Many studies have established and replicated the association of the 9p21-3 locus with CAD and myocardial infarction (MI). Of these, the variant on the p arm of chromosome 9 at position 21–3 (9p21-3) is the most well-known and replicated. Genome wide association studies (GWAS) have identified over 30 risk variants for CAD. The presence of a positive family history as a strong risk factor in CAD points to underlying genetic risk factors. Modification of major environmental risks such as smoking and high cholesterol reduces CAD mortality by 20% to 30%. However the effect of this allele on CAD progression and disease specific clinical outcomes are not observed possibly due to diminishing genetic risk following dietary modification and therapy.Ĭoronary artery disease (CAD) remains a worldwide leading cause of mortality. Patients of coronary atherosclerosis who carry the high risk genotype of the 9p21-3 allele may be more likely to have multi-vessel CAD. HR genotype did not predict ∆MLD or number of new lesions at follow-up.
There was no significant difference between HR and LR genotypes in terms of all-cause mortality, recurrent myocardial infarction or the frequency of coronary revascularization. ResultsĢ3 cohorts enrolling 16,860 participants were analyzed. Relative risks (RR) and weighted mean difference (WMD) were pooled using the random effects models. We extracted the association of the 9p21-3 locus with measures of severity of coronary atherosclerosis, angiographic outcomes, and key clinical outcomes (all-cause mortality, recurrent myocardial infarction and the need for coronary revascularization). Studies examining 9p21-3 genotype in patients with known coronary artery disease were included. Multiple electronic databases were searched from inception through August 2012. We performed a systematic review and meta-analysis to assess whether this locus is associated with severity of coronary atherosclerosis and adverse clinical outcomes in those with known coronary disease. Studies suggest that the 9p21-3 locus may influence susceptibility to myocardial infarction.
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