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Prevention of stroke in rheumatoid arthritis
Namrata Dhillon1, Kimberly Liang
1Division of Rheumatology and Clinical Immunology, University of Pittsburgh Medical Center, 3500 Terrace St. BST South, S723, Pittsburgh, PA, 15261, USA, dhillonn@upmc.edu.
Insights
Systemic inflammation in rheumatoid arthritis (RA) significantly increases cardiovascular disease (CVD) risk. Early, aggressive inflammation control and risk factor management are crucial for preventing stroke and CVD in RA patients.
Area of Science:
- Rheumatology
- Cardiology
- Public Health
Background:
- Systemic inflammation in rheumatoid arthritis (RA) is a primary driver of increased cardiovascular disease (CVD) risk, including stroke.
- RA itself may act as an independent risk factor for cerebrovascular accident (CVA).
- Traditional cardiovascular risk factors are compounded by RA-specific inflammatory processes.
Purpose of the Study:
- To outline prevention strategies for cerebrovascular disease in RA patients.
- To emphasize the importance of assessing and managing CVD risk in RA.
- To guide the use of RA-specific therapies in the context of cardiovascular risk.
Main Methods:
- Utilizing modified risk score calculators for CVD risk assessment in RA patients.
- Careful monitoring and control of systemic inflammation.
- Evaluating the benefits and risks of RA-directed therapies, including DMARDs and TNF-alpha inhibitors.
- Addressing modifiable risk factors as per general population guidelines.
Main Results:
- Early and aggressive inflammation control is vital, especially for RA patients with seropositivity, high inflammatory markers, long disease duration, or extra-articular manifestations.
- Disease-modifying antirheumatic drugs (DMARDs), particularly methotrexate, and TNF-alpha inhibitors show potential in mitigating CVD risk.
- Glucocorticoid therapy should aim for the minimal effective dose.
- Active RA may be considered a risk equivalent to diabetes mellitus for CVD risk stratification.
Conclusions:
- Integrated management of RA inflammation and cardiovascular risk is essential for preventing CVD and stroke.
- Timely and targeted therapeutic interventions, including DMARDs and anti-TNF agents, are key.
- Further research is needed on lipid management and primary aspirin use in RA.
Opinion Statement:
Recognizing that systemic inflammation is a major contributor to the increased risk of cardiovascular disease (CVD), including stroke, in rheumatoid arthritis (RA) serves as the basis for prevention strategies for cerebrovascular disease in RA. In addition to traditional cardiovascular risk factors, recognize that RA may be an independent risk factor for cerebrovascular accident (CVA). The risk of CVD should be assessed in each patient with RA, utilizing modified risk score calculators. Careful monitoring and control of systemic inflammation should be undertaken in conjunction with assessing each patient's CVD risk, acknowledging the benefits and risks of specific RA-directed therapies. Emphasis should be given to early and aggressive control of inflammation in RA patients, particularly those with seropositivity, increased inflammatory markers, long disease duration (>10 years), and/or extra-articular manifestations. In RA patients requiring glucocorticoid therapy, attempts should be made to use or wean to the minimal effective dose (preferably less than 7.5 mg/day). It should be recognized that both disease-modifying antirheumatic drugs (DMARDs), particularly methotrexate, and tumor necrosis factor (TNF)-alpha inhibitors partially mitigate the risk of CVD. In patients with inadequate control of inflammation with DMARDs, consideration should be given to switch to anti-TNF agents earlier in the disease process. Modifiable risk factors should be addressed as per guidelines for the general population. Active RA may be considered as a risk equivalent to diabetes mellitus when applying these guidelines. With regard to lipid management and use of statin therapy, further studies are required given the apparent "lipid paradox" in RA. Use of aspirin for primary prevention in RA has not been well studied; however, when aspirin is used for secondary prevention, one should recognize that concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) may decrease the antiplatelet effect. Given the cardiovascular risk associated with NSAIDs, the lowest possible dose for the shortest time should be used.
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