Conclusion Heart Failure is a clinical syndrome associated with significant morbidity and mortality that varies with age, gender, and ethnic- ity. The current understanding of HF pathophysiology allows for medications that reduce preload and afterload by curbing the compensatory response of the sympathoadrenergic and RAAS systems. Multiple agents in the treatment of HFrEF significantly reduce mortality. In the next decade, the percent of cases of HF- pEF will likely surpass those of HFrEF; unfortunately, treatment options to date are limited. More research on the pathophysiol- ogy of this condition and drugs with beneficial outcomes in this Case study CW is a 68-year-old African American female with a history of HFrEF, hypertension, T2DM, obesity, and seasonal allergies. She presents to the emergency room after Christmas dinner at her sister’s house. CW complains of increased symptoms of “difficulty in breathing, unable to walk to the mailbox without having to rest, and needing to sleep on two big pillows to get any rest.” Her cur- rent laboratory values are within normal limits, except her BNP is 1,200 pg/mL, prompting the ER provider to put in for a cardiology consult and admit the patient. Upon reviewing her home medi- cations with the busy ER provider, she states she does not have insurance but lists the following home medications: carvedilol 25 mg twice a day, metformin 500 mg twice a day, and loratadine 10 mg daily. She states she was prescribed captopril but is not taking it anymore because her sister “had her mouth swell up, and tak- ing all of these medications are expensive.” The provider told her, “Isosorbide dinitrate/hydralazine is better in the black population, and we may need to consider that since you cannot afford to take your captopril.” The provider quickly leaves the room to attend to a stroke alert next door. After hearing this, CW becomes irate and does not want to be admitted to the hospital. You come in to fin - ish her medication reconciliation prior to hospital admission, only to find her visibly upset. Question 1: What are some examples of implicit bias that the initial provider may have had upon evaluating CW? Discussion: According to recent studies, African Americans are associated with a higher incidence and prevalence of HF than Caucasians (Chan- dra et al., 2022; Virani et al., 2020). African American women also have a 2.5-fold higher rate of HF hospitalizations than Caucasians
setting is imperative. For the time being, clinicians can help curb the prevalence of HFpEF by preventing and controlling comorbid conditions. An update to the 2017 ACC/AHA guidelines is war- ranted, with newer pharmacotherapeutic options available for HF treatment. According to the ACC, the estimated release of new guidelines will occur by mid-2022. Until then, clinicians need to work together to close the gap between guideline recommenda- tions and actual clinical practice to provide the best outcomes for patients with heart failure. (Nayak et al., 2020). Furthermore, the majority (80%) of HF-related hospitalizations occur in individuals 65 years and above (Lesyuk et al., 2018). Because of these variances in demographics, discus- sions and further studies are needed to better understand factors contributing to this gap. Factors such as implicit bias towards race, age, and socioeconom- ic background lead to worse healthcare outcomes. In this case, an implicit bias towards the patient may be evident in the provider’s comments, such as a quick recommendation on isosorbide dini- trate/hydralazine without examining and explaining other options for CW. Additionally, we see that the provider states, “…since you cannot afford to take your captopril”. We do not know if the pro- vider is referring to her socioeconomic status or the inability of CW to take an ACE inhibitor due to what seems to be a family his- tory of angioedema. Having a conversation with the patient with clear word choices will alleviate perceived bias. Question 2: What is an evidence-based recommendation that is a better op- According to the African-American Heart Failure Trial, isosorbide dinitrate/hydralazine significantly reduced mortality in African American patients. This agent may not be the best choice for CW, however. The provider needs to investigate the history of “mouth swelling” and if CW has ever used an ACE inhibitor in the past and for how long. Furthermore, if a valid contraindication exists because of angioedema, it does not preclude using an ARB per guidelines. Using an ARB versus an isosorbide dinitrate/hydrala- zine combination can reduce pill burden and improve compliance. tion for CW? Discussion:
Appendix: Appendix A: Abbreviations in This Activity ACC American College of Cardiology ACE Angiotensin Converting Enzyme AHA American Heart Association ARB Angiotensin Receptor Blocker BNP B-type natriuretic peptide HF Heart Failure HTN Hypertension LVEF Left Ventricular Ejection Fraction LOE Level of Evidence MRA
Appendix B: ACC Classification and Level of Evidence Class of Recommendation Level of Evidence
I : Clear benefit that exceeds risk and treatment or proce- dure should be done IIa : Benefit is in favor, but ad - ditional studies are needed for treatment or procedure
Level A : Data from several randomized controlled trials or meta-analyses with multiple patient populations studied Level B : Data from single randomized controlled tri- als or non-randomized studies with limited pa- tient populations studied. B-R- denotes level B from ran- domized controlled trials Level C : Cases studies or con- sensus opinion with minimal patient populations studied.
IIb : Unclear benefit, but treat - ment or procedure may be considered III : No benefit or harm with treatment or procedure
Mineralocorticoid Receptor Antagonist
NT-proBNP N-terminal-proBNP NYHA
New York Heart Association
Note . Class of Recommendation and Level of Evidence from: 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure, by C.W. Yancy, M Jessup, B Bozkurt, et al. JACC, 70(6), 776-803.
RAAS SGLT2
Renin-angiotensin-aldosterone-system Sodium-glucose cotransporter-2 inhibitors
T2DM Type 2 diabetes mellitus
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