title: Role of genetic polymorphisms in myocardial infarction at young age.
abstract: Acute myocardial infarction (AMI) in young adult presents a typical pattern of risk factors, clinical, angiographic and prognostic characteristics. In the last years we demonstrated that hemorheological profile is altered in these patients in a persistent way and independently of the number of risk factors and of the extent of coronary lesions. Thus, the hyperviscosity syndrome following AMI could be considered an intrinsic characteristic of these patients. Consequently it is possible to hypothesise the presence of a genetic background at the origin of this predisposition. If this background is able to influence the risk of ischemic heart disease, this should be particularly evident in young subjects. Since inflammatory mechanisms play a central role in mediating all phases of atherosclerosis, genes encoding for inflammatory or anti-inflammatory molecules are candidates for the risk of developing atherosclerosis. As atherosclerosis is the first cause of mortality in Western countries and if pro-inflammatory genotypes contribute to risk of coronary heart disease, alleles associated to disease susceptibility should not be included in the genetic background favouring longevity: People genetically predisposed to a weak inflammatory activity have fewer chances to develop cardiovascular disease and, therefore, have better chance for a long-life. According to this hypothesis, we studied in our population of young patients with AMI, the distribution of some polymorphisms influencing a inflammation and found an higher prevalence of pro-inflammatory polymorphisms (SNP A2080G of pyrin gene, SNP Gly670Arg of PECAM gene, C1019T of Cx 37 gene, SNP G1059C of PCR gene) and a lower prevalence of anti-inflammatory polymorphisms (Asp299Gly of TLR4 gene, SNP -1082 G/A of IL10 gene, CCR5Δ32). Results of these studies show that early myocardial infarction could be associated with a genetic predisposition to an intense inflammatory response, associated also to an hyperviscosity syndrome.
authors.affiliation: Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università degli Studi di Palermo, Palermo, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Incalcaterra
authors.forename: M
authors.initials: M
authors.lastname: Caruso
authors.forename: C R
authors.initials: CR
authors.lastname: Balistreri
authors.forename: G
authors.initials: G
authors.lastname: Candore
authors.forename: R
authors.initials: R
authors.lastname: Lo Presti
authors.forename: E
authors.initials: E
authors.lastname: Hoffmann
authors.forename: G
authors.initials: G
authors.lastname: Caimi
mesh_terms: D000328:Adult; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000235:genetics; D017630:Connexins / Q000235:genetics; D003327:Coronary Disease / Q000235:genetics; D003598:Cytoskeletal Proteins / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D016753:Interleukin-10 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D000071198:Pyrin; D051197:Toll-Like Receptor 4 / Q000235:genetics; D000097006:Gap Junction alpha-4 Protein
chemical_list: D002097:C-Reactive Protein; D017630:Connexins; D003598:Cytoskeletal Proteins; D016753:Interleukin-10; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D000071198:Pyrin; D051197:Toll-Like Receptor 4; D000097006:Gap Junction alpha-4 Protein; C508609:IL10 protein, human; C000604192:MEFV protein, human; C495345:TLR4 protein, human