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Introduction:The FDA approved the use of sacubitril/valsartan and ivabradine among patients with HF and reduced ejection fraction (HFrEF) in 2015. However, after market introduction, early experiences suggested marked underutilization of these evidence-based therapies. Few nationally represented data are available examining their contemporary use & associated costs in the US.Methods:Publicly available data from the Medicare Part D Prescription Drug Event for 2016-17 was used to assess the use and associated costs of sacubitril/valsartan and ivabradine. The per-beneficiary cost of these newer agents was also compared with that of traditional guideline recommended medications for HFrEF (lisinopril, metoprolol succinate, and spironolactone).Results:The number of Medicare beneficiaries that were prescribed ivabradine and sacubitril/valsartan increased by 33% (3,637 to 4,820) and 156% (35,423 to 90,606) respectively from 2016 to 2017 (Figure 1A). The per beneficiary cost for ivabradine and sacubitril/valsartan were $1,947 and $1,838 respectively in 2016 to $2,400 and $2,511 in 2017, an increase of 23% and 37%. In contrast, the combined annual per-beneficiary spending on metoprolol succinate, lisinopril, spironolactone was $232 in 2016 and $221 in 2017, a 20-fold lower cost than either newer agent (Figure 1B). The estimated cost for transitioning all patients with HFrEF from lisinopril to sacubitril/valsartan, based on an estimated HFrEF prevalence of 2.65 million in the Medicare population, is $6.6 billion.Conclusions:The proportional use of sacubitril/valsartan and ivabradine has increased substantially from 2016 to 2017. Use of these agents among beneficiaries with HF is associated with high economic burden, with up to 20-fold higher cost than that for all three classes of GDMT. Further work is needed to lower the cost of these agents and to assess whether these agents avert downstream expenditures and clinical events among patients with HF.

Introduction:The 2019 Primary Prevention Guideline suggests selective use of low-dose aspirin (ASA) for primary prevention of ASCVD given increased bleeding risk. Higher coronary calcium (CAC) may identify those more likely to benefit from ASA, but whether higher CAC also associates with more bleeding is unclear.Methods:Participants of the Dallas Heart Study, free from ASCVD and not on ASA at baseline were included. Fatal and non-fatal major bleeding events (gastrointestinal, intracranial, major other) were identified from ICD9 and 10 codes. Adjudicated ASCVD events (non-fatal MI, coronary heart disease death, non-fatal and fatal stroke) were identified using ICD codes and phone surveys. Multivariable Cox models were used to assess the independent association of CAC with incident bleeding and ASCVD events.Results:The cohort included 2184 participants (mean age 44y, 57% female, 33% black) with 109 major bleeding events and 123 ASCVD events over a median follow-up of 17 years. Older age, black race, diabetes, smoking, blood pressure, peptic ulcer disease, corticosteroid and antacid use were associated with bleeding. Higher CAC categories (0, 1-100, >100) were associated with both ASCVD and bleeding events (p<0.001 each; Figure). CAC better discriminated ASCVD risk (c-statistic 0.79, 95% CI 0.74 to 0.83) than bleeding risk (c-statistic 0.61, 95% CI 0.55 to 0.66), and CAC ?100 (vs. CAC=0) remained associated with ASCVD [HR, 95%CI 3.98 (2.07-7.64)], but not bleeding [HR-1.24 (0.68-2.27)] after multivariable adjustment . In exploratory analyses applying meta-analysis estimates of the effect of ASA, the absolute 10-year reduction of ASCVD would be 1.7% and absolute increased bleeding 2.2% in those with CAC ?100.Conclusions:Higher CAC is associated with both ASCVD and bleeding events, with a stronger association with ASCVD. Additional studies are warranted to determine if there are CAC thresholds with favorable net benefit of ASA for primary prevention of ASCVD.

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.