that are required for transporting cholesterol. Reduced outward transport of cholesterol would lead to the accumulation of cholesterol in the inner arterial layers, as in atherosclerosis.