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Fibrinogen and cardiovascular disease: genetics and biomarkers

Dimitris Tousoulis1, Nikolaos Papageorgiou, Emmanuel Androulakis

  • 1Athens University Medical School, Hippokration Hospital,Vasilissis Sofias 114, 115 28, Athens, Greece. drtousoulis@hotmail.com

Blood Reviews
|June 10, 2011
PubMed

Insights

Fibrinogen is linked to coronary artery disease (CAD), but evidence for a causal relationship is uncertain. Genetic variations in fibrinogen show a modest impact on myocardial infarction (MI) risk, questioning the utility of gene screening for MI risk assessment.

Area of Science:

  • Cardiovascular Science
  • Genetics
  • Epidemiology

Background:

  • Prospective epidemiological studies and clinical observations suggest a strong correlation between fibrinogen levels and coronary artery disease (CAD).
  • The causal nature of the fibrinogen-CAD association remains uncertain, with possibilities including genetic variability and confounding by other risk factors.
  • Several fibrinogen gene polymorphisms influence fibrinogen levels, but only a few variants are linked to increased cardiovascular risk.

Purpose of the Study:

  • To evaluate the evidence regarding the association between fibrinogen and coronary artery disease (CAD).
  • To investigate the role of genetic variations in fibrinogen and their impact on myocardial infarction (MI) risk.
  • To assess the potential utility of fibrinogen gene screening for MI risk stratification.

Main Methods:

  • Review of prospective epidemiological studies and clinical observations.
  • Analysis of genetic variations (polymorphisms) in fibrinogen chain genes.
  • Examination of the association between specific genotypes, fibrinogen levels, and cardiovascular risk, including myocardial infarction (MI).

Main Results:

  • Many studies confirm a strong correlation between fibrinogen and CAD.
  • Genetic variations in fibrinogen have a modest impact on the process leading to MI.
  • Specific genotypes can lead to differences in fibrinogen levels but may not be directly linked to cardiovascular risk.

Conclusions:

  • The causality of fibrinogen in the pathogenesis of cardiovascular disease is complicated by findings where genetic differences in levels do not correlate with risk.
  • Screening of fibrinogen genes may not be a useful tool for assessing myocardial infarction (MI) risk.
  • Further research is needed to clarify the complex relationship between fibrinogen, its genetic underpinnings, and cardiovascular disease development.

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