PS24. ECOGENETICS AND PHARMACOGENETICS OF CORONARY ATHEROSCLEROSIS
PIER FRANCO PIGNATTI Section of Biology and Genetics, Department of Mother and Child, Biology and Genetics University of Verona, Italy e e-mail: Pierfranco.pignatti@univr.it
*Corresponding Author:
page: 29

Abstract

Family history is an important independent risk factor for coronary artery disease, and identification of susceptibility genes for this common disease is a vital goal (Watkins H & M Farrall 2006). Coronary atherosclerosis is a complex disease in which genetic and environmental factors play a role, and the study of interactions offer great promise for risk assessment, treatment, and understanding of pathophysiology. We will present a few examples from our work of some important emerging correlations between genetic and environmental factors which determine a modification of: i) disease risk, or ii) response to treatment.

i) Ecogenetics. MTHFR genotype is related to dietary pholate intake in determining hyperomocysteinemia (Girelli D et al 1998), a cardiovascular disease risk factor, and genotype-related threshold values of pholatemia could be indicated (Girelli D et al 2003). APOC3 genotypes are connected with coronary atherosclerosis (Olivieri O et al 2002) or metabolic syndrome (Olivieri O et al 2003) risk, as well as with apolipoprotein-CIII triglyceride lowering response to dietary Polyunsaturated Fatty Acids (Olivieri O et al 2005). PON (paraoxonase) genotypes may increase miocardial infarction risk in coronary atherosclerosis patients depending on their smoking habit (PON2, Martinelli N et al 2004), or on their metabolic syndrome status (PON1, Martinelli N et al 2005).

ii) Pharmacogenetics. Clopidogrel in combination with aspirin is the gold standard for prevention of stent thrombosis in patients undergoing percutaneous coronary interventions, however its effect is not uniform in all patients (Nguyen TA et al 2005). Response to clopidogrel used as a platelet antiaggregating therapy in patients who underwent coronary stenting was related to genotypes at several different genes involved in the drug’s mechanism of action or metabolism: GPIIIa (fibrinogen binding, Angiolillo DJ et al, 2004a), GPIa (collagen binding, Angiolillo DJ et al, 2004b and 2005a), and P2Y12 receptor (ADP binding inhibited by clopidogrel, Angiolillo J et al 2005b) genes, or 3A4 hepatic cytochrome P450 gene (Angiolillo DJ et al, 2006), respectively. 




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