Objective

Patients and physicians commonly differ in their assessments of rheumatoid arthritis (RA) activity. Clinically meaningful discordance thresholds or validation of their ability to predict functional outcomes are lacking. We explored whether an unbiased, person-centred latent profile analysis (LPA) approach could classify cases based on patient global assessment (PtGA) and physician global assessment (MDGA) assessments of RA activity. We further examined whether the LPA groups displayed greater differences in clinical outcomes compared with traditional threshold-based groups. Finally, we evaluated whether LPA yielded higher explanatory power for clinical outcomes.

Methods

LPA was performed in 618 patients with established RA from a single centre. A threshold-based discordance definition was used as a comparator, with patients classified into concordant (PtGA-MDGA within ± 3 cm), positively discordant (PtGA-MDGA ≥3 cm) and negatively discordant groups (PtGA-MDGA ≤-3 cm).

Results

LPA yielded five distinct groups: low PtGA/low MDGA (35.9%), moderate PtGA/moderate MDGA (18.6%), high PtGA/high MDGA (14.7%), high PtGA/low MDGA (23.3%) and low PtGA/high MDGA (7.4%). Groups differed across clinical, physical function, pain, fatigue, health-related quality of life, work productivity and activity impairment outcomes (p<0.001). Concordance groups, in particular, displayed marked heterogeneity in outcomes depending on the magnitude of disease activity reported, with the low/low group faring the best (p<0.001). The LPA solution demonstrated superior explanatory power for all outcomes (p<0.001).

Conclusions

We confirmed the validity and advantages of LPA in characterising the relationship between PtGA and MDGA over a conventional threshold-based definition. LPA yielded optimally distinct, clinically meaningful and cohesive groupings, demonstrating superior explanatory power for disease-related outcomes of interest.

Objective

To explore incidence and progression of coronary atherosclerosis and identify determinants in patients with rheumatoid arthritis (RA). We specifically evaluated the impact of inflammation, cardiac risk factors, duration of medication exposure, and their interactions on coronary plaque progression.

Methods

One hundred one participants with baseline coronary computed tomography angiography findings underwent follow-up assessment a mean ± SD of 83 ± 3.6 months after baseline. Plaque burden was reported as the segment involvement score (describing the number of coronary segments with plaque) and the segment stenosis score (characterizing the cumulative plaque stenosis over all evaluable segments). Plaque composition was classified as noncalcified, mixed, or calcified. Coronary artery calcium (CAC) was quantified using the Agatston method.

Results

Total plaque increased in 48% of patients, and progression was predicted by older age, higher cumulative inflammation, and total prednisone dose (P < 0.05). CAC progressors were older, more obese, hypertensive, and had higher cumulative inflammation compared to nonprogressors (P < 0.05). Longer exposure to biologics was associated with lower likelihood of noncalcified plaque progression, lesion remodeling, and constrained CAC change in patients without baseline calcification, independent of inflammation, prednisone dose, or statin exposure (all P < 0.05). Longer statin treatment further restricted noncalcified plaque progression and attenuated the effect of inflammation on increased plaque and CAC (P < 0.05). Stringent systolic blood pressure (BP) control further weakened the effect of inflammation on total plaque progression.

Conclusion

Inflammation was a consistent and independent predictor of coronary atherosclerosis progression in RA. It should therefore be specifically targeted toward mitigating cardiovascular risk. Biologic disease-modifying antirheumatic drugs, statins, and BP control may further constrain plaque progression directly or indirectly.

Objective

To evaluate whether biologic disease-modifying antirheumatic drugs (DMARDs) decrease cardiovascular disease (CVD) risk in rheumatoid arthritis (RA) and whether biologic DMARDs might have a beneficial effect on coronary plaque formation or progression.

Methods

In this single-center observational cohort study, 150 patients underwent computed tomographic angiography for evaluation of coronary atherosclerosis (total, noncalcified, mixed/calcified, and low-attenuation plaque); 101 had repeat assessments within a mean ± SD of 6.9 ± 0.3 years to evaluate plaque progression. All CVD events were prospectively recorded, including cardiac death, myocardial infarction, unstable angina, revascularization, stroke, claudication, and hospitalization for heart failure. The Framingham-D'Agostino score was used to assess cardiovascular risk. The segment stenosis score was used to measure plaque burden. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated.

Results

After adjustment for the segment stenosis score, the Framingham-D'Agostino score, and time-varying Disease Activity Score in 28 joints using the C-reactive protein level using marginal structural models, current biologic DMARD use was associated with lower long-term CVD risk (OR 0.15 [95% CI 0.04-0.60]). Noncalcified and low-attenuation plaque presence moderated the effect of biologic DMARDs on CVD risk; specifically, biologic DMARD use was associated with lower CVD risk in patients with noncalcified or low-attenuation plaque at baseline (OR 0.21 [95% CI 0.04-0.99] and OR 0.08 [95% CI 0.01-0.70], respectively), but not in those without noncalcified or low-attenuation plaque. Per-segment plaque progression analyses showed that biologic DMARD exposure was associated with transition of noncalcified to mixed/calcified plaque (OR 4.00 [95% CI 1.05-15.32]). Biologic DMARD exposure predicted a lower likelihood of new plaque forming in segments without plaque among patients without mixed/calcified plaque in other coronary segments (OR 0.40 [95% CI 0.17-0.93]), but not among those with calcification. Biologic DMARD treatment also predicted low-attenuation plaque loss (P = 0.042).

Conclusion

Our findings indicate that in RA, biologic DMARD use is associated with reduced CVD risk, protective calcification of noncalcified lesions, and lower likelihood of new plaque formation in patients with early atherosclerosis.

Objective

This study was designed to evaluate the determinants of patient and physician global assessments (PtGA and MDGA, respectively) of disease activity, their discordance and change over 2 years in Hispanics with rheumatoid arthritis (RA). We further examined the impact of discordance and its persistence on health-related quality of life (HRQOL) and work productivity on final visit.

Methods

We studied 536 Hispanics with established RA from a single centre. PtGA and MDGA were measured annually on 10 cm visual analogue scales and discordance was defined as absolute difference between them ≥3 cm. Associations between predictors and outcomes of interest were evaluated using multivariable regression and analysis of covariance for cross-sectional and longitudinal data, respectively.

Results

Independent predictors of baseline PtGA were pain, fatigue, depression, general health perceptions and tender joint count. MDGA was predicted by swollen joint count, tender joint count, erythrocyte sedimentation rate, fatigue and depression. Both PtGA and MDGA improved over time (all p<0.001). Discordance was observed in 43% at baseline, with fair stability over 2 years. Higher (worse) patient ratings were most prevalent; their presence at any time and increasing persistence predicted lower physical and mental HRQOL, decreased work productivity and more activity impairment at 2-year follow-up (all p<0.001).

Conclusions

Determinants of PtGA, MDGA and changes over 2 years were disparate in Hispanics with RA yielding significant discordance. Higher patient ratings at any time contributed to worse HRQOL, work productivity and activity impairment on final visit.

Objective

To examine a model addressing the roles of rheumatoid arthritis (RA) disease burden, mood disturbance, and disability as determinants of impairments in role functioning.

Methods

In a cross-sectional design, 103 RA patients recruited from the community to participate in a clinical trial completed assessments of self-assessed disease burden (total joint pain and disease activity), mood disturbance (Center for Epidemiological Studies Depression Scale depressed mood, somatic symptoms, lack of positive affect, and interpersonal problems), disability (Health Assessment Questionnaire disability index gross and fine motor), and role functioning (Short Form 36 health survey physical and social). Structural equation modeling (SEM) was used to examine direct and indirect mechanisms linking disease burden to role functioning.

Results

SEM results indicated that the model had excellent fit: S-Bχ(2)(30) = 38.59, P = 0.135; comparative fit index = 0.977, standardized root mean residual = 0.062, and root mean square error of approximation = 0.053. Mediational analyses demonstrated that, while disease burden was associated with poor role functioning, its effects were jointly mediated by mood disturbance and disability. After the effects of mood disturbance and disability were taken into account, the effect of disease burden on role functioning was not significant.

Conclusion

The results indicate that mood disturbance and disability may serve as important pathways through which RA disease burden affects role functioning. Future longitudinal research is suggested to replicate these findings and further explore the mediational mechanisms examined in this study.