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Introduction:One in four individuals with HFpEF are diagnosed with depression. The prognostic implications of prevalent and new onset depression in patients with HFpEF are unknown.Methods:Participants from the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist Trial (TOPCAT) with available PHQ-9 Depression Scale data at baseline were stratified according to depression severity: minimal (score: 1-4), mild (5-9), moderate (10-14), and severe (>15). Depression status at 1-year follow up was also determined in the subgroup with available follow up data using the PHQ-9 Depression Scale. The association of prevalent depression, change in depression status with risk of all-cause mortality and HF-hospitalization was evaluated using multivariable adjusted Cox models.Results:The study included 1431 participants, of which 15.9% had moderate depression and 10.8% had severe depression at baseline. Participants with severe depression at baseline had higher BMI, were more commonly women, and had higher burden of diabetes, and worse NYHA functional status. In adjusted Cox models, there was a significant graded association between depression severity and risk of mortality, with the highest risk noted among those with severe depression (See Fig 1A). Among participants with 1-year follow up data, participants with new-onset depression on follow-up had significantly higher risk of all-cause mortality [HR (95% CI) = 2.00 (1.27 - 3.14), ref group: no depression at baseline and follow up]. Prevalent depression at baseline or new onset depression on follow up was not significantly associated with risk of HF-related hospitalization in the study cohort.Conclusions:Prevalent and new onset depression is associated with higher risk of all-cause mortality in patients with HFpEF. Future studies are needed to determine if early identification and treatment of depression may modify the risk of all-cause mortality in patients with HFpEF.

Introduction:HTN and higher arterial stiffness are more common among self-reported black individuals compared to whites. The degree to which genetic African ancestry accounts for racial disparities in these phenotypes is not well known.Methods:Self-identified black participants from the Dallas Heart Study (DHS) free from CVD with available genotyping (Infinium HumanExome, Illumina) and arterial stiffness assessment by cardiac MRI were included. Genetic ancestry proportions were quantified from genome-wide genotyping data. Multivariable linear regression models were used to assess the association of African ancestry with arterial stiffness parameters [aortic pulse wave velocity (PWV), proximal aortic impedance (Zc), pulse pressure (PP)]. Among participants free from HTN at baseline, the association of African ancestry with HTN at follow-up 7 years later was assessed using adjusted logistic regression models.Results:The cohort included 1120 self-identified black participants (mean age 45y, 57% women) with a mean African ancestry proportion of 86% (SD 9%). In adjusted analyses, proportion of African ancestry was not significantly associated with arterial stiffness (PWV, Zc & PP) [Table]. In contrast, among participants free from HTN at baseline, a higher proportion of African ancestry was significantly associated with higher odds of HTN on follow-up independent of age, sex, SES factors, and CV risk factors (Table).Conclusions:Among self-reported black participants, higher proportion of genetic African Ancestry was associated with higher odds of HTN independent of biological and SES factors. However, African ancestry was not associated with measures of arterial stiffness. Genetic ancestry accounts for at least part of the higher burden of HTN but not arterial stiffness in black individuals. Future studies are needed to confirm these findings and better understand the contribution of genetic factors toward racial disparities in hypertension.