| Abstrakt: |
The authors start from the clinical fact that fibrinogen shall be considered today as a major and independent cardiovascular risk factor. Based on this assumption, they re-examine the latest studies and the modern theories on the role that fibrinogen would play in the atherothrombotic process. Among the various theories taken into consideration, the authors particularly emphasize the lesion reaction theory which, revised and re-interpreted in the light of the recent acquisitions, seems to give the most plausible explanation to the events leading to atheromatous plate formation and to subsequent thrombosis. Furthermore, the various causes leading to hyperfibrinogenemia are taken into consideration. On this subject, the authors wonder which alternatives, can be adopted to reduce high fibrinogen levels. It is ascertained that no specific drugs are available for pharmacologic treatment of hyperfibrinogenemia. Instead, there are various active principles capable of reducing fibrinogen levels, in addition to their primary action. The authors stress that in the cardiovascular branch, for example, both ticlopidine and bezabifrate can help reduce hyperfibrinogenemia, in addition to their respective antiplatelet and anti-hyperlipoproteinemic action. |
