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Role of genetic polymorphisms in myocardial infarction at young age
E Incalcaterra1, M Caruso, C R Balistreri
1Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche, Università degli Studi di Palermo, Palermo, Italy.
Insights
Young adults experiencing acute myocardial infarction (AMI) show a genetic predisposition to intense inflammation, linked to hyperviscosity syndrome. This suggests genetic factors influence early heart disease risk.
Area of Science:
- Cardiovascular Genetics
- Inflammation and Atherosclerosis
- Hemodynamics
Background:
- Acute myocardial infarction (AMI) in young adults exhibits distinct risk factor, clinical, angiographic, and prognostic profiles.
- Persistent hemorheological alterations, including hyperviscosity syndrome, are observed in young AMI patients, independent of traditional risk factors or lesion extent.
- This suggests a potential genetic predisposition underlying hyperviscosity and AMI susceptibility in younger individuals.
Purpose of the Study:
- To investigate the hypothesis that a genetic background influences the risk of ischemic heart disease, particularly in young adults with AMI.
- To examine the association between specific gene polymorphisms related to inflammatory pathways and the occurrence of early myocardial infarction.
- To explore the link between genetic predisposition to inflammation, hyperviscosity syndrome, and cardiovascular disease risk in young populations.
Main Methods:
- Analysis of genetic polymorphisms in candidate genes involved in inflammatory and anti-inflammatory pathways.
- Comparison of the prevalence of pro-inflammatory and anti-inflammatory polymorphisms in young AMI patients versus control groups.
- Assessment of hemorheological profiles and their correlation with genetic markers and clinical characteristics.
Main Results:
- A higher prevalence of pro-inflammatory polymorphisms (e.g., pyrin gene SNP A2080G, PECAM gene Gly670Arg, Cx 37 gene C1019T, PCR gene SNP G1059C) was found in young AMI patients.
- A lower prevalence of anti-inflammatory polymorphisms (e.g., TLR4 gene Asp299Gly, IL10 gene SNP -1082 G/A, CCR5Δ32) was observed in the same patient group.
- These genetic findings were associated with an observed hyperviscosity syndrome in young AMI patients.
Conclusions:
- Early myocardial infarction in young adults may be linked to a genetic predisposition for an intense inflammatory response.
- This genetic susceptibility to inflammation appears to be associated with the development of hyperviscosity syndrome.
- Understanding these genetic factors could offer new insights into the pathogenesis and prevention of early-onset cardiovascular disease.
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.
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