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Seven haemostatic gene polymorphisms in coronary disease: meta-analysis of 66 155 cases and 91 307 controls

Variants of certain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coronary disease have reported apparently conflicting results. We did meta-analyses on seven such haemostatic genetic variants for which... Full description

Journal Title: The Lancet (British edition) 2006, Vol.367 (9511), p.651-658
Main Author: Ye, Zheng
Other Authors: Liu, Eugene HC , Higgins, Julian PT , Keavney, Bernard D , Lowe, Gordon DO , Collins, Rory , Danesh, John
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: London: Elsevier Ltd
ID: ISSN: 0140-6736
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title: Seven haemostatic gene polymorphisms in coronary disease: meta-analysis of 66 155 cases and 91 307 controls
format: Article
creator:
  • Ye, Zheng
  • Liu, Eugene HC
  • Higgins, Julian PT
  • Keavney, Bernard D
  • Lowe, Gordon DO
  • Collins, Rory
  • Danesh, John
subjects:
  • Abridged Index Medicus
  • Analysis
  • Biological and medical sciences
  • Blood Coagulation Factors - genetics
  • Cardiology. Vascular system
  • Care and treatment
  • Case-Control Studies
  • Clinical outcomes
  • Coronary Disease - genetics
  • Coronary heart disease
  • Coronary vessels
  • Factor V - genetics
  • Factor VII - genetics
  • General aspects
  • Genes
  • Genotype
  • Heart
  • Heart attacks
  • Humans
  • Medical sciences
  • Meta-analysis
  • Myocardial Infarction - genetics
  • Polymorphism
  • Polymorphism, Genetic - genetics
  • Research
  • Studies
  • Systematic review
ispartof: The Lancet (British edition), 2006, Vol.367 (9511), p.651-658
description: Variants of certain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coronary disease have reported apparently conflicting results. We did meta-analyses on seven such haemostatic genetic variants for which the available evidence on each comprises at least 5000 coronary disease cases and at least 5000 controls. Meta-analyses were done of 191 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210A, plasminogen activator inhibitor-1 (PAI-1) [−675] 4G/5G, and three platelet glycoprotein (GP) receptor variants (GPIa C807T, GPIbα T[−5]C, GPIIIa C1565T), involving a total of 66 155 coronary disease cases and 91 307 controls. We explored potential sources of heterogeneity. In a combined analysis of all studies, the per-allele relative risks (RR) for coronary disease of factor V 1691A and of prothrombin 20210A were 1·17 (95% CI 1·08–1·28) and 1·31 (1·12–1·52), respectively. Combined analyses of studies of the PAI-1 [−675] 4G variant yielded a per-allele relative risk for coronary disease of 1·06 (1·02–1·10), but there was an indication of publication bias in these studies. Combined analyses of the factor VII 10976A, GPIa 807T, GPIbα [−5]C, and GPIIIa 1565T variants showed no significant overall associations with coronary disease, yielding per-allele RRs of 0·97 (0·91–1·04), 1·02 (0·97–1·08), 1·05 (0·96–1·13), and 1·03 (0·98–1·07), respectively. The 1691A variant of the factor V gene and the 20210A variant of the prothrombin gene, both of which increase circulating thrombin generation, might each be moderately associated with the risk of coronary disease. Further studies are merited to assess these associations in greater detail (including any gene–gene and gene–environment interactions) and to determine any implications with regard to potential therapies designed to reverse patients' prothrombotic phenotype, such as selective plasma factor V or factor Xa inhibition.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0140-6736
fulltext: fulltext
issn:
  • 0140-6736
  • 1474-547X
url: Link


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titleSeven haemostatic gene polymorphisms in coronary disease: meta-analysis of 66 155 cases and 91 307 controls
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creatorYe, Zheng ; Liu, Eugene HC ; Higgins, Julian PT ; Keavney, Bernard D ; Lowe, Gordon DO ; Collins, Rory ; Danesh, John
creatorcontribYe, Zheng ; Liu, Eugene HC ; Higgins, Julian PT ; Keavney, Bernard D ; Lowe, Gordon DO ; Collins, Rory ; Danesh, John
descriptionVariants of certain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coronary disease have reported apparently conflicting results. We did meta-analyses on seven such haemostatic genetic variants for which the available evidence on each comprises at least 5000 coronary disease cases and at least 5000 controls. Meta-analyses were done of 191 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210A, plasminogen activator inhibitor-1 (PAI-1) [−675] 4G/5G, and three platelet glycoprotein (GP) receptor variants (GPIa C807T, GPIbα T[−5]C, GPIIIa C1565T), involving a total of 66 155 coronary disease cases and 91 307 controls. We explored potential sources of heterogeneity. In a combined analysis of all studies, the per-allele relative risks (RR) for coronary disease of factor V 1691A and of prothrombin 20210A were 1·17 (95% CI 1·08–1·28) and 1·31 (1·12–1·52), respectively. Combined analyses of studies of the PAI-1 [−675] 4G variant yielded a per-allele relative risk for coronary disease of 1·06 (1·02–1·10), but there was an indication of publication bias in these studies. Combined analyses of the factor VII 10976A, GPIa 807T, GPIbα [−5]C, and GPIIIa 1565T variants showed no significant overall associations with coronary disease, yielding per-allele RRs of 0·97 (0·91–1·04), 1·02 (0·97–1·08), 1·05 (0·96–1·13), and 1·03 (0·98–1·07), respectively. The 1691A variant of the factor V gene and the 20210A variant of the prothrombin gene, both of which increase circulating thrombin generation, might each be moderately associated with the risk of coronary disease. Further studies are merited to assess these associations in greater detail (including any gene–gene and gene–environment interactions) and to determine any implications with regard to potential therapies designed to reverse patients' prothrombotic phenotype, such as selective plasma factor V or factor Xa inhibition.
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publisherLondon: Elsevier Ltd
subjectAbridged Index Medicus ; Analysis ; Biological and medical sciences ; Blood Coagulation Factors - genetics ; Cardiology. Vascular system ; Care and treatment ; Case-Control Studies ; Clinical outcomes ; Coronary Disease - genetics ; Coronary heart disease ; Coronary vessels ; Factor V - genetics ; Factor VII - genetics ; General aspects ; Genes ; Genotype ; Heart ; Heart attacks ; Humans ; Medical sciences ; Meta-analysis ; Myocardial Infarction - genetics ; Polymorphism ; Polymorphism, Genetic - genetics ; Research ; Studies ; Systematic review
ispartofThe Lancet (British edition), 2006, Vol.367 (9511), p.651-658
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descriptionVariants of certain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coronary disease have reported apparently conflicting results. We did meta-analyses on seven such haemostatic genetic variants for which the available evidence on each comprises at least 5000 coronary disease cases and at least 5000 controls. Meta-analyses were done of 191 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210A, plasminogen activator inhibitor-1 (PAI-1) [−675] 4G/5G, and three platelet glycoprotein (GP) receptor variants (GPIa C807T, GPIbα T[−5]C, GPIIIa C1565T), involving a total of 66 155 coronary disease cases and 91 307 controls. We explored potential sources of heterogeneity. In a combined analysis of all studies, the per-allele relative risks (RR) for coronary disease of factor V 1691A and of prothrombin 20210A were 1·17 (95% CI 1·08–1·28) and 1·31 (1·12–1·52), respectively. Combined analyses of studies of the PAI-1 [−675] 4G variant yielded a per-allele relative risk for coronary disease of 1·06 (1·02–1·10), but there was an indication of publication bias in these studies. Combined analyses of the factor VII 10976A, GPIa 807T, GPIbα [−5]C, and GPIIIa 1565T variants showed no significant overall associations with coronary disease, yielding per-allele RRs of 0·97 (0·91–1·04), 1·02 (0·97–1·08), 1·05 (0·96–1·13), and 1·03 (0·98–1·07), respectively. The 1691A variant of the factor V gene and the 20210A variant of the prothrombin gene, both of which increase circulating thrombin generation, might each be moderately associated with the risk of coronary disease. Further studies are merited to assess these associations in greater detail (including any gene–gene and gene–environment interactions) and to determine any implications with regard to potential therapies designed to reverse patients' prothrombotic phenotype, such as selective plasma factor V or factor Xa inhibition.
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4Cardiology. Vascular system
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15Genotype
16Heart
17Heart attacks
18Humans
19Medical sciences
20Meta-analysis
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authorYe, Zheng ; Liu, Eugene HC ; Higgins, Julian PT ; Keavney, Bernard D ; Lowe, Gordon DO ; Collins, Rory ; Danesh, John
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abstractVariants of certain haemostatic genes (such as that encoding factor V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coronary disease have reported apparently conflicting results. We did meta-analyses on seven such haemostatic genetic variants for which the available evidence on each comprises at least 5000 coronary disease cases and at least 5000 controls. Meta-analyses were done of 191 studies in relation to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210A, plasminogen activator inhibitor-1 (PAI-1) [−675] 4G/5G, and three platelet glycoprotein (GP) receptor variants (GPIa C807T, GPIbα T[−5]C, GPIIIa C1565T), involving a total of 66 155 coronary disease cases and 91 307 controls. We explored potential sources of heterogeneity. In a combined analysis of all studies, the per-allele relative risks (RR) for coronary disease of factor V 1691A and of prothrombin 20210A were 1·17 (95% CI 1·08–1·28) and 1·31 (1·12–1·52), respectively. Combined analyses of studies of the PAI-1 [−675] 4G variant yielded a per-allele relative risk for coronary disease of 1·06 (1·02–1·10), but there was an indication of publication bias in these studies. Combined analyses of the factor VII 10976A, GPIa 807T, GPIbα [−5]C, and GPIIIa 1565T variants showed no significant overall associations with coronary disease, yielding per-allele RRs of 0·97 (0·91–1·04), 1·02 (0·97–1·08), 1·05 (0·96–1·13), and 1·03 (0·98–1·07), respectively. The 1691A variant of the factor V gene and the 20210A variant of the prothrombin gene, both of which increase circulating thrombin generation, might each be moderately associated with the risk of coronary disease. Further studies are merited to assess these associations in greater detail (including any gene–gene and gene–environment interactions) and to determine any implications with regard to potential therapies designed to reverse patients' prothrombotic phenotype, such as selective plasma factor V or factor Xa inhibition.
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pubElsevier Ltd
pmid16503463
doi10.1016/S0140-6736(06)68263-9