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Published on: May 31, 2016
Vascular calcification in rheumatoid arthritis: prevalence, pathophysiological aspects and potential targets
J Paccou1, M Brazier, R Mentaverri
1Department of Rheumatology, University Hospital of Amiens, FR-80054 Amiens, France. julienpaccou@yahoo.fr
Insights
Rheumatoid arthritis (RA) patients experience accelerated vascular calcification due to specific inflammatory mediators, not just general inflammation. This review explores RA-associated vascular calcification and potential therapeutic targets.
Area of Science:
- Rheumatology
- Cardiovascular Medicine
- Immunology
Background:
- Rheumatoid arthritis (RA) significantly elevates cardiovascular disease (CVD) risk.
- Conventional CVD risk factors do not fully account for excess mortality in RA patients.
- Vascular calcification is a key contributor to CVD in RA.
Purpose of the Study:
- To review current understanding of vascular calcification prevalence in RA.
- To explore the pathophysiological mechanisms driving vascular calcification in RA.
- To identify potential therapeutic targets for mitigating vascular calcification in RA.
Main Methods:
- Literature review of recent studies on vascular calcification in rheumatoid arthritis.
- Analysis of pathophysiological aspects, focusing on specific mediators.
- Discussion of emerging therapeutic strategies.
Main Results:
- RA patients exhibit earlier and more widespread vascular calcification than controls.
- Proinflammatory cytokines, rather than global inflammation, are implicated in RA vascular calcification pathogenesis.
- Specific molecular pathways contributing to calcification are being elucidated.
Conclusions:
- Vascular calcification is a significant, accelerated complication in RA.
- Targeting specific inflammatory pathways may reduce cardiovascular risk in RA patients.
- Further research is needed to develop effective interventions against RA-associated vascular calcification.
Abstract:
Individuals with rheumatoid arthritis (RA) are at increased risk for morbidity and mortality from cardiovascular disease. Excess cardiovascular mortality in RA patients cannot be fully explained by conventional cardiovascular risk factors. The purpose of this review is to discuss recent progress concerning the prevalence and pathophysiological aspects of vascular calcification in RA. RA patients have early-onset diffuse calcification involving multiple vascular beds compared to age and sex-matched controls. Pathogenesis of vascular calcification in RA patients is not fully understood, but specific mediators such as proinflammatory cytokines and not global inflammation could be involved. The possible link between osteoporosis and vascular calcification in RA will not be discussed. Finally, potential targets to reduce vascular calcification in RA will be discussed.
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