• 1980: Survival Trends in RA Patients
• 1919: Incidence of Cancer in RA Patients on Anti-TNF Therapy (see RA Treatments)
• 1933: Cause of Fatigue in RA Patients
• 1899: Mortality Rates Following 1st Acute Cardiovascular Event
• 1901: Effect of Carotic Atherosclerosis on the Incidence of Acute Coronary Syndromes in RA

Abstract 1980: Survival Trends in Rheumatoid Arthritis Patients: Is the Mortality Gap Widening?
A Gonzalez, HM Kremers, CS Crowson, KV Ballman, VL Roger, SJ Jacobsen, & SE Gabriel
summarized by Kevin Fontaine, Ph.D.

Purpose: While life expectancy has increased substantially over the past several decades, it is unclear whether RA patients have experienced a similar increase in longevity. This study determined the absolute and relative survival trends in a cohort of RA patients ascertained over a 40-year period.

Methods: A population-based RA incidence cohort (1955-1995) was followed longitudinally until death or January, 2005. Expected mortality rates were estimated using age, sex, and calendar year-specific mortality rates based on the states white population to the person-time experience of the RA cohort. Poisson regression was used to model the observed mortality rates and relative survival after adjusting for age, sex, and disease duration.

Results: This cohort was comprised of 603 RA patients (73% female) with a mean follow-up time of 15 years (with 384 patient deaths). Mortality rate for RA patients over the 40 years of data collection remained constant at 2.1 per 100 person-years. However, the overall expected mortality rate for the general population decreased from 1.7 per 100 person-years in 1965 to 1.1 per 100 person-years in 2000. This indicates a widening mortality gap between RA and general population adults.

Conclusions: RA patients have not enjoyed the same increase in longevity experienced by the general population.

Editorial Comments: The apparent widening mortality gap between RA patients and the general population is of great concern. However, it is important to note that the majority of patients in this cohort were enrolled prior to the recent widespread use of RA disease-modifying agents. As such, it is unknown whether or how these new agents might influence mortality rate. Nonetheless, the results of this analysis underscore the need to better understand the reasons for the increased mortality risk imposed by RA so we can develop treatments to attenuate the RA-associated mortality risks. Cardiovascular disease is thought to be a major contributor to the increased mortality among RA patients and studies are underway to investigate how RA might promote increased risk for cardiovascular disease.

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Abstract 1933: The Cause of Fatigue in Patients with Rheumatoid Arthritis (RA)
H Repping-Wuts, J Fransen, T van Achterberg, G Bleijenberg, & P van Riel
summarized by Kevin Fontaine, Ph.D.

Purpose: To determine whether changes in fatigue among adults with RA occur over one year and to evaluate potential correlates of persistent severe fatigue in RA.

Methods: One hundred and thirty-seven patients reported their fatigue using the Checklist Individual Strength (CIS) at baseline and 1-year later. A score on the CIS of > 35 was used to indicate severe fatigue. RA disease activity was assessed quarterly using a VAS pain scale and the DAS28. Disability was also assessed at baseline and at 1-year using the Health Assessment Questionnaire (HAQ).

Results: The majority (86%) of patients completed all assessments and 69% of the sample was female. Overall, fatigue levels did not change significantly over the course of the study (baseline and 1-year CIS scores correlated at .73). Forty-nine patients (40% of the sample) were classified as severely fatigued at both baseline and at 1-year. Logistic regression models among this sub-sample of severely fatigued patients indicated that mean DAS28, baseline HAQ and age were significant predictors of persistent severe fatigue.

Conclusions: Persistent severe fatigue is present in a substantial proportion of RA patients and this fatigue appears to relate to disability and disease severity.

Editorial Comments: This cross-sectional study suggests that there is a sub-sample of RA patients that experience severe, persistent fatigue and that increased age, disability, and disease activity predict this fatigue. The fatiguing nature of RA is not well-established but this study suggests that fatigue is a significant issue for a substantial proportion of RA patients. What is less clear from this study is whether fatigue is empirically distinct from RA disease activity and/or disability or simply a proxy that correlates modestly with disease activity markers. Nonetheless, this study suggests that it might be worthwhile to assess fatigue at least periodically in RA patients both as a marker of disease and to identify the sub-sample of patients that might benefit from therapies to reduce their fatigue. It would also be valuable to develop and validate objective markers (i.e., performance tests) of fatigue in RA to determine whether questionnaire measures of adequately assess fatigue.

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Abstract 1899: Mortality Rates Following a First Acute Cardiovascular Event A Comparison between Rheumatoid Arthritis and the General Population
S Van Doornum, B King, C Brand, V Sundararajan
summarized by Jon Giles, M.D.

Several epidemiological investigations have identified an increased risk of cardiovascular mortality in RA patients. This increase in mortality could be secondary to both an increased prevalence of cardiovascular disease in the RA population, an increase in case fatality rate after a cardiovascular event, or both. An increased prevalence of cardiovascular disease in RA patients has been confirmed in multiple investigations. However, case fatality rates after cardiovascular events have not been well studied in RA patients. Here, Van Doornum et al examine cardiovascular mortality in Australian RA patients.

Methods: Administrative data was accessed for the population of approximately 5 million persons of Victoria, Australia. Data linkage was used to identify RA patients undergoing inpatient hospital admissions (from ICD coding), all inpatient admissions for first myocardial infarction (MI) or stroke (from ICD coding), and deaths (from the Victoria Death Index) for the period July 1, 2001 to November 30, 2003. Mortality in the 30 day period after the hospitalization for first cardiovascular event was considered to be secondary to the event.

Results: 29,924 first cardiovascular events were identified, 359 (1.2%) of which were patients identified to have RA. RA patients significantly differed from non-RA patients in gender (66.9% vs. 41.6% female, respectively), age (74.8 vs. 71.4 years, respectively) and were less likely to be smokers or be coded as having dyslipidemia.

Outcomes following first cardiovascular event: RA vs. non-RA

Conclusions: RA patients were 60% more likely than non-RA patients to die in the 30 day period following their first cardiovascular event. This increased mortality was accounted for entirely by an increase in the case fatality rate following MI. As a possible explanation, RA patients were significantly less likely to undergo angioplasty than non-RA patients, even after adjusting for pertinent confounding variables.

Editorial Comment: These results are compelling and highlight the need for further research into the possible explanations why this disparity in case fatality after MI exists. This investigation suffers from the same inherent potential biases that plague all studies arising from administrative data sets. In particular, the likelihood of miscoding for RA is high as RA is often only coded for inpatient hospital admissions when disease is very active, severe, or when RA complications arise during the hospitalization. Thus, selection bias may identify only the sickest RA patients and those most at risk for post-MI mortality, while milder or less complicated RA patients may be classified with the non-RA patients.

The underutilization of angioplasty in RA patients is particularly intriguing, and begs further study. Because RA patients are accustomed to a baseline level of musculoskeletal discomfort, or because analgesic and glucocorticoid use is more common in these patients, it is possible that the level of chest discomfort necessary to prompt emergent angioplasty is not occurring in these patients. Another possible explanation for the increase in MI mortality is that typical post-MI therapies (i.e. anti-platelet medications, beta-blockers, statins) are not being utilized effectively or their efficacy is affected by the RA disease process or by RA directed therapies. Unfortunately, this type of investigation is inherently unable to provide the degree of detail necessary to answer these questions.

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Abstract 1901: Effect of Carotid Atherosclerosis on the Incidence of Acute Coronary Syndromes in Rheumatoid Arthritis
I del Rincon, G Freeman, R Haas, D OLeary, D Battafarano, R Arroyo, A Escalante
summarized by Jon Giles, M.D.

Previous studies have identified an increased prevalence of carotid atherosclerosis in RA patients. In the general population, carotid atherosclerosis is a strong predictor of coronary atherosclerosis and subsequent cardiac events. However, this relationship has not been established in RA. Here, del Rincon et al examine the relationship between carotid atherosclerosis and incident acute coronary syndromes (ACS) in RA.

Methods: A prospective cohort of RA patients recruited from rheumatology clinics in San Antonio, TX underwent bilateral carotid ultrasound for the measurement if intimal-medial thickness (IMT) and assessment for the presence of carotid plaque. Subjects were followed in time for the development of ACS (myocardial infarction, unstable angina, cardiac arrest, and sudden cardiac death).

Results: Of the 779 RA patients enrolled, 636 underwent carotid ultrasound. During an observation period amounting to 3416 patient-years, 122 subjects who underwent baseline carotid ultrasound developed an ACS during follow-up corresponding to an incidence of 3.6 ACS events per 100 patient-years of follow-up (95% CI 2.96 4.23)

Relationship of carotid plaque to incidence of ACS

In multivariable models, a statistically significant association between carotid plaque and ACS was observed even after adjusting for age, gender, cardiovascular risk factors, past history of ACS, IMT, RA clinical manifestations (nodules, deformed joint count), and ESR.

Conclusions: The extent of carotid atherosclerosis is associated with an increased incidence of ACS in RA patients.

Editorial Comment: These findings are an important contribution to the literature, particularly as multiple investigations have established that carotid atherosclerosis is increased in RA, but few have directly investigated coronary atherosclerosis. With this investigation, the important surrogate relationship between carotid and coronary atherosclerosis can be made in RA patients. However, whether carotid atherosclerosis is a stronger or weaker predictor of coronary atherosclerosis in RA compared to non-RA patients requires a non-RA control group that is not presented in this investigation. In addition, the authors do not account for the use of plaque stabilizing medications (i.e. statins and beta-blockers) that could potentially confound the relationship between prevalent carotid plaque and incident ACS in these patients.

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