Are myocardial infarction-associated single-nucleotide polymorphisms associated with ischemic stroke?
Cheng, YC
Anderson, CD
Bione, S
Keene, K
Maguire, JM
Nalls, M
Rasheed, A
Zeginigg, M
Attia, J
Baker, R
Barlera, S
Biffi, A
Bookman, E
Brott, TG
Brown, RD
Chen, F
Chen, WM
Ciusani, E
Cole, JW
Cortellini, L
Danesh, J
Doheny, K
Ferrucci, L
Franzosi, MG
Frossard, P
Furie, KL
Golledge, J
Hankey, GJ
Hernandez, D
Holliday, EG
Hsu, FC
Jannes, J
Kamal, A
Khan, MS
Kittner, SJ
Koblar, SA
Lewis, M
Lincz, L
Lisa, A
Matarin, M
Moscato, P
Mychaleckyj, JC
Parati, EA
Parolo, S
Pugh, E
Rost, NS
Schallert, M
Schmidt, H
Scott, RJ
Sturm, JW
Yadav, S
Zaidi, M
Boncoraglio, GB
Levi, CR
Meschia, JF
Rosand, J
Sale, M
Saleheen, D
Schmidt, R
Sharma, P
Worrall, B
Mitchell, BD
- Publication Type:
- Journal Article
- Citation:
- Stroke, 2012, 43 (4), pp. 980 - 986
- Issue Date:
- 2012-04-01
Closed Access
Filename | Description | Size | |||
---|---|---|---|---|---|
_ Stroke.pdf | Published Version | 2.47 MB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Cheng, YC | en_US |
dc.contributor.author | Anderson, CD | en_US |
dc.contributor.author | Bione, S | en_US |
dc.contributor.author | Keene, K | en_US |
dc.contributor.author |
Maguire, JM |
en_US |
dc.contributor.author | Nalls, M | en_US |
dc.contributor.author | Rasheed, A | en_US |
dc.contributor.author | Zeginigg, M | en_US |
dc.contributor.author | Attia, J | en_US |
dc.contributor.author | Baker, R | en_US |
dc.contributor.author | Barlera, S | en_US |
dc.contributor.author | Biffi, A | en_US |
dc.contributor.author | Bookman, E | en_US |
dc.contributor.author | Brott, TG | en_US |
dc.contributor.author | Brown, RD | en_US |
dc.contributor.author | Chen, F | en_US |
dc.contributor.author | Chen, WM | en_US |
dc.contributor.author | Ciusani, E | en_US |
dc.contributor.author | Cole, JW | en_US |
dc.contributor.author | Cortellini, L | en_US |
dc.contributor.author | Danesh, J | en_US |
dc.contributor.author | Doheny, K | en_US |
dc.contributor.author | Ferrucci, L | en_US |
dc.contributor.author | Franzosi, MG | en_US |
dc.contributor.author | Frossard, P | en_US |
dc.contributor.author | Furie, KL | en_US |
dc.contributor.author |
Golledge, J |
en_US |
dc.contributor.author | Hankey, GJ | en_US |
dc.contributor.author | Hernandez, D | en_US |
dc.contributor.author | Holliday, EG | en_US |
dc.contributor.author | Hsu, FC | en_US |
dc.contributor.author | Jannes, J | en_US |
dc.contributor.author | Kamal, A | en_US |
dc.contributor.author | Khan, MS | en_US |
dc.contributor.author | Kittner, SJ | en_US |
dc.contributor.author | Koblar, SA | en_US |
dc.contributor.author | Lewis, M | en_US |
dc.contributor.author | Lincz, L | en_US |
dc.contributor.author | Lisa, A | en_US |
dc.contributor.author | Matarin, M | en_US |
dc.contributor.author | Moscato, P | en_US |
dc.contributor.author | Mychaleckyj, JC | en_US |
dc.contributor.author | Parati, EA | en_US |
dc.contributor.author | Parolo, S | en_US |
dc.contributor.author | Pugh, E | en_US |
dc.contributor.author | Rost, NS | en_US |
dc.contributor.author | Schallert, M | en_US |
dc.contributor.author | Schmidt, H | en_US |
dc.contributor.author | Scott, RJ | en_US |
dc.contributor.author | Sturm, JW | en_US |
dc.contributor.author | Yadav, S | en_US |
dc.contributor.author | Zaidi, M | en_US |
dc.contributor.author | Boncoraglio, GB | en_US |
dc.contributor.author | Levi, CR | en_US |
dc.contributor.author | Meschia, JF | en_US |
dc.contributor.author | Rosand, J | en_US |
dc.contributor.author | Sale, M | en_US |
dc.contributor.author | Saleheen, D | en_US |
dc.contributor.author | Schmidt, R | en_US |
dc.contributor.author | Sharma, P | en_US |
dc.contributor.author | Worrall, B | en_US |
dc.contributor.author | Mitchell, BD | en_US |
dc.date.issued | 2012-04-01 | en_US |
dc.identifier.citation | Stroke, 2012, 43 (4), pp. 980 - 986 | en_US |
dc.identifier.issn | 0039-2499 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/111450 | |
dc.description.abstract | Background and Purpose-Ischemic stroke (IS) shares many common risk factors with coronary artery disease (CAD). We hypothesized that genetic variants associated with myocardial infarction (MI) or CAD may be similarly involved in the etiology of IS. To test this hypothesis, we evaluated whether single-nucleotide polymorphisms (SNPs) at 11 different loci recently associated with MI or CAD through genome-wide association studies were associated with IS. Methods-Meta-analyses of the associations between the 11 MI-associated SNPs and IS were performed using 6865 cases and 11 395 control subjects recruited from 9 studies. SNPs were either genotyped directly or imputed; in a few cases a surrogate SNP in high linkage disequilibrium was chosen. Logistic regression was performed within each study to obtain study-specific βs and standard errors. Meta-analysis was conducted using an inverse variance weighted approach assuming a random effect model. Results-Despite having power to detect odds ratio of 1.09-1.14 for overall IS and 1.20-1.32 for major stroke subtypes, none of the SNPs were significantly associated with overall IS and/or stroke subtypes after adjusting for multiple comparisons. Conclusions-Our results suggest that the major common loci associated with MI risk do not have effects of similar magnitude on overall IS but do not preclude moderate associations restricted to specific IS subtypes. Disparate mechanisms may be critical in the development of acute ischemic coronary and cerebrovascular events. © 2012 2012 American Heart Association, Inc. | en_US |
dc.relation.ispartof | Stroke | en_US |
dc.relation.isbasedon | 10.1161/STROKEAHA.111.632075 | en_US |
dc.subject.classification | Neurology & Neurosurgery | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Brain Ischemia | en_US |
dc.subject.mesh | Myocardial Infarction | en_US |
dc.subject.mesh | Linkage Disequilibrium | en_US |
dc.subject.mesh | Polymorphism, Single Nucleotide | en_US |
dc.subject.mesh | Adolescent | en_US |
dc.subject.mesh | Adult | en_US |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Aged, 80 and over | en_US |
dc.subject.mesh | Middle Aged | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Stroke | en_US |
dc.subject.mesh | Genome-Wide Association Study | en_US |
dc.title | Are myocardial infarction-associated single-nucleotide polymorphisms associated with ischemic stroke? | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 4 | en_US |
utslib.citation.volume | 43 | en_US |
utslib.for | 1103 Clinical Sciences | en_US |
utslib.for | 1109 Neurosciences | en_US |
utslib.for | 1102 Cardiorespiratory Medicine and Haematology | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health | |
utslib.copyright.status | closed_access | |
pubs.issue | 4 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 43 | en_US |
Abstract:
Background and Purpose-Ischemic stroke (IS) shares many common risk factors with coronary artery disease (CAD). We hypothesized that genetic variants associated with myocardial infarction (MI) or CAD may be similarly involved in the etiology of IS. To test this hypothesis, we evaluated whether single-nucleotide polymorphisms (SNPs) at 11 different loci recently associated with MI or CAD through genome-wide association studies were associated with IS. Methods-Meta-analyses of the associations between the 11 MI-associated SNPs and IS were performed using 6865 cases and 11 395 control subjects recruited from 9 studies. SNPs were either genotyped directly or imputed; in a few cases a surrogate SNP in high linkage disequilibrium was chosen. Logistic regression was performed within each study to obtain study-specific βs and standard errors. Meta-analysis was conducted using an inverse variance weighted approach assuming a random effect model. Results-Despite having power to detect odds ratio of 1.09-1.14 for overall IS and 1.20-1.32 for major stroke subtypes, none of the SNPs were significantly associated with overall IS and/or stroke subtypes after adjusting for multiple comparisons. Conclusions-Our results suggest that the major common loci associated with MI risk do not have effects of similar magnitude on overall IS but do not preclude moderate associations restricted to specific IS subtypes. Disparate mechanisms may be critical in the development of acute ischemic coronary and cerebrovascular events. © 2012 2012 American Heart Association, Inc.
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