Current reports of research into the problem of atheroma deal largely with abnormalities and peculi-arities of lipid metabolism. As atheromatous plaques are rich in lipids, and can be produced in most experimental animals by a high cholesterol diet, it is reasonable to suppose that atheroma and lipid metabolism are related. There will, however, be some disagreement with Hess (1964) who stated that" atherosclerosis is now rather generally accepted to be a disorder of lipid metabolism", because there are several features of the disease that are not explained in terms of lipid disturbance. The main alternative theory is that atheroma is the result of intravascular clotting or thrombosis. This was originally expounded byRokitansky in a paper in 1844, and it has been supported by several authors since, in particular byDuguid (1955) and Osborn (1963) in this country. The two theories mentioned have appeared to compete with one another for acceptance, and it has not hitherto been possible to suggest a way in which they might be related.

The development of atheroma is undoubtedly related to hypertension as well as to lipid disturbance (Corcoran et al., 1956; Schettler, 1961). Two explanations of this relationship have been offered: Masson et al.(1958) believed that hypertension produced widespread vascular damage which facili-tated lipid deposition, while Page (1954) suggested that hypertension would lead to an increased transarterial filtration of some of the contents of the circulating fluid, either plasma lipids (Page) or protein (Duncan, Cornfield, and Buck, 1962), which would initiate the local formation ofatheroma. Any explanation of atheroma must account for