General recognition of the thrombotic component in ischaemic heart disease (IHD) is comparatively recent. Despite the obvious role of platelets, it has in many ways--and certainly epidemiologically--been work on the coagulation system that has been more rewarding in characterising those at high risk of IHD on account of haemostatic abnormalities. Raised plasma fibrinogen levels are clearly and independently associated with the onset of both clinically manifest IHD and stroke and probably with lower extremity arterial disease as well. High fibrinogen levels also increase recurrence rates and the progression of these conditions. High factor VII activity levels are associated with increased mortality from IHD but not with non-fatal episodes. Low fibrinolytic activity and raised factor VIII levels are also associated with increased IHD incidence. High fibrinogen levels predispose to thrombosis by effects on viscosity, platelet aggregability, fibrin deposition and the atherogenic process. There is increasing evidence that raised factor VII activity levels lead to increased thrombin production. Associations of several personal characteristics--notably smoking in the case of fibrinogen and dietary fat intake in the case of factor VII activity--influence the coagulation system in ways that are likely to predispose to thrombosis. Besides well known agents such as aspirin and anticoagulants, increasing attention ought now to be given to the antithrombotic potential of fibrinogen-lowering agents.