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[An update on the role of fibrinogen in the atherothrombotic process]
E Gatto1, R Gatto, E Maragliano
1II Divisione Cardiologica, Ospedale Regionale S. Martino, Genova.
Insights
Fibrinogen is a key cardiovascular risk factor. This review highlights the lesion reaction theory for atherothrombosis and discusses strategies to lower high fibrinogen levels, including drugs with dual actions.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Context:
- Fibrinogen is recognized as a significant independent cardiovascular risk factor.
- Atherothrombosis involves complex pathophysiological processes.
- Hyperfibrinogenemia contributes to cardiovascular disease development.
Purpose:
- To re-examine the role of fibrinogen in atherothrombosis.
- To evaluate theories explaining atherothrombotic events.
- To explore methods for reducing elevated fibrinogen levels.
Summary:
- The lesion reaction theory provides a plausible explanation for atheromatous plaque formation and thrombosis.
- Current therapeutic options do not specifically target hyperfibrinogenemia.
- Certain medications, like ticlopidine and bezafibrate, can lower fibrinogen levels as a secondary effect.
Impact:
- Enhanced understanding of fibrinogen's role in cardiovascular disease.
- Identification of potential therapeutic avenues for managing hyperfibrinogenemia.
- Informs clinical practice regarding cardiovascular risk assessment and management.
Abstract:
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.