Interactions amongst insulin, lipoproteins and haemostatic function relevant to coronary heart disease.

Interest has increased considerably in the past few years in the possible interactions amongst insulin, plasma lipoproteins and several components of the haemostatic system. There is now consistent epidemiological, clinical and experimental evidence that hypertriglyceridaemia, in particular, may represent a procoagulant state involving derangements of both blood coagulation and fibrinolysis. Imbalance in the haemostatic system secondary to increased clotting activity, impaired fibrinolytic function, or a combination thereof, should influence the growth and final size of evolving thrombi and predispose to arterial occlusion. This might be of particular significance in the coronary circulation, where a hypercoagulable state is likely to promote thrombosis at the site of a suddenly ruptured atherosclerotic plaque. In addition, there is accumulating experimental evidence that the haemostatic system plays a part in plaque formation and plaque growth. Basic research on the link between haemostasis and atherosclerosis should be given high priority, because modulation of haemostatic function will probably be a potent complementary approach to the prevention of coronary heart disease.