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Thrombophilia in young patients with acute myocardial infarction

Murat Celik1, Abdullah Altintas, Yusuf Celik

  • 1Internal Medicine, Clinical of Internal Diseases, Nusaybin State Hospital, Faculty of Medicine, Dicle University, Diyarbakir, Turkey.

Saudi Medical Journal
|January 8, 2008
PubMed

Insights

In young myocardial infarction (MI) patients, traditional coronary artery disease (CAD) risk factors significantly increased risk. However, thrombophilia mutations like Factor V Leiden and prothrombin G20210A did not elevate CAD risk in this population.

Area of Science:

  • Cardiology
  • Genetics
  • Thrombosis

Background:

  • Coronary artery disease (CAD) remains a leading cause of mortality, particularly in younger populations.
  • Thrombophilia, a predisposition to blood clots, is increasingly recognized as a potential contributor to cardiovascular events.
  • Understanding the interplay between genetic thrombotic risk factors and CAD in young individuals is crucial for effective prevention strategies.

Purpose of the Study:

  • To investigate the association between specific thrombophilic mutations and the occurrence of coronary artery disease (CAD) in patients who experienced myocardial infarction (MI) before the age of 45.
  • To identify whether genetic thrombophilia predispositions contribute to early-onset CAD.
  • To compare the prevalence of traditional CAD risk factors and thrombophilic mutations in young MI patients versus controls.

Main Methods:

  • A case-control study involving 129 male patients under 45 years with MI and 107 age-matched controls.
  • Assessment of traditional CAD risk factors including obesity, smoking, lipid profiles, family history, hypertension, and diabetes.
  • Genetic analysis for thrombophilia markers: Factor V Leiden (FV Leiden), prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations, as well as deficiencies in protein C, S, and antithrombin III.

Main Results:

  • Significant differences were observed in traditional CAD risk factors (obesity, smoking, lipids, family history, hypertension, diabetes, LVH) between MI patients and controls.
  • No deficiencies in protein C, protein S, or antithrombin III were found in either group.
  • The prevalence of heterozygote FV Leiden mutation, homozygous prothrombin G20210A, homozygous MTHFR C677T, and heterozygous MTHFR C677T mutations did not show a statistically significant difference between MI patients and controls.

Conclusions:

  • Traditional risk factors are strongly associated with an increased risk of CAD in young individuals.
  • Specific thrombophilic mutations, including Prothrombin G20210A, FV Leiden, and MTHFR C677T, along with deficiencies in protein C, S, and AT-III, were not found to significantly increase the risk of CAD in this young population.
  • The findings suggest that genetic thrombophilia may not be a primary driver of early-onset CAD, emphasizing the importance of managing conventional risk factors.
Abstract

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