Title: Polymorphism PlA of platelet glycoproteins is not a risk factor for ischaemic heart disease and myocardial infarction
- Krzysztof Chiżyński, Marcin Różalski, Cezary Watała, Jacek Golański, Ryszard Golański, Alicja Iwaszkiewicz-Zasłonka
- Original articles
- Polish Journal of Cardiology
- Start page:
- Final page:
- thrombocytes, GPIIb/IIIa, PIA polymorphism, fibrinogen receptor, ischaemic heart disease, myocardial infarction
Introduction: Some reports indicate the association between the presence of PIA2allele of GPIIIa polymorphism in blood platelet fibrinogen receptor and the accompanying stenosis of more than one vessel. The aim of the study was to analyze the frequencies of PIA (Leu/Pro33 substitution in GPIIIa) in ischemic heart disease patients as well as in patients with previous myocardial infarction (including both Q wave and non-Q wave infarction). Another objective of this study was to evaluate the possible association between the frequen-cies of PIA genotypes and alleles and the extent of coronary artery stenosis.
Material and methods: 222 patients with IHD were studied and 33 patients with normal coronary vessels were included ascontrols. Analysis was performed in 164 patients with unstable angina (68 - IV CCS classand 96 - III CCS class) and in 138 patients with the history of myocardial infarction (79 patients - Q wave and 59 patients - non-Q wave MI). PIA1/A2 polymorphism of platelet GPIIIa was detected in study group and in controls using polymerase chain reaction method. The significance of differences between the frequencies of p|Ai/A2 genotypes and alleles was estimated by chi2 test with Yates' correction.
Results: In patient with ischemic heart disease group the most frequent genotype was the "wild-type" P|ai/ai homozygote (70.7%); PIA2 allele was observed in this group both in the heterozygous form (28.4%) and in the homozygous form (0.9%). The frequencies of PIA1 and PIA2 alleles were 0.849 and 0.151, respectively. Differences in the frequencies of genotypes and alleles were not statistically significant between the patients with ischemic heart disease and control group. In our study comprising the population of central Polandthe frequencies of genotypes and alleles observed in IHD patients were not associated with the numbers of stenosed arteries. In accordance with previous reports, we did not reveal any significant differences in the distributions of genotypes and alleles of the PIA1/A2 polymorphism in patients with previous Q wave and non-Q wave infarction and in control group.
Conclusions: The lack of statistically significant differences in the distribution of PIA allelic variants between the group of ischemic heart disease patients vs. controls suggests that PIA1/A2 polymorphism of platelet GPIIIa is apparently of no significance with respect to the IHD. Based on our observations, the presence of PIA2 allele may not be regarded as a coronary risk factor. There is no obvious association between the extent of coronary artery stenosis (a number of vessels with >75% stenosis) and the occurrence of PIA2 allele.