Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2024 May 23;13(11):3056.
doi: 10.3390/jcm13113056.

Guideline-Optimised Treatment in Heart Failure-Do Higher Doses Reduce Systemic Inflammation More Significantly?

Affiliations

Guideline-Optimised Treatment in Heart Failure-Do Higher Doses Reduce Systemic Inflammation More Significantly?

Alexandru Mircea Arvunescu et al. J Clin Med. .

Abstract

Background: Chronic inflammation is a constant phenomenon which accompanies the heart failure pathophysiology. In all phenotypes of heart failure, irrespective of the ejection fraction, there is a permanent low-grade activation and synthesis of proinflammatory cytokines. Many classes of anti-remodelling medication used in the treatment of chronic heart failure have been postulated to have an anti-inflammatory effect. Methods: This retrospective study enrolled 220 patients and focused on evaluating the effect of the most used active substances from these classes in reducing the level of inflammatory biomarkers (C reactive protein, erythrocyte sedimentation rate and fibrinogen) after initiation or up-titration. Our research is evaluating if this anti-inflammatory effect intensifies while raising the dose. The evaluation was performed at two visits with an interval between them of 6 months. Results: From the beta-blockers class, carvedilol showed a reduction in erythrocyte sedimentation rate (ESR), in low (6.25 mg, bi daily) and medium (12.5 mg, bi daily) doses. At the same time, sacubitril/valsartan showed a reduction in CRP levels. This effect was obtained only in the medium (49/51 mg, bi daily) and high (97/103 mg, bi daily) doses, with the maximum reduction being observed in the high dose. Conclusions: From the classes of medication evaluated, the study showed a significant reduction in ESR levels in the low and medium doses of carvedilol and a reduction in CRP values in the cases of medium and high doses of ARNI.

Keywords: ACE-I; ARB; ARNI; CRP; ESR; MRA; SGLT2i; beta-blockers; fibrinogen; heart failure; inflammation; left ventricular ejection fraction.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The dynamics of ESR from T0 to T1 in patients who did not receive carvedilol vs. those with 6.25 mg/12.5 mg/25 mg bi daily of carvedilol.
Figure 2
Figure 2
The dynamics of CRP from T0 to T1 in patients who did not receive sacubitril/valsartan versus those with 24/26 mg bi daily, 49/51 mg bi daily or 97/103 mg bi daily of sacubitril/valsartan.

Similar articles

Cited by

References

    1. Paraskevaidis I., Farmakis D., Papingiotis G., Tsougos E. Inflammation and Heart Failure: Searching for the Enemy-Reaching the Entelechy. J. Cardiovasc. Dev. Dis. 2023;10:19. doi: 10.3390/JCDD10010019. - DOI - PMC - PubMed
    1. Adamo L., Rocha-Resende C., Prabhu S.D., Mann D.L. Reappraising the Role of Inflammation in Heart Failure. Nat. Rev. Cardiol. 2020;17:269–285. doi: 10.1038/S41569-019-0315-X. - DOI - PubMed
    1. Zhang Y., Bauersachs J., Langer H.F. Immune Mechanisms in Heart Failure. Eur. J. Heart Fail. 2017;19:1379–1389. doi: 10.1002/EJHF.942. - DOI - PubMed
    1. Reina-Couto M., Pereira-Terra P., Quelhas-Santos J., Silva-Pereira C., Albino-Teixeira A., Sousa T. Inflammation in Human Heart Failure: Major Mediators and Therapeutic Targets. Front. Physiol. 2021;12:746494. doi: 10.3389/FPHYS.2021.746494. - DOI - PMC - PubMed
    1. Aimo A., Castiglione V., Borrelli C., Saccaro L.F., Franzini M., Masi S., Emdin M., Giannoni A. Oxidative Stress and Inflammation in the Evolution of Heart Failure: From Pathophysiology to Therapeutic Strategies. Eur. J. Prev. Cardiol. 2020;27:494–510. doi: 10.1177/2047487319870344. - DOI - PubMed