Farideh Malakootikhah1,2, Hossein Naghavi1, Negar Firouzabadi3, Mohsen Maadani4, Massoumeh Shafiei5, Nader Tajik6. 1. Immunology Research Center (IRC), Institute of Immunology and Infectious Disease, Iran University of Medical Sciences, Shahid Hemmat Highway 14496, Tehran, Iran. 2. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 3. Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran. 4. Cardiovascular Intervention Research Center, Shaheed Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran. 5. Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. 6. Immunology Research Center (IRC), Institute of Immunology and Infectious Disease, Iran University of Medical Sciences, Shahid Hemmat Highway 14496, Tehran, Iran. tajik.n@iums.ac.ir.
Abstract
BACKGROUND: Coronary artery disease (CAD) is characterized by narrowing/ blockade of coronary arteries that is mainly caused by atherosclerotic plaques. Considering the involvement of platelet abnormalities, such as defective aggregation and adhesion, in the cardiovascular-related disorders, genetic variations in human platelet alloantigens (HPA) have been implicated in the CAD susceptibility. Herein, we intended to determine the association of HPA-1 to -6, -9, and -15 biallelic polymorphisms with CAD in an Iranian population. METHODS: In this retrospective case-control study, 200 CAD subjects and 100 matched healthy individuals were enrolled. DNA samples were isolated from peripheral blood samples and genotyping of HPA polymorphisms was accomplished using polymerase chain reaction-sequence-specific primers. RESULTS: The alleles and genotypes of studied HPA polymorphisms were equally distributed among cases and controls and therefore no statistically significant differences were detected. Univariate analysis identified no association of combined haplotypes with CAD risk. However, multivariate analysis showed a positive association of the HPA1b/2a/3b haplotype with CAD after adjustment for some covariates (including BMI, TG, LDL, FBS and blood pressure) that conferred a CAD susceptibility haplotype (P = 0.015; OR = 2.792; 95% CI 1.45-8.59). CONCLUSIONS: Although alleles, genotypes, and haplotypes of HPA polymorphisms were not associated with CAD risk, HPA1b/2a/3b haplotype was found to be a dependent disease risk haplotype in Iranian population after correcting for confounding factors.
BACKGROUND:Coronary artery disease (CAD) is characterized by narrowing/ blockade of coronary arteries that is mainly caused by atherosclerotic plaques. Considering the involvement of platelet abnormalities, such as defective aggregation and adhesion, in the cardiovascular-related disorders, genetic variations in human platelet alloantigens (HPA) have been implicated in the CAD susceptibility. Herein, we intended to determine the association of HPA-1 to -6, -9, and -15 biallelic polymorphisms with CAD in an Iranian population. METHODS: In this retrospective case-control study, 200 CAD subjects and 100 matched healthy individuals were enrolled. DNA samples were isolated from peripheral blood samples and genotyping of HPA polymorphisms was accomplished using polymerase chain reaction-sequence-specific primers. RESULTS: The alleles and genotypes of studied HPA polymorphisms were equally distributed among cases and controls and therefore no statistically significant differences were detected. Univariate analysis identified no association of combined haplotypes with CAD risk. However, multivariate analysis showed a positive association of the HPA1b/2a/3b haplotype with CAD after adjustment for some covariates (including BMI, TG, LDL, FBS and blood pressure) that conferred a CAD susceptibility haplotype (P = 0.015; OR = 2.792; 95% CI 1.45-8.59). CONCLUSIONS: Although alleles, genotypes, and haplotypes of HPA polymorphisms were not associated with CAD risk, HPA1b/2a/3b haplotype was found to be a dependent disease risk haplotype in Iranian population after correcting for confounding factors.
Authors: J L Anderson; G J King; T L Bair; S P Elmer; J B Muhlestein; J Habashi; J F Carlquist Journal: J Am Coll Cardiol Date: 1999-03 Impact factor: 24.094
Authors: C Böttiger; A Kastrati; W Koch; J Mehilli; H Seidl; K Schömig; N von Beckerath; A Schömig Journal: Thromb Haemost Date: 2000-04 Impact factor: 5.249
Authors: E J Weiss; P F Bray; M Tayback; S P Schulman; T S Kickler; L C Becker; J L Weiss; G Gerstenblith; P J Goldschmidt-Clermont Journal: N Engl J Med Date: 1996-04-25 Impact factor: 91.245