Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose
Patients with rheumatoid arthritis (RA) are at increased risk of cardiovascular disease (CVD). Longitudinal studies assessing the effect of changes of RA activity on CVD risk are lacking. We aimed to examine the impact of RA flare, remission, and cumulative burden of RA severity on CVD in RA.
Methods
In a population-based cohort of patients with RA (age≥30 years; 1987 ACR criteria met in 1988-2007) with no history of CVD we performed a retrospective medical records review of each clinical visit to estimate flare/remission status. RA flare was defined as any worsening of RA activity leading to initiation/change/increase of therapy (OMERACT 9). Remission was defined as the absence of disease activity (i.e. tender joint count [TJC]=0 + swollen joint count [SJC]=0 + ESR<10 mm/hr) (OMERACT 7). The previously validated RA medical Records-Based Index of Severity (RARBIS) and Claims-based Index of RA Severity (CIRAS) were used to estimate RA severity. Data on joint surgeries, erosions, extra-articular manifestations, RA flares, morning stiffness, rheumatoid factor (RF), acute phase reactants, antirheumatic drugs were gathered to calculate RARBIS. Claims data were used to calculate the CIRAS based on the number of rheumatology visits, rehabilitation visits; tests for inflammatory markers, RF, platelet counts, chemistry panels. The comparison cohort included age- and sex-matched non-RA subjects without CVD from the same underlying population. Data on CVD risk factors and incident CVD (i.e. myocardial infarction, cardiovascular death, angina, heart failure, stroke, intermittent claudication) were collected. All subjects were followed until death, migration or 07/01/2012. The association of RA activity/severity measures with CVD was examined using Cox models with time-dependent covariates, adjusting for age, sex, calendar year of RA, CVD risk factors and antirheumatic drug use.
Results
The study included 525 RA patients and 524 non-RA subjects (mean age 54.5 yrs; 71% female in both groups). During the mean follow-up of 10.3 years in RA cohort and 8.8 years in the non-RA cohort, 129 RA patients and 77 non-RA subjects developed CVD. There was a significant increase in CVD risk in RA per each acute flare vs remission (hazard ratio [HR] 1.07 per 6-week flare; 95% confidence interval [CI] 1.01-1.15). The CVD risk for RA patients during remission was not significantly different from the non-RA subjects adjusting for age, sex and calendar year (HR 0.90; 95%CI 0.51-1.59). Increased cumulative moving average of daily RARBIS (HR 1.16, 95%CI 1.03-1.30) and CIRAS (HR 1.38, 95%CI 1.12-1.70) was associated with CVD. RA patients who spent more time in medium and high CIRAS tertiles tended to have higher CVD risk vs those in the lower tertile (HR 1.08, 95%CI 0.98-1.20 and HR 1.18, 95%CI 1.06-1.31, respectively, per 1yr increase).
Conclusion
There was a meaningful 7%-increase in CVD risk with the exposure to each acute flare, but not remission, in RA vs general population highlighting the pivotal role of RA flares in shaping CVD risk in RA. Higher long-term burden of RA severity was associated with significantly increased CVD risk in RA suggesting accrued detrimental impact of RA severity over time.
Disclosure:
E. Myasoedova,
Roche Pharmaceuticals,
2;
A. K. Chandran,
Roche Pharmaceuticals,
2;
B. İlhan,
None;
B. T. Major,
Roche Pharmaceuticals,
2;
C. J. Michet III,
None;
E. L. Matteson,
None;
C. S. Crowson,
Roche Pharmaceuticals,
2.
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