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Review
. 2022 Oct;19(5):267-278.
doi: 10.1007/s11897-022-00560-3. Epub 2022 Jul 15.

Heart Failure in Chronic Infectious and Inflammatory Conditions: Mechanistic Insights from Clinical Heterogeneity

Nour Beydoun  1 , Matthew J Feinstein  2   3   4   5
Affiliations
Review

Heart Failure in Chronic Infectious and Inflammatory Conditions: Mechanistic Insights from Clinical Heterogeneity

Nour Beydoun et al. Curr Heart Fail Rep. 2022 Oct.

Abstract

Purpose of review: The balance between inflammation and its resolution plays an important and increasingly appreciated role in heart failure (HF) pathogenesis. In humans, different chronic inflammatory conditions and immune-inflammatory responses to infection can lead to diverse HF manifestations. Reviewing the phenotypic and mechanistic diversity of these HF presentations offers useful clinical and scientific insights.

Recent findings: HF risk is increased in patients with chronic inflammatory and autoimmune disorders and relates to disease severity. Inflammatory condition-specific HF manifestations exist and underlying pathophysiologic causes may differ across conditions. Although inflammatory disease-specific presentations of HF differ, chronic excess in inflammation and auto-inflammation relative to resolution of this inflammation is a common underlying contributor to HF. Further studies are needed to phenotypically refine inflammatory condition-specific HF pathophysiologies and prognoses, as well as potential targets for intervention.

Keywords: Chronic inflammatory and autoimmune disorders; Heart failure pathogenesis; Inflammation resolution; Persistent inflammation; Trained immunity.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Diversity of heart failure immunopathogenesis: infection, auto-inflammation, and impaired injury responses
See this image and copyright information in PMC

References

    1. Shah SJ, Katz DH, Selvaraj S, et al. Phenomapping for novel classification of heart failure with preserved ejection fraction. Circulation. 2015;131(3):269–279. doi: 10.1161/circulationaha.114.010637. - DOI - PMC - PubMed
    1. Ahmad T, Pencina MJ, Schulte PJ, et al. Clinical implications of chronic heart failure phenotypes defined by cluster analysis. J Am Coll Cardiol. 2014;64(17):1765–1774. doi: 10.1016/j.jacc.2014.07.979. - DOI - PMC - PubMed
    1. Dick SA, Epelman S. Chronic heart failure and inflammation: what do we really know? Circ Res. 2016;119(1):159–176. doi: 10.1161/CIRCRESAHA.116.308030. - DOI - PubMed
    1. Van Linthout S, Tschöpe C. Inflammation - cause or consequence of heart failure or both? Curr Heart Fail Rep. 2017;14(4):251–265. doi: 10.1007/s11897-017-0337-9. - DOI - PMC - PubMed
    1. •• Adamo L, Rocha-Resende C, Prabhu SD, Mann DL. Reappraising the role of inflammation in heart failure. Nat Rev Cardiol. 2020;17(5):269–285. 10.1038/s41569-019-0315-xIn-depth review on the role of the immune system and inflammation in heart failure, with a focus on immune cell subsets. Emerging therapies to target inflammation in heart failure are also discussed. - PubMed

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