Despite marked progress in cardiovascular disease management in the last several decades, there remain significant, persistent disparities in cardiovascular health in historically marginalized racial and ethnic groups. Here, we outline current state of health disparities in cardiovascular disease, discuss the interplay between social determinants of health, structural racism, and cardiovascular outcomes, and highlight strategies to address these issues. Across the continuum of atherosclerotic cardiovascular disease (ASCVD) prevention, there remain significant disparities in outcomes including morbidity and mortality by race, ethnicity, and socioeconomic status (SES). These disparities begin early in childhood (primordial prevention) and continue with a higher prevalence of cardiovascular risk factors (primary prevention), and in the uptake of evidence-based therapies (secondary prevention). These disparities are driven by social determinants of health and structural racism that disproportionately disadvantage historically marginalized populations. Structural racism and social determinants of health contribute to significant disparities in cardiovascular morbidity and mortality.

Although cardiovascular disease (CVD) is the leading cause of death in women, cardiovascular risk factors remain underrecognized and undertreated. Hyperlipidemia is one of the leading modifiable risk factors for CVD. Statins are the mainstay of lipid lowering therapy (LLT), with additional agents such as ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors as additive or alternative therapies. Clinical trials have demonstrated that these LLTs are equally efficacious in lipid lowering and cardiovascular risk reduction in women as they are in men. Although the data on statin teratogenicity is evolving, in times of pregnancy or attempted pregnancy, most lipid-lowering agents are generally avoided due to lack of high-quality safety data. This leads to limited treatment options in pregnant women with hyperlipidemia or cardiovascular disease. During the perimenopausal period, the mainstay of lipid management remains consistent with guidelines across all ages. Hormone replacement therapy for cardiovascular risk reduction is not recommended. Future research is warranted to target sex-based disparities in LLT initiation and persistence across the life course.

Adrenal insufficiency is a rare cause of heart failure. We describe a young patient who presented with new-onset biventricular systolic heart failure due to primary adrenal insufficiency. The patient was initiated on hydrocortisone, with rapid improvement of both left and right ventricular systolic function. (Level of Difficulty: Beginner.).

Objectives: The Fontan operation has increased survival in patients with single-ventricle congenital heart defects. However, Fontan survivors are at risk of other organ dysfunctions, such as renal dysfunction (RD). The objectives of this study are to assess the prevalence of and potential risk factors for RD among Fontan survivors. Design, setting, and patients: We performed a two-center, cross-sectional study that included Fontan survivors evaluated in outpatient-clinics for routine follow up between 01/08-12/16. Outcome measures: The primary outcome was the presence of RD defined by estimated glomerular filtration rate (eGFR) of <90 ml/min/1.73 m(2) derived using the serum creatinine-based Full Age Spectrum equation. Chi-square and t-tests were used to compare groups with and without RD. A multivariable logistic regression model was derived to identify risk factors associated with the presence of RD using stepwise variable selection methods. Additionally, using eGFR as a continuous variable, a linear regression model was derived to evaluate risk factors that negatively correlate with eGFR. Results: We included 402 Fontan survivors; 61% male; median age 13.7 (2.3-49.9) years; median time since initial Fontan 9.8 (0.1-36.9) years. RD was present in 27.4% (110/402) of patients. Risk factors for RD included single ventricle with right ventricular morphology [odds ratio 2.04; 95% CI (1.26,3.3)], ascites [2.99 (1.04,8.59)] and sildenafil therapy [2.22 (1.05,4.67)]. Risk factors that negatively correlate with eGFR included history of Stage 1 Norwood palliation (-7.6 ml/min/1.73 m2; p = 0.003); "failing Fontan physiology" defined by ascites, protein-losing enteropathy and/or plastic bronchitis (-8.9 ml/min/1.73 m(2); p = 0.01) and moderate or greater ventricular dysfunction (-16.7 ml/min/1.73 m(2); p = 0.02). Conclusions: One-fourth of Fontan survivors demonstrate RD within ten years after Fontan. Risk factors for RD included right ventricular morphology of the single ventricle, history of Stage 1 Norwood palliation, "failing Fontan physiology," or ventricular dysfunction. Therefore, comprehensive screening for RD in Fontan survivors is needed, particularly in those identified at a higher risk for RD.