Three main atherogenic processes are recognised today: hyperlipemia, arterial wall injury and parietal thrombosis. The role of hyperlipemia is supported, among other things, by the following: 1. Experimentally, protracted hyperlipemia can reproduce faithfully the lesions and all complications of advanced human atherosclerosis. 2. Immunohistochemically, plaque lipoproteins are identical with certain blood lipoproteins. 3. The incidence of atherosclerosis in different populations roughly parallels the average blood lipid levels of these populations. 4. Dietary and pharmacological reductions of blood lipid levels in certain populations have reduced the clinical manifestations of atherosclerosis in these populations. Prolonged hyperlipemia generates arterial plaques by causing penetration of blood lipids into the myocytes of the inner arterial wall, immigration of lipid-laden monocytes into the subendothelial space, and increased endothelial permeability for blood lipoproteins and mitogens. All types of arterial wall injury diminish the endothelial barrier and increase endothelial permeability for blood lipoproteins and mitogenic factors. Seven groups of naturally occurring arterial insults are recognised today: hemodynamic turbulence, hypertension, metabolic insults (including hyperlipemia), immune insults, viruses, exogenous chemicals, and obstruction of adventitial lymphatics. These insults usually cause a functional increase of endothelial permeability (when mild) or a loosening of interendothelial junctions (when intense). Parietal thrombosis develops practically only in atherosclerotic-almost never in normal-arteries. It is most frequently initiated by tiny breaks of plaque surfaces, breaks which expose blood to the highly thrombogenic collagen and lipid masses that abound in the atherosclerotic--but are absent from the normal arterial wall. parietal thrombi are overgrown by endothelium, turned into fibrous tissue and incorporated into the underlying plaques, whose thickness they can thus greatly increase.