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Nutrition and platelet function in atherogenesis

Platelets are undoubtedly involved in the final occlusion of atheromatous arteries forming the major component of the occlusive thrombus (Davies & Thomas, 1981). This sudden and often catastrophic event is most likely precipitated by fissuring of an atheromatous plaque, as detailed post-mortem analysis of obstructed coronary arteries invariably shows the thrombus in association with plaque haemorrhage (Constantinides, 1966; Davies & Thomas, 1981). Platelets have also been implicated in cases of sudden cardiac death by the finding of platelet aggregates in the coronary microcirculation (Haerem, 1972; El-Maraghi & Genton, 1980). Platelets may also participate in the early stages of atheroma. There is ample evidence, beginning with the work of Duguid (1946), that mural thrombi composed of platelets and fibrin can be incorporated into more advanced lesions (Woolf, 1983). Moreover, the recognition, both in humans and experimental animals, of platelet interactions with the arterial wall at sites which show a predilection for atherosclerosis (Packham & Mustard, 1986) and of the platelet production of powerful smooth-muscle-cell mitogens such as platelet-derived growth factor (Ross et al. 1974) has focused attention on arterial endothelial-cell damage, platelet adhesion and aggregation and release of mitogens as early events in the atherosclerotic process (Ross & Glomset, 1976). In the response-to-injury hypothesis, breach of the endothelial barrier would expose subendothelial smooth muscle cells and connective tissue to plasma constituents including lipoproteins, platelets and macrophage-type mononuclear cells (Harker & Ross, 1979). Platelets would adhere to the injured site, form microthrombi and release their granular contents including platelet-derived growth factor which stimulates migration and focal proliferation of intimal and medial smooth muscle cells (Ross & Vogel, 1978). Subsequently there would be synthesis of collagen, elastin and proteoglycans by smooth muscle cells and intracellular and extracellular lipid accumulation. Support for this sequence of events has come from animal models of atherosclerosis and studies using cell-culture techniques and caution is necessary in translating these findings to the human situation. However, there does seem to be considerable evidence linking platelets to the development of proliferative arterial lesions following experimental removal of endothelium in animals either mechanically or chemically (Mustard et al. 1983). In addition the emerging information regarding the properties of the plateletderived growth factor suggests an important role for this mitogen in the atherogenic process (Bowen-Pope & Ross, 1984). It should be emphasized here that other cells such as monocytes and endothelial cells may secrete cellular mitogens, and macrophage interaction with the vessel wall may be the first demonstrable lesion in experimental atherogenesis (Faggiotto & Ross, 1984; Faggiotto et al. 1984; Ross et al. 1984). Support for the possible role of platelets in atherogenesis is not available from large-scale epidemiological studies which have implicated the traditional risk factors such as hypertension, cigarette smoking, hypercholesterolaemia and diabetes mellitus. This is because there is no entirely satisfactory test of platelet function and those tests that are available would be difficult to apply to the study of large population groups. Nevertheless there is some circumstantial epidemiological evidence linking platelets to atherogenesis stemming mainly from observations of the Greenland Eskimos.