# Heart failure in autoimmune rheumatic diseases

**Authors:** Yuliya Fedorchenko, Olena Zimba, Mykhailo Fedorchenko, Bekzhan A. Permenov, Burhan Fatih Kocyigit

PMC · DOI: 10.1007/s00296-026-06101-8 · 2026-03-26

## TL;DR

Heart failure is a growing problem in autoimmune rheumatic diseases, often appearing at younger ages and linked to inflammation and immune-related heart damage.

## Contribution

The paper highlights the unique mechanisms and risk factors for heart failure in various autoimmune rheumatic diseases.

## Key findings

- Heart failure risk is significantly increased in rheumatic diseases like rheumatoid arthritis and lupus.
- Subclinical heart involvement is common and often precedes overt heart failure.
- Early detection tools like echocardiography and biomarkers help identify at-risk patients.

## Abstract

Heart failure (HF) is an increasingly important cause of morbidity and mortality in patients with autoimmune rheumatic diseases. Despite advances in cardiovascular prevention and treatment, HF incidence continues to rise in this population, driven by chronic systemic inflammation, immune-mediated myocardial injury, microvascular dysfunction, fibrosis, and treatment-related cardiotoxicity. Epidemiological studies consistently demonstrate a markedly increased HF risk across a broad spectrum of rheumatic diseases—including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, idiopathic inflammatory myopathies, ankylosing spondylitis, and primary Sjögren syndrome—often manifesting at younger age and independently of traditional cardiovascular risk factors. Subclinical myocardial involvement is frequent and commonly precedes overt HF, with preserved ejection fraction representing the dominant phenotype, particularly in inflammatory arthritis and systemic sclerosis. Advances in speckle-tracking echocardiography, cardiac magnetic resonance, and circulating biomarkers such as natriuretic peptides and cardiac troponins have enabled earlier detection and refined risk stratification. Although anti-inflammatory therapies, including conventional and biologic disease-modifying antirheumatic drugs, may mitigate HF risk, optimal control of traditional cardiovascular risk factors and cautious use of cardiotoxic agents remain essential.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252), rheumatoid arthritis (MONDO:0008383), systemic lupus erythematosus (MONDO:0007915), systemic sclerosis (MONDO:0005100), idiopathic inflammatory myopathies (MONDO:0020122), ankylosing spondylitis (MONDO:0005306)

## Full-text entities

- **Genes:** NEDD8 (NEDD8 ubiquitin like modifier) [NCBI Gene 4738] {aka NEDD-8}, UBC (ubiquitin C) [NCBI Gene 7316] {aka HMG20}, HSP90AB1 (heat shock protein 90 alpha family class B member 1) [NCBI Gene 3326] {aka D6S182, HSP84, HSP90B, HSPC2, HSPCB}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, UBB (ubiquitin B) [NCBI Gene 7314] {aka HEL-S-50}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, RPLP0 (ribosomal protein lateral stalk subunit P0) [NCBI Gene 6175] {aka L10E, LP0, P0, PRLP0, RPP0, uL10}
- **Diseases:** right ventricular systolic dysfunction (MESH:D018497), autoimmune rheumatic condition (MESH:D012216), arterial hypertension (MESH:D000081029), systolic and diastolic HF (MESH:D054144), fibrosis (MESH:D005355), lupus nephritis (MESH:D008181), DM (MESH:D009223), PSD (MESH:D013180), autoimmunity (MESH:D001327), Lupus (MESH:D008180), Valvular abnormalities (MESH:D006349), Polymyositis (MESH:D017285), ischemic heart disease (MESH:D017202), PM/DM (MESH:D003882), endothelial dysfunction (MESH:D014652), arrhythmias (MESH:D001145), Chronic systemic inflammation (MESH:D007249), Diastolic dysfunction (MESH:D018487), cardiotoxic (MESH:D066126), Congestive HF (MESH:D006333), aortic stenosis (MESH:D001024), pulmonary hypertension (MESH:D006976), hypertension (MESH:D006973), mitral insufficiency (MESH:D008944), systolic (MESH:D000092244), biventricular impairment (MESH:D018754), cardiac affections (MESH:D006331), obesity (MESH:D009765), inflammatory dyslipidemia (MESH:D050171), telangiectasia (MESH:D013684), idiopathic inflammatory myopathies (MESH:D009220), interstitial lung disease (MESH:D017563), myocardial alterations (MESH:D004408), diabetes mellitus (MESH:D003920), microvascular dysfunction (MESH:D017566), gastrointestinal involvement (MESH:D005767), diastolic abnormalities (MESH:D006337), Myocardial perfusion defects (MESH:D009202), RA (MESH:D001172), SSc (MESH:D012595), Cardiovascular complications (MESH:D002318), autoimmune myocarditis (MESH:D009205), myopericarditis (MESH:D010146), PSS (MESH:D012859), ankylosing spondylitis (MESH:D013167), Myocardial involvement (MESH:C564676), aortic insufficiency (MESH:D001022), Dilated cardiomyopathy (MESH:D002311), inflammatory arthritis (MESH:D001168)
- **Chemicals:** natriuretic peptides (MESH:D045265), steroid (MESH:D013256), hydroxychloroquine (MESH:D006886), TNF-alpha inhibitors (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13018076/full.md

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Source: https://tomesphere.com/paper/PMC13018076