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.

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