size was determined using linear measurements as outlined by the American 
Society of Echocardiography. Severity of mitral regurgitation was determined using color Doppler and the PISA method as outlined by the American Society of Echocardiography. Aldosterone assay Samples for aldosterone were assayed using a commercially available kit containing I-125-labeled aldosterone, as previously described. All samples were assayed in duplicate. Intra-assay and inter-assay coefficients of variation for this assay were 1.5% and 1.9% respectively. Study population African Americans at least18 years of age, with a diagnosis of heart failure for at least 3 months were included. Additional inclusion criteria were treatment with an ACE inhibitor or angiotensin Genotyping Genomic DNA was isolated from buccal cells or whole blood using a PuregeneH kit. Hardy-Weinberg equilibrium was tested by x2 analysis. Normally distributed continuous data are presented as mean 6 SD and were compared by unpaired t-tests and analysis of variance. Continuous data that were non-normally distributed are presented as median and were compared with Mann Whitney U and Kruskal Wallis tests. The x2 or Fischer’s exact test was used to compare categorical data, and the Cochran-Armitage trend test was used to compare allele frequencies buy Debio1347 between groups. Multiple logistic regression permitted tests of association between CYP11B2 344T.C and presence of AF while holding clinical factors, echocardiographic measurements, and genetic ancestry constant. Dominant, additive, recessive and genotypic effects models were all used to test the association of CYP11B2 2344T.C genotype and presence of AF. Based on previous data, risk factors for AF included as covariates in the multiple logistic regression models were age, sex, body size, systemic hypertension, diabetes, coronary artery disease, creatinine clearance, left atrial size, mitral regurgitation and genetic ancestry. Marginal standardization was used for the final logistic regression model to estimate adjusted prevalence differences between genotype groups. Bootstrapping was used to quantify the confidence intervals of the prevalence difference generated from the marginal standardization. Given the low prevalence of the CC homozygous genotype, we used permutation 17804190 to generate a distribution genotypic effects under the assumption of a true null hypothesis, which creates an empirical p value for the association of the CYP11B2 2344T.C recessive effects model and AF. For the exploratory analysis of serum aldosterone, linear regression was used to examine the association between genetic ancestry and aldosterone levels. Serum aldosterone was naturallog transformed to produce a more normal distribution of regression residuals, as done previously. Mean log serum aldosterone was compared between genotype and AF groups by the unpaired t-test. We also examined the association between genotype and extreme elevation of log aldosterone despite standard heart failure therapy, which was defined as a serum log aldosterone level at or above the 90th percentile for the study population, 7906496 using Fisher’s exact test. A two-sided p value of less than 0.05 was considered as statistical significance. Adjusted for age, sex, body size, mitral regurgitation, systemic hypertension, coronary artery disease, diabetes mellitus, left atrial size, creatinine clearance, and percent European ancestry. Empirical p value generated by permuting the CC genotype term in the logist
