Last update:
11-Jul-2004

Arch Hellen Med, 2000, 17(Supplement):51-56

LECTURE

Hemostasis and inflammation in cardiovascular risk
Εmerging concepts from genetic epidemiology

M.B. DONATI
"Angela Valenti" Laboratory of Genetic and Environmental Risk Factors for Thrombotic Disease,
Department of Vascular Medicine and Pharmacology, Instituto di Ricerche
Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy

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.

Key words: Gene/environment interactions, Gene polymorphisms, Infection, Inflammation, Myocardial infarction.