Thromb Haemost 2004; 92(02): 384-386
DOI: 10.1160/TH03-12-0744
Platelets and Blood Cells
Schattauer GmbH

Platelet glycoprotein Ibα polymorphisms modulate the risk for myocardial infarction

Margareth C. Ozelo
1   State University of Campinas, Campinas, Brazil
,
Andrea F. Origa
1   State University of Campinas, Campinas, Brazil
,
Francisco J. P. Aranha
1   State University of Campinas, Campinas, Brazil
,
Antonio P. Mansur
2   University of São Paulo, São Paulo, Brazil
,
Joyce M. Annichino-Bizzacchi
1   State University of Campinas, Campinas, Brazil
,
Fernando F. Costa
1   State University of Campinas, Campinas, Brazil
,
Eleanor S. Pollak
3   University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
,
Valder R. Arruda
3   University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
4   The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
› Author Affiliations
Financial support: This study was supported by grant from FAPESP Fundação de Apoio a Pesquisa do Estado de São Paulo (95/09112-6) to V.R.A.
Further Information

Publication History

Received 06 December 2003

Accepted after resubmission 06 May 2004

Publication Date:
30 November 2017 (online)

Summary

Platelet glycoprotein Iba (GPIba) gene polymorphisms have been reported to affect the risk of developing coronary heart disease. Here, within the GPIba gene, we determine the association between the variable number of tandem repeats (VNTR), the -5C/T Kozak sequence dimorphism, and the human platelet antigen (HPA)-2 polymorphisms with occurrence of myocardial infarction (MI). Patients (n=180) presenting survivors of MI were compared to 180 controls matched by age, gender, and race. Carriers of VNTR-CD genotype had a 2-fold higher risk for MI compared to controls. The prevalence of VNTR-BC was lower among patients than among controls (P=.007). These data are in agreement with recent reports of increased plug formation by human platelets containing VNTRCD but no other VNTR genotypes. Among patients, the number of vessels severely occluded was greater among carriers of the D-allele (P=.019) or VNTR-CD (P=.026) and lower among carriers of the C-allele (P=.003) or VNTR-CC (P=.0009) compared to non-carriers of these alleles. No influence was seen with the Kozak or HPA-2 polymorphisms. Determination of VNTR of the GPIba gene may prove useful for identifying high-risk individuals for MI.

 
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