Cardiovascular disease in patients with chronic inflammation: mechanisms underlying premature cardiovascular events in rheumatologic conditions
Open accessAbstract
A variety of systemic inflammatory rheumatic diseases associate with an increased risk of atherosclerotic events and premature cardiovascular (CV) disease. Although this recognition has stimulated intense basic science and clinical research, the precise nature of the relationship between local and systemic inflammation, their interactions with traditional CV risk factors, and their role in accelerating atherogenesis remains unresolved. The individual rheumatic diseases have both shared and unique attributes that might impact CV events. Understanding of the positive and negative influences of individual anti-inflammatory therapies remains rudimentary. Clinicians need to adopt an evidence-based approach to develop diagnostic techniques to identify those rheumatologic patients most at risk of CV disease and to develop effective treatment protocols. Development of optimal preventative and disease-modifying approaches for atherosclerosis in these patients will require close collaboration between basic scientists, CV specialists, and rheumatologists. This interface presents a complex, important, and exciting challenge.
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Chronic inflammation triggers endothelial dysfunction and initiates premature atherosclerosis.
“Chronic inflammation triggers endothelial dysfunction and initiates premature atherosclerosis.”
From Risk of cardiovascular outcomes among women with endometriosis in the United Kingdom: a retrospective matched cohort study (2021) · cites this paper as [9]
The Rheumatoid arthritis section (page unavailable) reports endothelial dysfunction in patients with RA and says vascular impairments may predispose to atherosclerosis. The Conclusion’s Figure 1 caption says systemic inflammatory rheumatic disorders predispose to premature, accelerated atherosclerosis. The claim overstates these qualified findings as a definite causal sequence in which chronic inflammation triggers endothelial dysfunction and initiates atherosclerosis. (LLM, conf=0.87)
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- Authors
- Mason, J. C., & Libby, P.
- Affiliations
- Hammersmith Hospital (GB)
- Brigham and Women's Hospital (US)
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-11-27
- Volume
- 36
- Issue
- 8
- Pages
- 482-489
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- PMC
- PMC4340364
- OpenAlex
- W2072453475
- Cited by
- 420
- References
- 130
- Citations by year
- 2026: 13 · 2025: 27 · 2024: 53 · 2023: 38 · 2022: 50 · 2021: 29 · 2020: 42 · 2019: 44 · 2018: 40 · 2017: 31 · 2016: 28 · 2015: 22 · 2014: 2 · 2012: 1
- FWCI
- 4.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Heart Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NIHR Biomedical Research Centre, Royal Marsden NHS Foundation Trust/Institute of Cancer Research
- National Institute for Health and Care Research
- British Heart Foundation
- Imperial College London
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL080472, R01HL080472)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Risk Factors
- Keywords
- cardiovascular disease, chronic inflammation, atherosclerosis, atherogenesis, cardiovascular risk factors, anti-inflammatory therapy, cardiovascular risk prediction, cardiovascular disease prevention
- MeSH terms
- Anti-Inflammatory Agents, Non-Steroidal, Arthritis, Rheumatoid, Biological Factors, Coronary Artery Disease, Gout, Humans, Immunosuppressive Agents, Lupus Erythematosus, Systemic, Rheumatic Diseases, Risk Factors, Vasculitis, Biomarkers, Antirheumatic Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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