g African Americans with heart failure, greater European ancestry was correlated with higher serum aldosterone concentrations, and greater West African ancestry was correlated with lower aldosterone levels. These finding are consistent with previous observations of lower plasma aldosterone in African Americans compared to Europeans with various stages of hypertension. Moreover, the link between European ancestry and elevated aldosterone may provide insight into the mechanism underlying the association between European ancestry and increased risk of AF in African Americans in the Atherosclerosis Risk in Communities Study. In particular, our data support the hypothesis that the genetic ancestry effect on incident 8913470 AF could be due, in part, to differences in aldosterone levels by ancestry. However, we did not observe a significant association between ancestry and AF in our study, which is in contrast to data from the ARIC study. It is possible that our study was underpowered to detect such an association, especially with the modest effect size observed in ARIC between European ancestry and incident AF. The implication of our findings that CYP11B2 genotype is associated with both AF risk and elevated aldosterone is that CYP11B2 may be a Sodium laureth sulfate site useful biomarker to identify heart failure patients at risk for AF in whom aldosterone antagonism may attenuate such risk. In addition to increasing the risk for stroke, AF can also exacerbate heart failure symptoms and reduce exercise capacity. As such, the ability to predict patients at greater risk for AF, in whom modalities could be instituted to ameliorate this risk, could potentially lessen heart failure-related morbidity. There is strong evidence that aldosterone antagonism with an MRA in systolic heart failure improves survival and reduces heart failure -related morbidity, including AF. There are also data that the MRA spironolactone attenuates the deleterious effects of aldosterone in AF at the level of atrial tissue, where mineralocorticoid receptors appear to be up-regulated, lending support to the idea that an MRA may attenuate the risk for AF in heart failure patients with a 2344CC genotype. However, the role of MRAs in heart failure patients with the CYP11B2 2344 CC genotype-associated AF risk has yet to be ascertained. It is important to note that there have been discrepant results with the CYP11B2 2344T.C 18000030 variant and its association with aldosterone secretion and the presence of cardiovascular disease. Along with type-I error due to sample size, one of several explanations is confounding association due to population admixture, which we have addressed by adjusting for genetic ancestry. Allele and genotype frequencies in our study are similar to those from the African American Heart Failure Trial . However, there are significant differences in CYP11B2 2344T.C allele and genotype frequencies among ethnic groups. African 
Americans have a lower frequency of the CC genotype than both Europeans and Asians, which may explain the intra-ancestral discrepancy in certain association studies. Some of the previous studies focused on patient populations with cardiovascular diseases other than heart failure, and failed to find an association between 2344CC genotype and AF. It is possible that aldosterone regulation plays a greater role in the pathogenesis of AF in heart failure patients than patients with other diseases considering the significant aldosterone involvement in the ventricular remodeling and car