Association of the platelet glycoprotein receptor IIIa (PlA1/PlA1) genotype with coronary artery disease in Arabs.

The PlA2 allele (heterozygotes or homozygotes) resulting from a genetic polymorphism in the glycoprotein IIIa gene has been proposed as a potential genetic factor linked to platelet hyperaggregability and increased risk of coronary artery disease (CAD). Such an association could only be established in some ethnic groups. There were no previous reports investigating the distribution of this allele and its possible link to CAD in Arabs. We used the polymerase chain reaction and allele-specific restriction digestion for determining the prevalence of this allele in 509 healthy blood donors (BD) and 451 angiographically confirmed CAD patients of Arabic ethnic background. For the BD group (n = 509), 70.7% were homozygous PlA1/PlA1, 26.9% were heterozygous PlA1/PlA2 and 2.4% were homozygous PlA2/PlA2. Within the CAD group (n = 451), 77.2% were homozygous PlA1/PlA1, 19.5% were heterozygous PlA1/PlA2 and 3.3% were homozygous PlA2/PlA2. The PlA1 allele frequency was 0.84 and 0.87, and for the PlA2 was 0.16 and 0.13 for the BD and CAD groups, respectively. In conclusion, our results suggest that the PlA1/PlA1 genotype (P = 0.029) is associated with CAD in Saudi Arabs.

Prevalence of the 20210 G-->A prothrombin variant and its association with coronary artery disease in a Middle Eastern Arab population.

BACKGROUND: No reports are available on the distribution of the 20210 G-->A prothrombin variant among Middle Eastern Arabs. Additionally, to date, studies that attempt to establish this polymorphism as an independent risk factor or as a predictor for coronary artery disease (CAD) have yielded conflicting results. OBJECTIVE: To determine the prevalence of the 20210 G-->A prothrombin variant among Middle Eastern Arabs and to evaluate the potential relevance of this variant to Arab patients with angiographically documented CAD. METHODS AND RESULTS: We used the polymerase chain reaction and restriction enzyme digestion to determine the prevalence of this polymorphism in 613 individuals from Arabic ethnic origin with CAD and from 593 healthy blood donors (BDs) from an identical ethnic background. Within the BD group (n = 593), 10 individuals (1.7%) were heterozygous, 583 individuals (98.3%) were normal, and none were homozygous for the 20210 G-->A prothrombin variant. Within the CAD group (n = 613), 13 individuals (2.1%) were heterozygous, 600 individuals (97.9%) were normal, and none were homozygous for the 20210 G-->A prothrombin variant. A chi(2) analysis was used to evaluate any significance in the distribution of genotypes. A value of 1.23 was obtained. Values less than 3.84 indicate no statistically significant difference between the heterozygous carriers of the 20210A allele in both study groups. CONCLUSIONS: In our population of Middle Eastern Arabs, the presence of the 20210 G-->A prothrombin variant is not associated with patients with angiographically documented CAD. Therefore, this variant cannot be considered as an independent risk factor or as a predictor for CAD in this population.

Prevalence and role of methylenetetrahydrofolate reductase 677 C-->T and 1298 A-->C polymorphisms in coronary artery disease in Arabs.

CONTEXT: Previous studies reported an association of 677 C-->T and 1298 A-->C methylenetetrahydrofolate reductase (MTHFR) variants with coronary artery disease (CAD). No previous studies concerning the prevalence of these 2 MTHFR variants or their possible association with CAD in Arabs are currently available in the literature. OBJECTIVE: To determine the prevalence of MTHFR variants and their potential relevance to CAD among Arabs. DESIGN: We used polymerase chain reaction and restriction enzyme digestion to determine the prevalence of these 2 MTHFR polymorphisms in 625 healthy blood donors (BDs) and 545 angiographically confirmed CAD patients of Arab origin. RESULTS: For the 677 C-->T variant within the CAD group, 64.2% were homozygous wild-type C/C, 32.1% were heterozygous C/T, and 3.7% were homozygous T/T genotype. Within the BD group tested for the 677 C-->T variant, 72.2% were homozygous wild-type C/C, 25.8% were heterozygous C/T, and 2% were homozygous T/T genotype. Within the CAD group tested for the 1298 A-->C variant (n = 540), 45.7% were homozygous wild-type A/A, 46.9% were heterozygous A/C, and 7.4% were homozygous C/C genotype. Within the BD group tested for the 1298 A-->C variant (n = 625), 39.4% were homozygous wild-type A/A, 51.5% were heterozygous A/C, and 9.1% were homozygous C/C genotype. The distribution and allele frequency of these 2 MTHFR variants followed the Hardy-Weinberg equilibrium and were similar in the CAD and BD study groups. The prevalence of the 677 C-->T and 1298 A-->C compound heterozygosity was 9.6% for the BD group and 12.3% for the CAD group. CONCLUSION: The 2 MTHFR variants tested in this study, individually or compound, are not associated with CAD. Therefore, neither of these 2 variants can be considered an independent risk factor or a predictor for CAD in this population.

Lack of association of lipoprotein lipase gene polymorphisms with coronary artery disease in the Saudi Arab population.

CONTEXT: Previous studies reported an association of certain polymorphisms in the lipoprotein lipase (LPL) gene with the risk of coronary artery disease (CAD); however, these studies were small and inconsistent. In addition, none of these studies attempted to establish such an association in the Arab population. OBJECTIVE: To determine whether 2 LPL polymorphisms (LPL-HindIII and LPL-PvuII located on introns 8 and 6, respectively, of the LPL gene) can be considered as independent risk factors or as predictors for CAD in Arabs. DESIGN: We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the LPL-HindIII and LPL-PvuII polymorphisms among healthy blood donors of Arabic origin (BD group) and angiographically confirmed CAD patients (CAD group) with identical ethnic backgrounds. RESULTS: For the HindIII genotypes, within the BD group (n = 410), the +/+ genotype was found in 206 individuals (50.2%), 173 (42.2%) carried the +/- genotype, and 31 (7.6%) carried the -/- genotype. Within the CAD group (n = 352), the +/+ genotype was found in 189 individuals (53.7%), 138 (39.2%) carried the +/- genotype, and 25 (7.1%) carried the -/- genotype. P values of.38,.45, and.92 were obtained for the +/+, +/-, and -/- genotypes, respectively. For the PvuII genotypes, within the BD group (n = 511), the +/+ genotype was found in 182 individuals (35.6%), 248 (48.5%) carried the +/- genotype, and 81 (15.9%) carried the -/- genotype. Within the CAD group (n = 431), the +/+ genotype was found in 138 individuals (32%), 225 (52.2%) carried the +/- genotype, and 68 (15.8%) carried the -/- genotype. P values of.28,.29, and.98 were obtained for the +/+, +/-, and -/- genotypes, respectively. The distribution and the allele frequency of these 2 LPL variants were similar in CAD and BD study groups and followed the Hardy-Weinberg equilibrium. CONCLUSION: There was no difference in the distribution of both LPL polymorphisms between the healthy group and the CAD group. Therefore, these 2 LPL polymorphisms cannot be considered as independent risk factors or as predictors for CAD in this population.