People with HF LVEF ≥40% deserve to take center stage

Heart failure graphic banner with display “People with HF LVEF ≥40% deserve to take center stage”
Patient burden
Pathophysiology
Complexity of care
Commitment from Bayer

A serious condition that deserves more attention

Treatment options are limited for people with HF LVEF ≥40%
1-7

Heart failure can manifest with a reduced ejection fraction <40% (HFrEF), mildly reduced ejection fraction of 41% to 49% (HFmrEF), or with a preserved ejection fraction ≥50% (HFpEF). People with HF LVEF ≥40% account for approximately half of the total heart failure population.1,8  They often have overlapping comorbidities, such as kidney disease, hypertension, obesity, type 2 diabetes, and atrial fibrillation that increase their risk of mortality and morbidity.1-3,5,9 Evidence suggests that these comorbidities are among many factors that contribute to the different pathophysiology in patients with HF LVEF ≥40% vs patients with HF LVEF <40%.1-3,7,10

People with HF LVEF ≥40% are impacted in ways similar to what people with
HF LVEF <40% face1,3,4,11:

  • Downward arrow icon in a purple circle
    Functional limitations that affect daily activities1,3,4,11,12
  • Hospital building icon in a purple circle symbolizing rehospitalization charges
    Rehospitalization rate1,3
  • Purple colored heart icon with lightening symbolizing danger
    In an HF registry (2005 to 2009), approximately 75% of people hospitalized with HF LVEF ≥40% will die within 5 years1,13

The challenges in understanding the pathophysiology of HF LVEF ≥40% represent an unmet medical need.1-3,7,10

The complex pathophysiology of HF LVEF ≥40%
1-3,7,10

HF LVEF ≥40% is a multifaceted condition involving multiple important mechanisms
14

HF LVEF ≥40% does not represent a single pathological process but is a complex
disease with many contributing factors.14 Current evidence suggests systemic comorbid conditions (such as obesity, age, diabetes, etc)—and the interplay between them—drive myocardial dysfunction. While the mechanistic link is not fully understood, the current studies suggest a proinflammatory and profibrotic state as an important factor of
HF LVEF ≥40%.6,15-17

Graphic of a heart with table titled HF LVEF ≥40% and a list on possible contributing factors and pathways

While HF LVEF ≥40% is a multifaceted condition, inflammation and fibrosis are important factors in its pathophysiology.14,16

People with HF LVEF ≥40% often face complexity of care
1-5,11,18

Most clinical studies evaluating medical treatments for HF LVEF ≥40% have followed positive studies with the same drugs studied in HF LVEF <40%.1,19 However, due to major differences in fundamental pathophysiology, there is not enough high-quality evidence for guidelines to support a Class I recommendation for most of these therapies in HF LVEF ≥40%.1,3

 

Commitment from Bayer

Bayer is committed to the specific needs of people with HF.

  • CKD=chronic kidney disease; HF=heart failure; HF LVEF ≥40%=heart failure left ventricle ejection fraction greater than or equal to 40%—includes HFpEF (heart failure with preserved ejection fraction) and HFmrEF (heart failure with mid-range ejection fraction); HF LVEF <40%=heart failure left ventricle ejection fraction less than 40%—includes HFrEF (heart failure with reduced ejection fraction); RAAS=renin-angiotensin-aldosterone system; ROS=reactive oxygen system.

    1. Heidenreich PA, et al. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063.
    2. O’Gallagher K, et al. Cardiovasc Res. 2018;114(7):919-921. doi:10.1093/cvr/cvy095.
    3. Upadhya B, et al. Clin Cardiol. 2020;43(2):145-155. doi:10.1002/clc.23321.
    4. Forsyth F, et al. Eur J Cardiovasc Nurs. 2023;22(5):529-536. doi:10.1093/eurjcn/zvac081.
    5. Borlaug BA. Nat Rev Cardiol. 2020;17(9):559-573. doi:10.1038/s41569-020-0363-2.
    6. Parra-Lucares A, et al. Biomedicines. 2022;11(1):70. doi:10.3390/biomedicines11010070.
    7. Sanders-van Wijk S, et al. Eur J Heart Fail. 2015;17(10):1006-1014. doi:10.1002/ejhf.414.
    8. Bozkurt B, et al. J Card Fail. 2023;29(10):1412-1451. doi:10.1016/j.cardfail.2023.07.006.
    9. Méndez AB, et al. Clin Kidney J. 2022;15(10):1807-1815. doi:10.1093/ckj/sfac133.
    10. Palazzuoli A, et al. Prog Cardiovasc Dis. 2021;67:89-97 doi:10.1016/j.pcad.2021.03.007.
    11. Desai N, et al. Heart Fail Rev. 2024;29(3):631-662. doi:10.1007/s10741-024-10385-y.
    12. Fotos NV, et al. Scand J Caring Sci. 2013;27(3):686-694. doi:10.1111/j.1471-6712.2012.01078.x.
    13. Shah KS, et al. JACC. 2017;70(20):2476-2486. doi:10.1016/j.jacc.2017.08.074.
    14. Sweeney M, et al. EMBO Mol Med. 2020;12(10):e10865. doi:10.15252/emmm.201910865.
    15. Paulus WJ, et al. JACC. 2013;62(4):263-271. doi:10.1016/j.jacc.2013.02.092.
    16. van de Wouw J, et al. Front Physiol. 2019:10:1108. doi:10.3389/fphys.2019.01108. 
    17. Ferreira NS, et al. Am J Hypertens. 2021;34(1):15-27. doi:10.1093/ajh/hpaa137.
    18. Devadoss R, et al. J Cardiovasc Dev Dis. 2024;11(1):15. doi:10.3390/jcdd11010015.
    19. Varnado S, et al. Methodist Debakey Cardiovasc J. 2022;18(5):17-26. doi:10.14797/mdcvj.1162.