CARDIOVASCULAR disease remains the chief cause of death in the United States and Western Europe, and atherosclerosis, the principal cause of myocardial and cerebral infarction, accounts for the majority of these deaths.1 This review, like its predecessor,2 will not attempt to cover all literature on atherosclerosis. In a previous review of the pathogenesis of atherosclerosis,2 Glomset and I discussed various hypotheses of atherogenesis2 3 4 5 6 7 and emphasized the importance of intimal smooth-muscle proliferation as the key event in the development of the advanced lesions of atherosclerosis. The response-to-injury hypothesis of atherogenesis2 3 4 5 6 proposes that "injury" to the endothelium is the initiating event in . . .

The Pathogenesis of Atherosclerosis — An Update

The pathogenesis of atherosclerosis (first of two parts).

The compositions of lesion types that precede and that may initiate the development of advanced atherosclerotic lesions are described and the possible mechanisms of their development are reviewed. While advanced lesions involve disorganization of the intima and deformity of the artery, such changes are absent or minimal in their precursors. Advanced lesions are either overtly clinical or they predispose to the complications that cause ischemic episodes; precursors are silent and do not lead directly to complications. The precursors are arranged in a temporal sequence of three characteristic lesion types. Types I and II are generally the only lesion types found in children, although they may also occur in adults. Type I lesions represent the very initial changes and are recognized as an increase in the number of intimal macrophages and the appearance of macrophages filled with lipid droplets (foam cells). Type II lesions include the fatty streak lesion, the first grossly visible lesion, and are characterized by layers of macrophage foam cells and lipid droplets within intimal smooth muscle cells and minimal coarse-grained particles and heterogeneous droplets of extracellular lipid. Type III (intermediate) lesions are the morphological and chemical bridge between type II and advanced lesions. Type III lesions appear in some adaptive intimal thickenings (progression-prone locations) in young adults and are characterized by pools of extracellular lipid in addition to all the components of type II lesions.

A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

Au cours de la contraction du tissu de granulation, de nombreux fibroblastes acquierent des caracteristiques ultrastructurelles qui les rendent semblables a des cellules musculaires lisses. Il est probable que ces elements modifies jouent un role dans le processus de contraction des plaies.

Presence of modified fibroblasts in granulation tissue and their possible role in wound contraction.

Dietary-induced atherosclerosis in miniature swine.

Production of early atherosclerotic lesions in rats characterized by proliferation of "modified smooth muscle cells".

Lecithin fatty acid composition in bile and plasma of man, dogs, rats, and oxen

Short-term feeding of unsaturated versus saturated fat in the production of atherosclerosis in the rat

Fatty Acids of Serum and Adipose Tissue in Six Groups Eating Natural Diets Containing 7 to 40 Per Cent Fat

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