Background and PurposeIschemic 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. MethodsMeta-analyses of the associations between the 11 MI-associated SNPs and IS were performed using 7,080 cases and 11,395 controls 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 betas and standard errors. Meta-analysis was conducted using an inverse variance weighted approach assuming a random effect model. ResultsDespite 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. ConclusionsOur 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.
Are myocardial infarction-associated single nucleotide polymorphisms associated with ischemic stroke?
Bione S;Lisa A;Parolo S;
2012
Abstract
Background and PurposeIschemic 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. MethodsMeta-analyses of the associations between the 11 MI-associated SNPs and IS were performed using 7,080 cases and 11,395 controls 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 betas and standard errors. Meta-analysis was conducted using an inverse variance weighted approach assuming a random effect model. ResultsDespite 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. ConclusionsOur 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.