BACKGROUND: The Pl(A2) allele of the gene encoding for GPIIIa subunit of the platelet membrane receptor glycoprotein (GP) IIb/IIIa has been suggested as a significant risk factor for thrombotic complications of coronary artery disease (CAD). The aim of the current investigation was to investigate the association between Pl(A) GPIIIa polymorphism and the extent of angiographically confirmed CAD in patients from the north region of Poland. METHODS: The study was performed in 397 male Caucasian patients. All subjects had significant coronary artery stenosis confirmed by elective coronary angiography. Screening for the Pl(A) GPIIIa genotypes was performed by polymerase chain reaction of genomic DNA, followed by NciI digestion and agarose gel electrophoresis. RESULTS: The genotype distribution of the Pl(A) GPIIIa polymorphism in our study group was Pl(A1/A1)-75%, Pl(A1/A2)-24% and Pl(A2/A2)-1% with Pl(A1) and Pl(A2) allele frequencies of 0.87 and 0.13, respectively. The prevalence of the homozygous Pl(A1/A1) genotype among subjects with multiple-vessel CAD (two or three vessels with at least 50% stenosis) was significantly higher than in patients with single-vessel disease; the odds ratio of Pl(A2/A2) or Pl(A1/A2) patients for having multiple-vessel CAD was 0.46 (95% CI 0.27-0.77, P<0.01). The mean CAD score for Pl(A1/A1) patients was significantly higher in comparison to Pl(A2/A2) and Pl(A1/A2) patients (7.58+/-2.20 and 6.98+/-2.37, respectively, P<0.05). CONCLUSIONS: Our results suggest, that the Pl(A1/A1) genotype of Pl(A) GPIIIa polymorphism is associated with more severe CAD in male Caucasian patients from the north region of Poland.
BACKGROUND: The Pl(A2) allele of the gene encoding for GPIIIa subunit of the platelet membrane receptor glycoprotein (GP) IIb/IIIa has been suggested as a significant risk factor for thrombotic complications of coronary artery disease (CAD). The aim of the current investigation was to investigate the association between Pl(A) GPIIIa polymorphism and the extent of angiographically confirmed CAD in patients from the north region of Poland. METHODS: The study was performed in 397 male Caucasian patients. All subjects had significant coronary artery stenosis confirmed by elective coronary angiography. Screening for the Pl(A) GPIIIa genotypes was performed by polymerase chain reaction of genomic DNA, followed by NciI digestion and agarose gel electrophoresis. RESULTS: The genotype distribution of the Pl(A) GPIIIa polymorphism in our study group was Pl(A1/A1)-75%, Pl(A1/A2)-24% and Pl(A2/A2)-1% with Pl(A1) and Pl(A2) allele frequencies of 0.87 and 0.13, respectively. The prevalence of the homozygous Pl(A1/A1) genotype among subjects with multiple-vessel CAD (two or three vessels with at least 50% stenosis) was significantly higher than in patients with single-vessel disease; the odds ratio of Pl(A2/A2) or Pl(A1/A2) patients for having multiple-vessel CAD was 0.46 (95% CI 0.27-0.77, P<0.01). The mean CAD score for Pl(A1/A1) patients was significantly higher in comparison to Pl(A2/A2) and Pl(A1/A2) patients (7.58+/-2.20 and 6.98+/-2.37, respectively, P<0.05). CONCLUSIONS: Our results suggest, that the Pl(A1/A1) genotype of Pl(A) GPIIIa polymorphism is associated with more severe CAD in male Caucasian patients from the north region of Poland.