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Combined effect of hemostatic gene polymorphisms and the risk of myocardial infarction in patients with advanced coronary atherosclerosis.

Martinelli N, Trabetti E, Pinotti M, Olivieri O, Sandri M, Friso S, Pizzolo F, Bozzini C, Caruso PP, Cavallari U, Cheng S, Pignatti PF, Bernardi F, Corrocher R, Girelli D - PLoS ONE (2008)

Bottom Line: In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors.As compared to subjects with 3-7 alleles, those with few (</=2) alleles had a decreased MI risk (OR 0.34, 95%CIs 0.13-0.93), while those with more (>/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01).The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical and Experimental Medicine, University of Verona, Verona, Italy.

ABSTRACT

Background: Relative little attention has been devoted until now to the combined effects of gene polymorphisms of the hemostatic pathway as risk factors for Myocardial Infarction (MI), the main thrombotic complication of Coronary Artery Disease (CAD). The aim of this study was to evaluate the combined effect of ten common prothrombotic polymorphisms as a determinant of MI.

Methodology/principal findings: We studied a total of 804 subjects, 489 of whom with angiographically proven severe CAD, with or without MI (n = 307; n = 182; respectively). An additive model considering ten common polymorphisms [Prothrombin 20210G>A, PAI-1 4G/5G, Fibrinogen beta -455G>A, FV Leiden and "R2", FVII -402G>A and -323 del/ins, Platelet ADP Receptor P2Y12 -744T>C, Platelet Glycoproteins Ia (873G>A), and IIIa (1565T>C)] was tested. The prevalence of MI increased linearly with an increasing number of unfavorable alleles (chi(2) for trend = 10.68; P = 0.001). In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors. As compared to subjects with 3-7 alleles, those with few (/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01). The number of procoagulant alleles correlated directly (r = 0.49, P = 0.006) with endogenous thrombin potential.

Conclusions: The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD.

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Related in: MedlinePlus

Study population (n = 804) stratified on the basis of number of risk alleles (1A).The distribution of number of risk alleles in CAD-free (n = 315) and in CAD patients (n = 489) (1B) and in CAD patients with (n = 307) or without a history of MI (n = 182) (1C).
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pone-0001523-g001: Study population (n = 804) stratified on the basis of number of risk alleles (1A).The distribution of number of risk alleles in CAD-free (n = 315) and in CAD patients (n = 489) (1B) and in CAD patients with (n = 307) or without a history of MI (n = 182) (1C).

Mentions: Supplemental Table 1 (Table S1) shows the genotype frequencies for each of the 10 polymorphisms in CAD-free (n = 315; males 66.0%; mean age 59.2±11.9 years) and in CAD subjects (n = 489; males 83.6%; mean age 60.3±9.3 years). All alleles were in Hardy-Weinberg equilibrium. For each polymorphism there was no significant difference in genotype distribution between CAD and CAD-free groups. The distribution of the “prothrombotic score” (PS) in the whole study population (n = 804) is shown in figure 1A. The score ranged from 0 (1 subject) to 10 prothrombotic alleles (7 subjects), with a median level of 5. Figure 1B shows the distribution of the PS in CAD-free and in CAD subjects. No association was found between the PS and CAD (P = 0.889 by χ2-test).


Combined effect of hemostatic gene polymorphisms and the risk of myocardial infarction in patients with advanced coronary atherosclerosis.

Martinelli N, Trabetti E, Pinotti M, Olivieri O, Sandri M, Friso S, Pizzolo F, Bozzini C, Caruso PP, Cavallari U, Cheng S, Pignatti PF, Bernardi F, Corrocher R, Girelli D - PLoS ONE (2008)

Study population (n = 804) stratified on the basis of number of risk alleles (1A).The distribution of number of risk alleles in CAD-free (n = 315) and in CAD patients (n = 489) (1B) and in CAD patients with (n = 307) or without a history of MI (n = 182) (1C).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2211406&req=5

pone-0001523-g001: Study population (n = 804) stratified on the basis of number of risk alleles (1A).The distribution of number of risk alleles in CAD-free (n = 315) and in CAD patients (n = 489) (1B) and in CAD patients with (n = 307) or without a history of MI (n = 182) (1C).
Mentions: Supplemental Table 1 (Table S1) shows the genotype frequencies for each of the 10 polymorphisms in CAD-free (n = 315; males 66.0%; mean age 59.2±11.9 years) and in CAD subjects (n = 489; males 83.6%; mean age 60.3±9.3 years). All alleles were in Hardy-Weinberg equilibrium. For each polymorphism there was no significant difference in genotype distribution between CAD and CAD-free groups. The distribution of the “prothrombotic score” (PS) in the whole study population (n = 804) is shown in figure 1A. The score ranged from 0 (1 subject) to 10 prothrombotic alleles (7 subjects), with a median level of 5. Figure 1B shows the distribution of the PS in CAD-free and in CAD subjects. No association was found between the PS and CAD (P = 0.889 by χ2-test).

Bottom Line: In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors.As compared to subjects with 3-7 alleles, those with few (</=2) alleles had a decreased MI risk (OR 0.34, 95%CIs 0.13-0.93), while those with more (>/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01).The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical and Experimental Medicine, University of Verona, Verona, Italy.

ABSTRACT

Background: Relative little attention has been devoted until now to the combined effects of gene polymorphisms of the hemostatic pathway as risk factors for Myocardial Infarction (MI), the main thrombotic complication of Coronary Artery Disease (CAD). The aim of this study was to evaluate the combined effect of ten common prothrombotic polymorphisms as a determinant of MI.

Methodology/principal findings: We studied a total of 804 subjects, 489 of whom with angiographically proven severe CAD, with or without MI (n = 307; n = 182; respectively). An additive model considering ten common polymorphisms [Prothrombin 20210G>A, PAI-1 4G/5G, Fibrinogen beta -455G>A, FV Leiden and "R2", FVII -402G>A and -323 del/ins, Platelet ADP Receptor P2Y12 -744T>C, Platelet Glycoproteins Ia (873G>A), and IIIa (1565T>C)] was tested. The prevalence of MI increased linearly with an increasing number of unfavorable alleles (chi(2) for trend = 10.68; P = 0.001). In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors. As compared to subjects with 3-7 alleles, those with few (/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01). The number of procoagulant alleles correlated directly (r = 0.49, P = 0.006) with endogenous thrombin potential.

Conclusions: The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD.

Show MeSH
Related in: MedlinePlus