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  • Review Article
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Current understanding and management of cardiovascular involvement in rheumatic immune-mediated inflammatory diseases

Nature Reviews Rheumatology volume 20, pages 614–634 (2024)Cite this article

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Abstract

Immune-mediated inflammatory diseases (IMIDs) are a spectrum of disorders of overlapping immunopathogenesis, with a prevalence of up to 10% in Western populations and increasing incidence in developing countries. Although targeted treatments have revolutionized the management of rheumatic IMIDs, cardiovascular involvement confers an increased risk of mortality and remains clinically under-recognized. Cardiovascular pathology is diverse across rheumatic IMIDs, ranging from premature atherosclerotic cardiovascular disease (ASCVD) to inflammatory cardiomyopathy, which comprises myocardial microvascular dysfunction, vasculitis, myocarditis and pericarditis, and heart failure. Epidemiological and clinical data imply that rheumatic IMIDs and associated cardiovascular disease share common inflammatory mechanisms. This concept is strengthened by emergent trials that indicate improved cardiovascular outcomes with immune modulators in the general population with ASCVD. However, not all disease-modifying therapies that reduce inflammation in IMIDs such as rheumatoid arthritis demonstrate equally beneficial cardiovascular effects, and the evidence base for treatment of inflammatory cardiomyopathy in patients with rheumatic IMIDs is lacking. Specific diagnostic protocols for the early detection and monitoring of cardiovascular involvement in patients with IMIDs are emerging but are in need of ongoing development. This Review summarizes current concepts on the potentially targetable inflammatory mechanisms of cardiovascular pathology in rheumatic IMIDs and discusses how these concepts can be considered for the diagnosis and management of cardiovascular involvement across rheumatic IMIDs, with an emphasis on the potential of cardiovascular imaging for risk stratification, early detection and prognostication.

Key points

  • Cardiovascular manifestations of rheumatic immune-mediated inflammatory diseases (IMIDs) can be varied and include accelerated atherosclerotic cardiovascular disease and inflammatory cardiomyopathy. Cardio-rheumatology is an expanding subspecialist field underpinned by advancing our understanding of inflammation and cardiovascular pathology to improve the detection and treatment of cardiovascular involvement of rheumatic IMIDs and to enable knowledge transfer to support a targeted approach to cardiovascular disease in the general population.

  • Studies across rheumatic IMIDs and cardiovascular diseases in the general population have identified IL-6 as a key shared cytokine, with the upstream cytokines IL-1α and IL-1β also being involved in central pathogenic pathways. Contrasting observations on the results of targeting cytokines such as TNF, IL-12 and IL-23p40 and Janus kinases emphasize the need for continued study to elucidate mechanisms and local organ effects.

  • The sensitive imaging modalities CT, MRI and PET–CT have emerged as highly effective tools in the detection of involvement and monitoring of response in large-vessel vasculitis, with increasing use of MRI in inflammatory cardiomyopathy, but their application needs further development in other diseases.

  • Guideline-directed medical therapy of cardiovascular involvement in rheumatic IMIDs is important, alongside effective immunosuppressant treatment of the rheumatic IMIDs.

  • Translating inflammation biology of cardio-rheumatology into precision medicine strategies to address cardiovascular involvement in rheumatic IMIDs among wider organ manifestations is complex. Well-designed trials are needed to deliver tailored management.

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Fig. 1: Complex inter-relationship between rheumatic immune-mediated inflammatory disease, cardiovascular disease and associated treatment effects.
Fig. 2: Shared inflammatory mechanisms in rheumatic immune-mediated inflammatory disease and cardiovascular disease.
Fig. 3: Monitoring and management of atherosclerosis and inflammatory cardiomyopathy in patients with rheumatic immune-mediated inflammatory disease.
Fig. 4: Targeting cardiovascular involvement as part of heterogeneous organ manifestations in rheumatic immune-mediated inflammatory diseases.
Fig. 5: Theoretical model of precision medicine treatment to address cardiovascular risk and involvement in patients with rheumatic immune-mediated inflammatory diseases.

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Acknowledgements

All authors are recipients of the Medical Research Council (MRC)–British Heart Foundation (BHF) co-funded ‘CARDIO-IMID UK Network’ partnership grant (MR/X009955/1). They acknowledge the National Institute for Health Research (NIHR)–BHF Cardiovascular Partnership for its support in establishing a ‘CARDIO-IMID’ platform. M.H.B. is a NIHR Senior Investigator. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. M.R.D. is supported by the BHF (FS/SCRF/21/32010) and is the recipient of the Sir Jules Thorn Award for Biomedical Research 2015 (15/JTA). J.M.T. is supported by the Wellcome Trust (211100/Z/18/Z) and the Cambridge BHF Centre for Research Excellence (18/1/34212). D.P.O’R. is supported by the MRC (MC_UP_1605/13) and BHF (RG/19/6/34387, RE/18/4/34215). S.P. is funded by a BHF Chair Award CH/16/2/32089. The authors thank Mamta H. Buch for reviewing the manuscript and input into the development of the figures.

Author information

Authors and Affiliations

  1. Centre for Musculoskeletal Research, Division of Musculoskeletal & Dermatological Sciences, Faculty of Biology, Medicine & Health, University of Manchester, Manchester, UK

    Maya H. Buch

  2. NIHR Manchester Biomedical Research Centre, Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK

    Maya H. Buch

  3. Section of Cardiorespiratory Medicine, Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK

    Ziad Mallat & Jason M. Tarkin

  4. Centre for Cardiovascular Science, Chancellors Building, Little France Crescent, University of Edinburgh, Edinburgh, UK

    Marc R. Dweck

  5. MRC Laboratory of Medical Sciences, Imperial College London, London, UK

    Declan P. O’Regan

  6. Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK

    Vanessa Ferreira

  7. National Heart & Lung Institute, Imperial College London, London, UK

    Taryn Youngstein

  8. Department of Rheumatology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK

    Taryn Youngstein

  9. Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK

    Sven Plein

  10. School of Biomedical Engineering and Imaging Sciences, Kings College London, London, UK

    Sven Plein

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  1. Maya H. Buch
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  2. Ziad Mallat
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  5. Declan P. O’Regan
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  6. Vanessa Ferreira
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Contributions

M.H.B., M.R.D., J.M.T., Z.M. and S.P. researched data for the article, discussed the content, wrote, reviewed and edited the manuscript. T.Y. discussed the content, contributed to the writing, reviewed and edited the manuscript. D.P.O’R. and V.F. reviewed and edited the manuscript.

Corresponding author

Correspondence to Maya H. Buch.

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Competing interests

M.H.B. has received grant/research support paid to the University of Manchester from Gilead and has acted as an adviser or speaker with funds paid to the University of Manchester for AbbVie, Alfasigma, Boehringer Ingelheim, Galapagos, Gilead Sciences and Pfizer, Inc. M.R.D. has received speaker fees from Pfizer, Radcliffe Cardiology, Bristol Myers Squibb, Edwards and Novartis, and has received consultancy fees from Novartis, Jupiter Bioventures, Beren and Silence Therapeutics.

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Nature Reviews Rheumatology thanks Elena Bartoloni and the other, anonymous, reviewers for their contribution to the peer review of this work.

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Related links

IMID-Bio-UK: https://www.gla.ac.uk/research/az/imid/

Glossary

Cholesterol efflux pathway

The first step of reverse cholesterol transport, which is the removal of cholesterol from macrophage foam cells in the arterial wall by HDL, transport in plasma, uptake by the liver and ultimate secretion in bile.

Coronary artery disease

(CAD). Also known as ischaemic heart disease, in which coronary artery atherosclerosis leads to narrowing or occlusion of one or more of the coronary arteries. CAD can lead to angina pectoris or myocardial infarction.

Heart failure with preserved ejection fraction

(HFpEF). Heart failure with high left ventricular (LV) filling pressure despite normal or near-normal LV ejection fraction ≥50%.

Heart failure with reduced ejection fraction

(HFrEF). Systolic heart failure defined as left ventricular ejection fraction ≤40%.

Late gadolinium enhancement

(LGE). A cardiovascular MRI method in which images are acquired 10 min after the administration of gadolinium-based contrast agents, which identify focal myocardial fibrosis, scar and infarction.

Major adverse cardiovascular events

(MACE). Classical 3-point MACE is defined as a composite of nonfatal stroke, nonfatal myocardial infarction and cardiovascular death.

Myocarditis

Inflammation of the myocardium.

Pericarditis

Inflammation of the pericardium.

ST-elevation myocardial infarction

(STEMI). Acute STEMI occurs owing to occlusion of one or more coronary arteries, which results in myocardial injury and necrosis in the distribution of the infarct-related coronary artery.

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Buch, M.H., Mallat, Z., Dweck, M.R. et al. Current understanding and management of cardiovascular involvement in rheumatic immune-mediated inflammatory diseases. Nat Rev Rheumatol 20, 614–634 (2024). https://doi.org/10.1038/s41584-024-01149-x

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