Objective. To examine trends in the incidence and prevalence of rheumatoid arthritis (RA) from 1995 to 2007.Methods. To augment our preexisting inception cohort of patients with RA (1955-1994), we assembled a population-based incidence cohort of individuals >18 years of age who first fulfilled the American College of Rheumatology 1987 criteria for the classification of RA between January 1, 1995 and December 31, 2007 and a cohort of patients with prevalent RA on January 1, 2005. Incidence and prevalence rates were estimated and were age-and sex-adjusted to the white population in the US in 2000. Trends in incidence rates were examined using Poisson regression methods.Results. The 1995-2007 incidence cohort comprised 466 patients (mean age 55.6 years), 69% of whom were female and 66% of whom were rheumatoid factor positive. The overall age-and sex-adjusted annual RA incidence was 40.9/100,000 population. The ageadjusted incidence in women was 53.1/100,000 population (versus 27.7/100,000 population in men). During the period of time from 1995 to 2007, the incidence of RA increased moderately in women (P ‫؍‬ 0.02) but not in men (P ‫؍‬ 0.74). The increase was similar among all age groups. The overall age-and sex-adjusted prevalence on

Objectives-To examine the impact of systemic inflammation and serum lipids on cardiovascular disease (CVD) in rheumatoid arthritis (RA).Methods-In a population-based RA incident cohort (1987 ACR criteria first met between 1988 and 2007), we collected serum lipid measures, erythrocyte sedimentation rates (ESR), C-reactive protein (CRP) measures and cardiovascular events including ischemic heart disease, and heart failure. Cox models were used to examine the association of lipids and inflammation with the risk of CVD and mortality adjusting for age, sex and year of RA incidence.Results-The study included 651 RA patients (mean age 55.8 years, 69% female); 67% were rheumatoid factor positive. ESR was associated with the risk of CVD (hazard ratio [HR] 1.2 per 10 mm/hr increase, 95% confidence interval [CI] 1.1, 1.3). Similar findings, although not statistically significant, were seen with CRP (p=0.07). We found a significant nonlinear association for total cholesterol (TCh) on risk of CVD, with 3.3-fold increased risk for TCh<4 mmol/L (95%CI 1.5, 7.2) and no increased risk of CVD for TCh≥4 mmol/L (p=0.57). Low lowdensity cholesterol (LDL<2 mmol/L) was associated with marginally increased risk of CVD (p=0.10); there was no increased risk for LDL≥2 mmol/L (p=0.76).Conclusion-Inflammatory measures (particularly, ESR) are significantly associated with the risk of CVD in RA. Lipids may have paradoxical associations with the risk of CVD in RA, whereby lower TCh and LDL levels are associated with increased cardiovascular risk.

Objective. Understanding of the personal risks for rheumatoid arthritis (RA) and other rheumatic diseases remains poor, despite advances in knowledge with regard to their pathogenesis, therapeutics, and clinical impact, in part because the personal lifetime risk of developing these diseases is unknown. This study was undertaken to estimate the lifetime risk of RA, as well as other inflammatory autoimmune rheumatic diseases, including systemic lupus erythematosus, psoriatic arthritis, polymyalgia rheumatica (PMR), giant cell arteritis, ankylosing spondylitis, and Sjögren's syndrome, and to provide an overall estimate of the risk of developing inflammatory autoimmune rheumatic disease over a lifetime.Methods. Using the incidence rates obtained from our population-based studies of rheumatic diseases among residents of Olmsted County, Minnesota, and mortality rates from life tables for the general population, we estimated the sex-specific lifetime risk of rheumatic disease.Results. The lifetime risk of RA developing in US adults was 3.6% for women and 1.7% for men, and the lifetime risk of rheumatoid factor-positive RA was 2.4% for women and 1.1% for men. The second most common inflammatory autoimmune rheumatic disease was PMR, with a lifetime risk of 2.4% for women and 1.7% for men. The overall lifetime risk of inflammatory autoimmune rheumatic disease was 8.4% for women and 5.1% for men.Conclusion. One in 12 women and 1 in 20 men will develop an inflammatory autoimmune rheumatic disease during their lifetime. These results can serve as useful guides in counseling patients regarding their lifetime risk of these conditions and have important implications regarding disease awareness campaigns.

Objective To compare the prevalence of left ventricular (LV) diastolic dysfunction in subjects with and without rheumatoid arthritis (RA), among those with no history of heart failure (HF), and to determine risk factors for diastolic dysfunction in RA. Methods We conducted a cross-sectional, community-based study comparing cohorts of adult RA and non-RA subjects without a history of HF. Standard 2D/Doppler echocardiography was performed in all participants. Diastolic dysfunction was defined as impaired relaxation (with or without increased filling pressures) or advanced reduction in compliance or reversible or fixed restrictive filling. Results The study included 244 RA subjects and 1448 non-RA subjects. Mean age was 60.5 years in the RA cohort (71% female) and 64.9 years (50% female) in the non-RA cohort. The vast majority (>98%) of both cohorts had preserved ejection fraction (EF≥50%). Diastolic dysfunction was more common in RA subjects at 31% compared to 26% (age and sex adjusted) in non-RA subjects (OR 1.6; 95% CI 1.2, 2.4). RA subjects had significantly lower LV mass, higher pulmonary arterial pressure, and higher left atrial volume index than non-RA subjects. RA duration and IL-6 level were independently associated with diastolic dysfunction in RA even after adjustment for cardiovascular risk factors. Conclusion Subjects with RA have a higher prevalence of diastolic dysfunction than those without RA. RA duration and IL-6 are independently associated with diastolic dysfunction suggesting the impact of chronic autoimmune inflammation on myocardial function in RA. Clinical implications of these findings require further investigation.

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ObjectivesTo examine trends in the incidence of rheumatoid arthritis (RA) from 2005 to 2014 overall and by serological status as compared with 1995–2004 and 1985–1994.MethodsWe evaluated RA incidence trends in a population-based inception cohort of individuals aged ≥18 years who first fulfilled the 1987 American College of Rheumatology (ACR) criteria for RA between 1 January 1985 and 31 December 2014. Incidence rates were estimated and were age-adjusted and sex-adjusted to the white population in the USA in 2010. Trends in incidence were examined using Poisson regression methods.ResultsThe 2005–2014 incidence cohort comprised 427 patients: mean age 55.4 years, 68% female, 51% rheumatoid factor (RF) positive and 50% anti-cyclic citrullinated peptide antibody positive. The overall age-adjusted and sex-adjusted annual RA incidence in 2005–2014 was 41/100 000 population (age-adjusted incidence: 53/100 000 in women and 29/100 000 in men). While these estimates were similar to the 1995–2004 decade, there was a decline in the incidence of RF-positive RA in 2005–2014 compared with the previous two decades (p=0.004), with a corresponding increase in RF-negative cases (p<0.001). Smoking rates declined and obesity rates increased from earlier decades to more recent years.ConclusionsSignificant increase in incidence of RF-negative RA and decrease in RF-positive RA in 2005–2014 compared with previous decades was found using 1987 ACR criteria. The incidence of RA overall during this period remained similar to the previous decade. The changing prevalence of environmental factors, such as smoking, obesity and others, may have contributed to these trends. Whether these trends represent a changing serological profile of RA requires further investigation.

Objective To examine the role of rheumatoid arthritis (RA) flare, remission, and RA severity burden in cardiovascular disease (CVD). Methods In a population-based cohort of RA patients without CVD (age ≥30 years; 1987 ACR criteria met in 1988-2007) we performed medical records review at each clinical visit to estimate flare/remission status. The previously validated RA medical Records-Based Index of Severity (RARBIS) and Claims-based Index of RA Severity (CIRAS) were applied. Age- and sex-matched non-RA subjects without CVD comprised the comparison cohort. Cox models were used to assess the association of RA activity/severity with CVD, adjusting for age, sex, calendar year of RA, CVD risk factors, antirheumatic medications. Results Study included 525 RA patients and 524 non-RA subjects. There was a significant increase in CVD risk in RA per time spent in each acute flare vs remission (HR 1.07 per 6-week flare; 95% CI 1.01-1.15). The CVD risk for RA patients in remission was similar to the non-RA subjects (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. CVD risk was higher in RA patients who spent more time in medium (HR 1.08, 95% CI 0.98-1.20) and high CIRAS tertiles (HR 1.18, 95%CI 1.06-1.31) vs lower tertile. Conclusions Our findings show substantial detrimental role of exposure to RA flare and cumulative burden of RA disease severity in CVD risk in RA suggesting important cardiovascular benefits associated with tight inflammation control and improved flare management in RA patients.

Increased mortality in rheumatoid arthritis (RA) is widely recognized but not fully explained. Despite substantial improvements in management and growing knowledge of the determinants of increased mortality, evidence for reduction in mortality in RA has lagged behind. Indeed, most studies report no apparent reduction in mortality in RA. However, emerging evidence from some recent RA inception cohorts suggests no increased mortality, including cardiovascular mortality, but this awaits further confirmation. Although it is possible that recent advances in RA treatment may manifest in improvement of survival in the near future, other factors, including undertreated or unrecognized low-grade inflammation, comorbidities, and immunogenetic factors, may contribute to the excess mortality in RA and impede its improvement. In this review, we summarize the current knowledge of the rates and determinants of mortality in RA, identify and discuss potential explanations for excess mortality, and outline promising research avenues for targeting mortality in RA.