Overview of studies on regression of atherosclerosis.

Regression of the main components of atherosclerotic leseions is compared with regression of other related pathological masses in the body, notably the fatty liver, the large abscess, the large thrombus, the tuberculous granuloma, the lipid implantation granuloma, an the at first reversible but later irreversible proliferation of tissues in response to certain hydrocarbons. The unique obstacles to the regression of advanced artheromata -- as compared to regression of pathological masses elsewhere -- are identified as a lack of early capillarisation, a dependence on evacuation by a very slow unidirectional filtration across an extremely dense and contracted tissue, a lack of an unending imigration of leucocytes for the phagocytic or lysosomal removal of large extracellular lipid pools, and the massive deposits of collagen, an insulating material of extremely long half-life that seems, in addition, to promote wall fragility and supra-plaque thrombosis. The origin and the fate of the myocyte proliferation in hyperlipemia-induced plaques is scrutinized; arguments are presented in favor of its regenerative rather than platelet-induced origin and in favor of the possibility that protracted hyperlipemia may induce the development of some regression-resistsant myocytic mutants. The special difficulties and pitfalls of regression research are analysed. The current conclusions from the most critical experimental studies to date indicate that incipient or young lesions are capable of significant regression, but there is as yet no evidence that advanced or complicated plaques will regress in any species.