Genome-wide association analyses identify novel Brugada syndrome risk loci and highlight a new mechanism of sodium channel regulation in disease susceptibility

README chr: chromosome pos: genomic position in GRCh37 rsid: dbSNP ID (if available) effect_allele: effect allele other_allele: other allele beta: meta-analysis association regression coefficient se: standard error of beta p: P value of the association testing n_cohorts: number of cohorts included in the meta-analysis for the specific variant n_all: total number of samples n_cases: total number of cases n_controls: total number of controls direction: direction of effect for each of the 10 cohorts hetISq: I^2 from the meta-analysis heterogeneity test (METAL) hetChiSq: ChiSq from the meta-analysis heterogeneity test (METAL) hetDf: Degrees of freedom in the meta-analysis heterogeneity test (METAL) hetPVal: P-value of the meta-analysis heterogeneity test (METAL) eaf_all: effect allele frequency overall eaf_cases: effect allele frequency in cases eaf_controls: effect allele frequency in controls

The Brugada syndrome GWAS summary statistics Brugada syndrome is a cardiac arrhythmia disorder associated with sudden death in young adults. With the exception of SCN5A, encoding the cardiac sodium channel Na_V1.5, susceptibility genes remain largely unknown. We performed a genome-wide association meta-analysis comprising 2,820 unrelated cases with Brugada syndrome and 10,001 controls.