Are myocardial infarction-associated single-nucleotide polymorphisms associated with ischemic stroke?

Chingyu Cheng, Christopher Anderson, Silvia Bione, Keith Keene, Jane Maguire, Michael Nalls, Asif Rasheed, Marion Zeginigg, John Attia, Ross Baker, Simona Barlera, Alessandro Biffi, Ebony Bookman, Thomas Brott, Robert Brown, Fang Chen, Wei Min Chen, Emilio Ciusani, John Cole, Lynelle CortelliniJohn Danesh, Kimberly Doheny, Luigi Ferrucci, Maria Franzosi, Philippe Frossard, Karen Furie, Johnathan Golledge, Graeme Hankey, Dena Hernandez, Elizabeth Holliday, Fang-Chi Hsu, Jim Jannes, Ayeesha Kamal, Muhammad Khan, Steven Kittner, Simon Koblar, Martin Lewis, Lisa Lincz, Antonella Lisa, Mar Matarin, Pablo Moscato, Josyf Mychaleckyj, Eugenio Parati, Silvia Parolo, Elizabeth Pugh, Natalia Rost, Michael Schallert, Helena Schmidt, Rodney Scott, Jonathan Sturm, Sunaina Yadav, Moazzam Zaidi, Giorgio Boncoraglio, Christopher Levi, James Meschia, Jonathan Rosand, Michele Sale, Danish Saleheen, Reinhold Schmidt, Pankaj Sharma, Bradford Worrall, Braxton Mitchell

    Research output: Contribution to journalArticlepeer-review

    22 Citations (Scopus)


    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.

    Original languageEnglish
    Pages (from-to)980-986
    Number of pages7
    Issue number4
    Publication statusPublished - Apr 2012


    • cerebral infarct
    • genetics
    • ischemia


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