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The prevalence of the platelet glycoprotein IIIa Pl(A1/A2) polymorphism in three South African ethnic groups and its

Nitien H Naran1, Nanthakumarn Chetty, Nigel J Crowther

  • 1Department of Chemical Pathology, University of the Witwatersrand, Johannesburg, South Africa. nitien.naran@nhls.ac.za

Thrombosis Research
|July 29, 2008
PubMed

Insights

The platelet glycoprotein IIIa (GP) IIIa Pl(A2) allele is linked to increased platelet aggregation and higher coronary artery disease (CAD) risk. This genetic factor contributes to myocardial infarction risk, independent of other known risk factors.

Area of Science:

  • Cardiovascular Genetics
  • Platelet Biology
  • Population Health

Background:

  • Coronary artery disease (CAD) prevalence varies across ethnic groups in South Africa, with lower rates in African subjects compared to Indian or white individuals.
  • While metabolic factors are known contributors to CAD, the role of genetic factors remains less understood.
  • Specific polymorphisms in the platelet membrane glycoprotein (GP) IIIa gene, known as Pl(A1/A2), have been investigated for their potential link to CAD development.

Purpose of the Study:

  • To investigate the prevalence of platelet GPIIIa (Pl(A1/A2)) polymorphisms in Indian, white, and African populations in South Africa.
  • To determine the effect of these polymorphisms on platelet function.
  • To assess the association between platelet GPIIIa polymorphisms and the risk of coronary artery disease (CAD).

Main Methods:

  • Genotyping for platelet GPIIIa (Pl(A1/A2)) polymorphisms was performed in 313 Indian, 267 white, and 227 African subjects.
  • Subjects were categorized based on the presence or absence of a history of CAD.
  • Platelet function, including aggregation responses to ADP and collagen and thromboxane A2 (TXA2) production, was assessed.

Main Results:

  • The frequency of the unfavorable Pl(A2) allele was significantly higher in white subjects (14.8%) compared to Indian (8.0%) and African (8.7%) subjects without a history of CAD (p<0.05).
  • The Pl(A2) allele frequency was substantially higher in subjects with a history of CAD (23.0%) than in those without (10.0%; p<0.0001).
  • Platelets carrying the Pl(A2) allele exhibited hypersensitivity to ADP and collagen, with increased TXA2 production.

Conclusions:

  • The platelet GPIIIa Pl(A2) allele is associated with enhanced platelet function, suggesting it may be a genetic risk factor for myocardial infarction, particularly sudden death.
  • This polymorphism may contribute to CAD risk independently of other known risk factors.
  • However, the study findings do not fully explain the observed ethnic differences in CAD prevalence.
Abstract

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