Vehicle Control as a Measure of Real-World Driving Performance in Patients With Rheumatoid Arthritis.

OBJECTIVE: To quantify vehicle control as a metric of automobile driving performance in patients with rheumatoid arthritis (RA). METHODS: Naturalistic driving assessments were completed in patients with active RA and controls without disease. Data were collected using in-car, sensor-based instrumentation installed in the participants' own vehicles to observe typical driving habits. RA disease status, disease activity, and functional status were associated with vehicle control (lateral [steering] and longitudinal [braking/accelerating] acceleration variability) using mixed-effect linear regression models stratified by road type (defined by roadway speed limit). RESULTS: Across 1,292 driving hours, RA drivers (n = 33) demonstrated differences in vehicle control compared to controls (n = 23), with evidence of significant statistical interaction between disease status and road type (P < 0.001). On residential roads, participants with RA demonstrated overall lower braking/accelerating variability than controls (P ≤ 0.004) and, when disease activity was low, lower steering variability (P = 0.03). On interstates/highways, RA was associated with increased steering variability among those with moderate/high Clinical Disease Activity Index scores (P = 0.04). In models limited to RA, increases in disease activity and physical disability over 12 weeks of observation were associated with a significant increase in braking/accelerating variability on interstate/highways (both P < 0.05). CONCLUSION: Using novel naturalistic assessments, we linked RA and worsening RA disease severity with aberrant vehicle control. These findings support the need for further research to map these observed patterns in vehicle control to metrics of driver risk and, in turn, to link patterns of real-world driving behavior to diagnosis and disease activity.

Rheumatoid arthritis and cardiovascular disease: the role of systemic inflammation and evolving strategies of prevention.

PURPOSE OF REVIEW: The incidence and mortality of cardiovascular disease are increased in the context of rheumatoid arthritis. The purpose of this review is to examine our evolving understanding of the pathogenesis of cardiovascular disease in rheumatoid arthritis and to underscore the importance of tailored prevention of cardiovascular disease in this select population. RECENT FINDINGS: Recent reports have highlighted the shared pathobiology of cardiovascular disease and rheumatoid arthritis, both of which represent inflammatory disorders. Several reports have also provided much-needed insight into the deleterious impact that select therapies (including cyclo-oxygenase-2-specific inhibitors) may have in terms of the risk of cardiovascular disease in rheumatoid arthritis. Although further study is warranted, preliminary investigations also suggest that aggressive anti-inflammatory therapy, including the adjunctive use of statins, may play important cardioprotective roles in rheumatoid arthritis. SUMMARY: The pathogenesis of cardiovascular disease in rheumatoid arthritis is complex and involves several intermediate factors, including dyslipidemia, elevations in serum homocysteine, impaired insulin sensitivity, and endothelial dysfunction. Given the burden of cardiovascular disease in this population, it is important that health care providers caring for rheumatoid arthritis patients adopt a treatment course that is both comprehensive and individualized to address specific risk factors for cardiovascular disease.

Disseminated giant cell arteritis with inflammatory arthritis and C-ANCA.

Giant cell arteritis (GCA) is well known for its involvement of the proximal aorta and its branches, classically causing headache, visual impairment, and elevations in the erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). We describe a case of biopsy-proven GCA initially presenting with limb claudication, oligoarticular inflammatory arthritis, and a positive antineutrophil cytoplasmic antibody with cytoplasmic staining (C-ANCA), treated successfully with a combination of prednisone and weekly methotrexate. This case illustrates the wide spectrum of features that can be seen with GCA, including the occasional presence of C-ANCA. The C-ANCA became negative after treatment.