Mechanism and Prevention Possibilities in Coronary Thrombosis
If it is accepted that many myocardial infarctions (MI) are caused, in younger as in older patients, by coronary thrombosis (Davies et al. 1979), modern analysis is providing evidence (see Born 1979) that it depends on complex haemodynamic interactions between atherosclerotic lesions and blood constituents, primarily the platelets. These interactions have implications, both positive and negative, for prevention and treatment. Platelet aggregation as the immediate cause of arterial thrombosis is the basis for the world-wide interest in and large-scale trials of platelet-inhibiting agents as potential anti-thrombotic drugs. In principle, one approach to the prevention of arterial thrombosis should be through drugs capable of inhibiting platelet aggregation. Rapidly increasing biochemical and pharmacological knowledge about platelets has revealed potent inhibitors of aggregation with different modes of action. Encouraging results have been obtained recently with models of extra-corporeal circulation, e.g. artificial kidneys in which the thrombotic deposition of platelets can be prevented by adenosine (Richardson et al. 1976) or by prostacyclin (prostaglandin I2) (Bunting et al. personal communcation). It was on the basis of their platelet-inhibiting activities that three established drugs, acetylsalicylic acid (aspirin), dipyridamole (persantin) and sulphinpyrazone (anturane) have been undergoing extensive trials in different well-defined clinical situations arising in consequence of arterial thromboses. Results so far have left considerable uncertainties. All these drugs have actions on many other systems in the body, so that any therapeutic effectiveness need not be due to their actions on platelets.