Association of the Gene Polymorphisms of Platelet Glycoprotein Ia and IIb/IIIa with Myocardial Infarction and Extent of Coronary Artery Disease in the Korean Population

SummaryPlatelet glycoprotein (GP) Ia is the major receptor for collagen and plays an important role in platelet adhesion and aggregation. Different gene polymorphisms have been identified that induce either various expression levels (C807T) or alterations of the tertiary structure (A1648G) of GPIa. Previously, we could demonstrate an association of the GPIa C807T dimorphism with nonfatal myocardial infarction. We have now analysed the influence of the GPIa A1648G (Br, HPA-5) dimorphism on the risk of coronary artery disease (CAD) and acute myocardial infarction (AMI). DNA samples from 2163 male Caucasian patients who underwent coronary angiography were genotyped by polymerase chain reaction and restriction fragment length analysis. The relation of the GPIa A1648G dimorphism to the extent of CAD was determined by multiple regression analysis with adjustment for coronary risk factors. Odds ratios (OR) as an estimate of relative risk of CAD and AMI and two-tailed p-values were calculated by multiple logistic regression. In the total study sample, no association was detected between the A1648G dimorphism and CAD or AMI. However, upon analysis of low-risk patient subgroups we found an association of the GPIa A1648G polymorphism with the risk and the extent of CAD (patients with high apoAI/apoB ratio: OR 0.59, p = 0.0090; nonand ex-smokers: OR 0.66, p = 0.0131; both inclusion criteria: OR 0.44, p = 0.0003). The relative frequency of the A1648 allele was higher in controls whereas the GG1648 genotype was overrepresented in patients with CAD. This association was also detectable when individuals with low expression levels of GPIa (C807 homozygotes) were analysed (patients with high apoAI/apoB ratio: OR 0.44, p = 0.0045; nonand ex-smokers: OR 0.61, p = 0.0370). Our findings indicate that the A1648G polymorphism of the platelet collagen receptor plays a role in CAD in well defined patient groups.

Download Full-text

Lipoprotein lipase gene polymorphisms are predictors of risk of coronary artery disease and myocardial infarction

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(98)81284-9 ◽

1998 ◽

Vol 31 ◽

pp. 147-148

Author(s):

J.L. Anderson ◽

G.J. King ◽

S.P. Elmer ◽

T.L. Bair ◽

J.B. Muhlestein ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Lipoprotein Lipase ◽

Gene Polymorphisms ◽

Lipase Gene ◽

Lipoprotein Lipase Gene ◽

Artery Disease

Download Full-text

Association of the Platelet Glycoprotein IIIa PIA1/A2 Gene Polymorphism to Coronary Artery Disease but not to Nonfatal Myocardial Infarction in Low Risk Patients

Thrombosis and Haemostasis ◽

10.1055/s-0037-1615174 ◽

1998 ◽

Vol 80 (08) ◽

pp. 214-217 ◽

Cited By ~ 44

Author(s):

Jörg Humme ◽

Jürgen Stricker ◽

Quoc Nguyen ◽

Norbert Katz ◽

Monika Philipp ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Gene Polymorphism ◽

Total Population ◽

Low Risk ◽

Platelet Glycoprotein ◽

Risk Patients ◽

Artery Disease ◽

High Bmi

SummaryBackground. The platelet membrane glycoprotein IIb/IIIa functions as a receptor for fibrinogen and von Willebrand factor during platelet aggregation. In a small case-control study, evidence has been presented that the PlA2 allele of the platelet glycoprotein GPIIIa PlA1/A2 gene polymorphism might be an independent risk factor for acute myocardial infarction (MI). Methods and Results. We explored the association of the PlA1A2 to the severity of coronary artery disease (CAD), as assessed angiographically in 2252 male individuals, and to myocardial infarction (MI). The severity of coronary heart disease (CHD) was also estimated by calculating a CHD score according to Gensini. The PlA genotype was determined by allele specific restriction digestion. Relation of the PlA2 allele to CAD: In the total population, the frequency of the PlA2 allele was not associated to the presence or to the extent of CAD. Also the CHD scores of PlA1/PlA2 genotypes were essentially the same. However, after exclusion of individuals with high BMI (≥26.9 kg/m2) and/or low apoAI (<1.43 g/l) PlA2PlA2 carriers had clearly higher CHD scores than PlA1PlA1 genotypes; PlA1PlA2 heterozygotes had intermediate values (p <0.05). After division of the study population into one group of individuals without any angiographic signs of CAD (CHD score = 0) and into another group of patients with severe CAD (CHD score (≥120), a strong association of the PlA2 allele with severe CAD was also found in the same low risk groups; e.g. exclusion of persons with high BMI and low apoAI resulted in an Odds ratio of 5.37 (1.46-19.7) (p <0.02). Relation of the PlA2 allele to MI: No association was found between PlA1/PlA2 genotypes and risk of MI neither in the total population nor in low risk subgroups.Conclusions. Whereas no difference in the distribution of allele and genotype frequencies between controls and survivors of MI could be detected, the PlA2 allele is associated with CHD in low risk patients.

Download Full-text