Haemostatic factors and coronary heart disease

Elevation in the plasma concentration of fibrinogen in coronary heart disease (CHD) and in stroke has been found to be due to increased biosynthesis and turnover. The pathway of the increased turnover of fibrinogen is via formation of fibrin. A new method for detecting and measuring intravascular fibrin has shown a highly significant elevation in these patients. These elevated levels of fibrin formation, or intravascular clotting, are associated with depressed fibrinolysis or clot lysis. This increased formation of fibrin in the patient is not responsive to conventional oral anticoagulant therapy with Coumadin (Na Warfarin). Prospective studies on over 1,500 patients have shown elevated plasma fibrinogen to have at least as strong an association with cardiovascular death as raised cholesterol. Increased plasma fibrin is highly susceptive to control with low dose heparin and urokinase. These discoveries should provide the health care field with a new basis for detecting early warning signs of CHD and thrombotic stroke and for more effective preventive therapy.