49. Hyperfibrinogenemia and cardiovascular risk: possible strategies for intervention

Abstract

Summary Elevated plasma fibrinogen has been identified as an independent predictor of cardiovascular diseases. Although abundant evidence suggests a causal role of fibrinogen in the pathogenesis of atherothrombotic complications, this has not yet been proven. To overcome this dilemma, several strategies seem conceivable to intervene with hyperfibrinogenemia. Abstention from smoking and regular long-term endurance exercise significantly decrease fibrinogen. Treatment of chronic infections such as Helicobacter pylori, Chlamydia pneumoniae , or dental disease possibly influences cardiovascular risk indirectly by modifying fibrinogen levels. A number of drugs have been shown to reduce plasma fibrinogen besides their main therapeutic action; clinically, fibrates are by far the most important group. Other oral drugs with appreciable fibrinogen-lowering capacity include ticlopidine, pentoxifylline, beta-adrenergic blockers, ACE inhibitors, and several steroid hormones. Large clinical trials in patients post-myocardial infarction, with advanced periphonel arterial occlusive disease (POAD), and with diabetes mellitus, are under way, investigating in more detail the possible therapeutic efficacy of lowering fibrinogen on clinical endpoints. Aspirin might influence the physical properties of the fibrin gel structure, thereby rendering the clot more amenable to endogenous fibrinolysis. Chronic application of low dose urokinase or apheresis may be suitable in selected patient groups. Finally, a new approach consists in the interference with fibrinogen-dependent platelet aggregation through blockade of the glycoprotein IIb/IIIa-receptors.