Arterial thrombosis events, such as acute myocardial infarction (AMI), have a complex, multifactorial pathogenesis. Among the factors which may lead to activation of hemostatic components and thrombogenesis, inflammatory mediators have been recently recognized. On one hand, besides platelets, blood leukocytes appear increasingly important in atherosclerosis and thrombosis; on the other hand the levels of acute phase reactants (such as C-reactive protein) and inflammatory cytokines may influence remarkably clotting/fibrinolysis components and are associated with increased risk of AMI. The levels of inflammatory mediators (as well as of clotting factors), may be genetically modulated. Recent experience from our group has indicated that some polymorphisms in the genes of the cytokine system, able to influence the inflammatory response of monocytes, are associated with the risk of juvenile myocardial infarction, while fibrinogen genotypes associated with higher fibrinogen levels mediate the response to Helicobacter pylori infection and enhance the risk for familial myocardial infarction. Thus, from genetic epidemiology studies, new support is provided to the links between inflammation and arterial thrombosis.
|Journal||Archives of Hellenic Medicine|
|Issue number||SUPPL. A|
|Publication status||Published - 2000|
- Gene polymorphisms
- Gene/environment interactions
- Myocardial infarction
ASJC Scopus subject areas