The nature of atheroma

Atherosclerosis represents a heterogenous group of pathological phenomena involving degenerative, inflammatory and proliferative processes which produce lesions containing mainly cellular material, lipid, collagen and calcium. Despite the varying pathological forms, the clinical sequelae of atherosclerosis are well defined and affect coronary, cerebrovascular and peripheral arteries. The Office of Population Censuses and Surveys (1984) reported cardiovascular-related mortality of 42% of total mortality in England and Wales. Of these cardiological causes, 56% were due to ischaemic heart disease, i.e. 28% of total mortality (Table 1). Moreover, cerebrovascular disease represented 13% and peripheral vascular disease 4% of total mortality. With such a large proportion of our mortality therefore related to atherosclerotic disease there is a clear requirement for definition of pathology and pathogenesis in order to provide a framework for therapeutic intervention. The onset of atherosclerosis is an early event beginning with diffuse, regular thickening of the arterial intima in childhood. The smooth appearance of the arterial tree may be lost during teenage years with the formation of nodular aggregates or cushions of fibroelastic tissue (Stout & Thorpe, 1980). However, the hallmark of established atherosclerosis is formation of the fibrous plaque. The clinical sequelae of this relate to the complications of the fibrous plaque giving rise to slow or sudden vascular occlusion. These include haemorrhage into the plaque, calcification, p mural thrombus on its surface. The present paper will therefore highlight some of the controversial areas of the nature and the theories of atheroma formation.