Do antirheumatic drugs increase the risk of acute myocardial infarction?
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Comment↗
Biomedical subjects
Sherine E Gabriel
Publications and source records attributed to Sherine E Gabriel.
Contribution of congestive heart failure and ischemic heart disease to excess mortality in rheumatoid arthritis.
OBJECTIVE: Although mortality among patients with rheumatoid arthritis (RA) is higher than in the general population, the relative contribution of comorbid diseases to this mortality difference is not known. This study was undertaken to evaluate the contribution of congestive heart failure (CHF) and ischemic heart disease (IHD), including myocardial infarction, to the excess mortality in patients with RA, compared with that in individuals without RA. METHODS: We assembled a population-based inception cohort of individuals living in Rochester, Minnesota, in whom RA (defined according to the criteria of the American College of Rheumatology [formerly, the American Rheumatism Association]) first developed between 1955 and 1995, and an age- and sex-matched non-RA cohort. All subjects were followed up until either death, migration from the county, or until 2001. Detailed information from the complete medical records was collected. Statistical analyses included the person-years method, cumulative incidence, and Cox regression modeling. Attributable risk analysis techniques were used to estimate the number of RA deaths that would be prevented if the incidence of CHF was the same in patients with RA and non-RA subjects. RESULTS: The study population included 603 patients with RA and 603 subjects without RA. During followup, there was an excess of 123 deaths among patients with RA (345 RA deaths occurred, although only 222 such deaths were expected). The mortality rates among patients with RA and non-RA subjects were 39.0 and 29.2 per 1,000 person-years, respectively. There was a significantly higher cumulative incidence of CHF (but not IHD) in patients with RA compared with non-RA subjects (37.1% versus 27.7% at 30 years of followup, respectively; P < 0.001). The risk of death associated with either CHF or IHD was not significantly different between patients with RA and non-RA subjects. If the risk of developing CHF was the same in patients with RA and individuals without RA, the overall mortality rate difference between RA and non-RA hypothetically would be reduced from 9.8 to 8.0 excess deaths per 1,000 person-years; that is, 16 (13%) of the 123 excess deaths could be prevented. CONCLUSION: CHF, rather than IHD, appears to be an important contributor to the excess overall mortality among patients with RA. CHF contributes to this excess mortality primarily through the increased incidence of CHF in RA, rather than increased mortality associated with CHF in patients with RA compared with non-RA subjects. Eliminating the excess risk of CHF in patients with RA could significantly improve their survival.
Arthritis, Rheumatoid↗
Rheumatoid arthritis and the heart.
The risk of cardiovascular disease is increased in patients with rheumatoid arthritis (RA). Although the pathogenesis of cardiovascular disease in patients with RA is largely unknown, evidence to date indicates that it involves complex interactions between the traditional and nontraditional cardiovascular risk factors as well as various medications commonly used for the treatment of RA patients. This review provides an overview of the clinical studies that demonstrate increased risk of coronary heart disease and heart failure in patients with RA and also discusses the potential role of the various risk factors.
Arthritis, Rheumatoid↗
Patient, disease, and therapy-related factors that influence discontinuation of disease-modifying antirheumatic drugs: a population-based incidence cohort of patients with rheumatoid arthritis.
OBJECTIVE: A major challenge in management of rheumatoid arthritis (RA) is prediction of longterm response to disease-modifying antirheumatic drug (DMARD) treatment. Our objective was to identify the predictors of DMARD discontinuation in an incidence cohort of patients with RA followed continuously from their incidence date. METHODS: Members of a population-based incidence cohort of Rochester, Minnesota, residents aged > or = 18 years diagnosed with RA (by 1987 American College of Rheumatology criteria) from January 1, 1955, to January 1, 1995, were followed longitudinally through their complete medical records until January 1, 2001. Detailed drug exposure data were collected on all DMARD and glucocorticoid regimens. Subjects were considered exposed to a DMARD if duration of use was > or = 30 days. Time to discontinuation of DMARD was estimated using survival analysis techniques. Andersen-Gill models with multiple events per patient were used to assess the influence of demographics, calendar time, comorbidities, disease characteristics [disease duration, rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), joint counts, radiographic changes, nodules, RA complications], and therapy characteristics (DMARD use, singly or in combination, glucocorticoid use, first or subsequent regimen, effect of previous therapy) on time from DMARD initiation to discontinuation. RESULTS: The study population comprised 345 DMARD-treated patients (73% female) with mean age of 53.1 years and mean followup 15.4 years. Median time taking any DMARD was 16.0 months for the first, and 17.9 months for all regimens. Methotrexate (MTX) had the longest time to discontinuation, with a median of 30.3 months without folate, and 61.7 months with folate supplementation. Among the various disease characteristics examined, only higher ESR at DMARD initiation was significantly associated with a shorter time taking DMARD [hazard ratio (HR) 1.05 per 10 mm/h increase, 95% CI 1.02, 1.08]. In multivariable Andersen-Gill models considering all DMARD regimens, hydroxychloroquine use (HR 0.77, 95% CI 0.64, 0.92) and MTX use (HR with folate 0.39, 95% CI 0.30, 0.51; HR without folate 0.51, 95% CI 0.39, 0.67) were significantly associated with longer time to DMARD discontinuation, whereas prior MTX use (HR 1.96, 95% CI 1.57, 2.45) was associated with shorter time to DMARD discontinuation, after adjusting for age, sex, calendar year, Charlson comorbidity index, disease duration, and ESR at DMARD initiation. Disease duration was negatively associated with time to DMARD discontinuation; each 10 year increase in disease duration corresponded to a 14% decrease in the risk of discontinuation (HR 0.86, 95% CI 0.75, 0.98). CONCLUSION: Longer RA disease duration does not appear to increase the risk of DMARD discontinuation. However, high disease activity (as assessed by ESR) is associated with a higher likelihood of discontinuing DMARD. MTX failure may identify a subgroup of patients who are less likely to respond to other DMARD and therefore could be considered as candidates for biological therapies.
Antirheumatic Agents↗
Direct medical costs of polymyalgia rheumatica.
OBJECTIVE: To describe the patterns of care and direct medical costs of polymyalgia rheumatica (PMR) to test the hypothesis that the direct medical costs incurred by patients with PMR are higher than costs incurred by age- and sex-matched population-based controls from the same community. METHODS: The study population comprised 193 Olmsted County, Minnesota residents who were first diagnosed with PMR between January 1, 1987 and December 31, 1999. Inclusion criteria were as follows: age > or = 50 years; bilateral aching and morning stiffness (lasting > or = 30 minutes) persisting for at least 1 month and involving the neck, shoulders, or hip girdle regions; and an erythrocyte sedimentation rate (ESR) > or = 40 mm/hour. In patients who fulfilled the first 2 criteria, but had a normal ESR, a rapid response to low-dose corticosteroids served as the third criterion. A total of 695 age- and sex-matched subjects without PMR served as control subjects. Billing data from the Olmsted County Healthcare Expenditure and Utilization Database (OCHEUD) were used to provide estimates of nationally representative unit costs in the year 2002 inflation-adjusted dollars. All subjects were followed using the OCHEUD records until December 31, 2002 to assess the total direct medical costs. Generalized quantile regression modeling was used to estimate the effect of PMR on direct medical costs, after adjusting for age, sex, Charlson comorbidity score, number of hospital days, and number of radiographs. RESULTS: During the first year following diagnosis, subjects with PMR used a substantially higher number of outpatient services and laboratory tests compared with controls, but during the subsequent 4 years, there were no differences between the 2 groups. In age- and sex-adjusted analysis, PMR was associated with a significant incremental cost of 2,233 dollars at the 10th percentile of costs and 27,712 dollars at the 90th percentile of costs. However, further adjustments for comorbidities, number of hospital days, radiographs, and imaging eliminated the incremental cost difference between the subjects with PMR and control subjects. PMR subjects were significantly more likely to have a history of myocardial infarction (odds ratio [OR] 1.78, 95% confidence interval [95% CI] 1.13, 2.82), peripheral vascular diseases (OR 2.21, 95% CI 1.37, 3.60), and cerebrovascular diseases (OR 1.60, 95% CI 1.08, 2.39) compared with the controls. CONCLUSION: Incremental direct medical costs associated with the management of PMR can be substantial, especially early in the disease course. These incremental costs appear to originate mainly from comorbid cardiovascular conditions that were shown to be more prevalent among subjects with PMR.
Aged↗
Use of physician services in a population-based cohort of patients with polymyalgia rheumatica over the course of their disease.
OBJECTIVE: To describe the use of generalist and rheumatologist services in a population-based cohort of patients with polymyalgia rheumatica (PMR) and to identify predictors of rheumatology care. METHODS: We identified all incident cases of PMR among residents of Olmsted County, Minnesota between 1970 and 1999. Patients were followed for a maximum of 5 years after their incidence date. Logistic regression and zero-inflated Poisson regression models were used to assess the association between rheumatology care and age, sex, giant cell arteritis (GCA), PMR relapses, corticosteroid complications, comorbidity, and various laboratory findings, adjusting for the total number of visits. RESULTS: Of the 364 incident cases of PMR eligible for this analysis, 67% were women and the mean age at incidence was 73 years. Over a mean followup of 4.1 years, individuals in this cohort utilized a total of 5,108 physician office visits and 2,015 telephone calls. The mean number of generalist and rheumatologist visits per person-years of follow-up during the first year of PMR was 7.02 and 2.15, respectively. Thereafter, there was a steady decline in both generalist and rheumatologist visits. One hundred forty-four (40%) patients had no rheumatologist visits and 102 (28%) had only 1 rheumatologist visit, mostly for diagnostic confirmation. Men and patients with several comorbid conditions were significantly more likely to be seen by rheumatologists (P < 0.001). However, once referred, women, older patients, and those with GCA, PMR relapses, and corticosteroid complications had significantly more rheumatologist visits (P < 0.001). CONCLUSION: The use of physician services in PMR is considerable. Generalists provide the large majority of care. Rheumatologist involvement is generally limited to diagnostic confirmation and management of complications. The relative paucity of rheumatology care following the period of diagnosis may represent an opportunity for improving the care of patients with PMR.
Aged↗
The need for microsimulation to evaluate osteoporosis interventions.
Simulations play an increasingly important role in the evaluation of osteoporosis interventions. Existing evaluations have been based on "reduced-form" cohort simulations that do not reflect the complexity and heterogeneity of osteoporosis and its outcomes. Such simplified models offer parsimony and ease of use, but they also are limited in their ability to explain and extrapolate outcomes in a way that is most useful for both clinical and health policy decision makers. Alternatively, evaluations could be based on "structural" microsimulations, which explicitly model the underlying biology of osteoporosis at the individual level. The structural approach presents technical challenges, including the need to obtain more-detailed data and the requirement that underlying biological models be validated. However, evaluations based on structural microsimulation may ultimately provide substantially more useful information, resulting in improved decision making.
Computer Simulation↗
Increased unrecognized coronary heart disease and sudden deaths in rheumatoid arthritis: a population-based cohort study.
OBJECTIVE: To examine the risk of clinical coronary heart disease (CHD) in patients with rheumatoid arthritis (RA) compared with age- and sex-matched non-RA subjects, and to determine whether RA is a risk factor for CHD after accounting for traditional CHD risk factors. METHODS: We assembled a population-based incidence cohort of 603 Rochester, Minnesota residents ages >or=18 years who first fulfilled the American College of Rheumatology (ACR) 1987 criteria for RA between January 1, 1955 and January 1, 1995, and 603 age- and sex-matched non-RA subjects. All subjects were followed up through their complete inpatient and outpatient medical records, beginning at age 18 years until death, migration, or January 1, 2001. Data were collected on CHD events and traditional CHD risk factors (diabetes mellitus, hypertension, dyslipidemia, body mass index, smoking) using established diagnostic criteria. CHD events included hospitalized myocardial infarction (MI), unrecognized MI, coronary revascularization procedures, angina pectoris, and sudden CHD deaths. Conditional logistic regression and Cox regression models were used to estimate the risk of CHD associated with RA, both prior to and following RA diagnosis, after adjusting for CHD risk factors. RESULTS: During the 2-year period immediately prior to fulfillment of the ACR criteria, RA patients were significantly more likely to have been hospitalized for acute MI (odds ratio [OR] 3.17, 95% confidence interval [95% CI] 1.16-8.68) or to have experienced unrecognized MIs (OR 5.86, 95% CI 1.29-26.64), and less likely to have a history of angina pectoris (OR 0.58, 95% CI 0.34-0.99) compared with non-RA subjects. After the RA incidence date, RA patients were twice as likely to experience unrecognized MIs (hazard ratio [HR] 2.13, 95% CI 1.13-4.03) and sudden deaths (HR 1.94, 95% CI 1.06-3.55) and less likely to undergo coronary artery bypass grafting (HR 0.36, 95% CI 0.16-0.80) compared with non-RA subjects. Adjustment for the CHD risk factors did not substantially change the risk estimates. CONCLUSION: Patients with RA have a significantly higher risk of CHD when compared with non-RA subjects. RA patients are less likely to report symptoms of angina and more likely to experience unrecognized MI and sudden cardiac death. The risk of CHD in RA patients precedes the ACR criteria-based diagnosis of RA, and the risk cannot be explained by an increased incidence of traditional CHD risk factors in RA patients.
Adolescent↗
The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years.
OBJECTIVE: It is hypothesized that the systemic inflammation associated with rheumatoid arthritis (RA) promotes an increased risk of cardiovascular (CV) morbidity and mortality. We examined the risk and determinants of congestive heart failure (CHF) in patients with RA. METHODS: We assembled a population-based, retrospective incidence cohort from among all individuals living in Rochester, Minnesota, in whom RA (defined according to the American College of Rheumatology 1987 criteria) was first diagnosed between 1955 and 1995, and an age- and sex-matched non-RA cohort. After excluding patients in whom CHF occurred before the RA index date, all subjects were followed up until either death, incident CHF (defined according to the Framingham Heart Study criteria), migration from the county, or until January 1, 2001. Detailed information from the complete medical records (including all inpatient and outpatient care provided by all local providers) regarding RA, ischemic heart disease, and traditional CV risk factors was collected. Cox models were used to estimate the effect of RA on the development of CHF, adjusting for CV risk factors and/or ischemic heart disease. RESULTS: The study population included 575 patients with RA and 583 subjects without RA. The CHF incidence rates were 1.99 and 1.16 cases per 100 person-years in patients with RA and in non-RA subjects, respectively (rate ratio 1.7, 95% confidence interval [95% CI] 1.3-2.1). After 30 years of followup, the cumulative incidence of CHF was 34.0% in patients with RA and 25.2% in non-RA subjects (P< 0.001). RA conferred a significant excess risk of CHF (hazard ratio [HR] 1.87, 95% CI 1.47-2.39) after adjusting for demographics, ischemic heart disease, and CV risk factors. The risk was higher among patients with RA who were rheumatoid factor (RF) positive (HR 2.59, 95% CI 1.95-3.43) than among those who were RF negative (HR 1.28, 95% CI 0.93-1.78). CONCLUSION: Compared with persons without RA, patients with RA have twice the risk of developing CHF. This excess risk is not explained by traditional CV risk factors and/or clinical ischemic heart disease.
Arthritis, Rheumatoid↗
Cardiovascular death in rheumatoid arthritis: a population-based study.
OBJECTIVE: To determine whether systemic inflammation confers any additional risk for cardiovascular death among patients with rheumatoid arthritis (RA), after adjusting for traditional cardiovascular risk factors and comorbidities. METHODS: Using the population-based data resources of the Rochester Epidemiology Project, we assembled an incidence cohort of all Rochester, Minnesota residents ages >or=18 years who first fulfilled the American College of Rheumatology 1987 criteria for RA between January 1, 1955 and January 1, 1995. All subjects were followed up longitudinally through their complete (inpatient, outpatient) medical records, beginning at age 18 years and continuing until death, migration, or January 1, 2001. Detailed information on the occurrence of various cardiovascular risk factors (personal history of coronary heart disease [CHD], congestive heart failure, smoking, hypertension, dyslipidemia, body mass index [BMI], diabetes mellitus, menopausal status) as well as indicators of systemic inflammation and RA disease severity (rheumatoid factor [RF] seropositivity, erythrocyte sedimentation rate [ESR], joint swelling, radiographic changes, RA nodules, RA complications, RA treatments, disease duration) and comorbidities were collected on all subjects. Causes of death were ascertained from death certificates and medical records. Cox regression models were used to estimate the independent predictors of cardiovascular death. RESULTS: This inception cohort comprised a total of 603 RA patients whose mean age was 58 years, of whom 73% were women. During a mean followup of 15 years, 354 patients died and cardiovascular disease was the primary cause of death in 176 patients. Personal history of CHD, smoking, hypertension, low BMI, and diabetes mellitus, as well as comorbidities, including peripheral vascular disease, cerebrovascular disease, chronic pulmonary disease, dementia, ulcers, malignancies, renal disease, liver disease, and history of alcoholism, were all significant risk factors for cardiovascular death (P < 0.01 for each). Multivariable Cox regression analyses, controlled for cardiovascular risk factors and comorbidities, revealed that the risk of cardiovascular death was significantly higher among RA patients with at least 3 ESR values of >or=60 mm/hour (hazard ratio [HR] 2.03, 95% confidence interval [95% CI] 1.45-2.83), RA vasculitis (HR 2.41, 95% CI 1.00-5.81), and RA lung disease (HR 2.32, 95% CI 1.11-4.84). CONCLUSION: These results indicate that markers of systemic inflammation confer a statistically significant additional risk for cardiovascular death among patients with RA, even after controlling for traditional cardiovascular risk factors and comorbidities.
Adult↗
How much of the increased incidence of heart failure in rheumatoid arthritis is attributable to traditional cardiovascular risk factors and ischemic heart disease?
OBJECTIVE: To compare the proportion of the risk for the development of heart failure (HF) that is attributable to traditional cardiovascular (CV) risk factors, ischemic heart disease (IHD), and alcohol abuse between subjects with and subjects without rheumatoid arthritis (RA). METHODS: A population-based inception cohort of RA patients was assembled along with a similar cohort of subjects without RA. All individuals were followed up through their complete medical records, until HF incidence, death, migration, or January 1, 2001. The attributable risk of HF was estimated as the difference between the observed cumulative incidence of HF in each cohort (estimated from multivariable Cox models and adjusted for the competing risk of death) and the predicted cumulative incidence of HF in the absence of risk factors, with results expressed as a percentage of the observed cumulative incidence. RESULTS: A total of 575 RA subjects and 583 non-RA subjects (mean age 57 years, 73% women) without HF at incidence/index date had a mean followup of 15.1 and 17.0 years, respectively. During that period, 165 RA and 115 non-RA subjects had a first episode of HF, with a cumulative incidence of 36.3% and 20.4%, respectively, at age 80 years. Among non-RA subjects, 77% of the HF at age 80 years was attributable to CV risk factors, IHD, and alcohol abuse combined, whereas among RA subjects, only 54% of the HF at age 80 years was attributable to these factors (P < 0.01). CONCLUSION: The excess risk of HF among RA patients is not explained by an increased frequency or effect of CV risk factors and IHD.
Adult↗
Relapse in a population based cohort of patients with polymyalgia rheumatica.
OBJECTIVE: To determine the incidence and the clinical, laboratory, and treatment related predictors of relapse in polymyalgia rheumatica (PMR). METHODS: Using the population based resources of the Rochester Epidemiology Project, we assembled an incidence cohort of subjects with PMR first diagnosed between January 1, 1970, and December 31, 1999. For inclusion, subjects were required to fulfill 3 criteria: (1) age > or = 50 years; (2) bilateral aching and morning stiffness in neck, shoulders, or hip girdle regions; and (3) erythrocyte sedimentation rate (ESR) > or = 40 mm/h. In subjects who fulfilled the first 2 criteria but had a normal ESR, a rapid response to low dose corticosteroids (CS) served as the third criterion. Patients were followed until permanent remission, migration, or a maximum of 5 years after their incidence date. Relapse was defined as an exacerbation of PMR symptoms requiring an adjustment of CS dose (> or = 5 mg) occurring at least 30 days after the incidence date. Time to relapse was modeled using the Kaplan-Meier method. CS treatment patterns were modeled using linear and nonlinear models. Cox regression models were used to evaluate predictors of time to first and subsequent relapses. RESULTS: The study population included 364 patients with a mean age of 73.4 years and 244 (67%) were women. Among the 284 patients treated with CS, a higher initial CS dose and faster CS tapering rate were significant predictors of future relapses, after adjusting for age, sex, ESR, giant cell arteritis at PMR diagnosis, and the intensity of rheumatologist care. Every 5 mg/day increase in initial CS dose was associated with a 7% increase in the risk of relapse [hazard ratio (HR) 1.07, 95% CI 1.02, 1.13]. The hazard of having a relapse was 4-fold higher when the CS tapering rate was fast (HR 4.27, 95% CI 2.84, 6.44), and 2-fold higher when the CS tapering rate was medium (HR 2.19, 95% CI 1.54, 3.11) compared to slow tapering. CONCLUSION: Higher initial CS doses and faster tapering are significant predictors of future relapses. Our results suggest that efforts should be made to minimize initial CS dose and taper CS slowly in order to avoid disease relapses.
Aged↗
Use of low-dose glucocorticoids and the risk of cardiovascular morbidity and mortality in rheumatoid arthritis: what is the true direction of effect?
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Anti-Inflammatory Agents↗
Reappraisal of the epidemiology of giant cell arteritis in Olmsted County, Minnesota, over a fifty-year period.
OBJECTIVE: To investigate time trends in the incidence and survival of giant cell arteritis (GCA) over a 50-year period in Olmsted County, Minnesota. METHODS: Using the unified record system at the Mayo Clinic, we identified all incident cases of GCA first diagnosed between 1950 and 1999. Incidence rates were estimated and adjusted to the 1980 United States white population for age and sex. The annual incidence rates were graphically illustrated using a 3-year centered moving average. Survival rates were computed and compared with the expected rates in the population. RESULTS: There were 173 incident cases of GCA during the 50-year study period. Of these, 79% were women and the mean age at diagnosis was 74.8 years. The overall age- and sex-adjusted incidence per 100,000 persons 50 years of age or older was 18.8 (95% confidence interval [95% CI] 15.9-21.6). Incidence was higher in women (24.4; 95% CI 20.3-28.6) than in men (10.3; 95% CI 6.9-13.6). Incidence rates increased significantly over the study period (P = 0.017); in particular, a progressive increase was observed from 1950 to 1979; subsequently, no substantial increases in incidence rates were observed. A cyclic pattern of annual incidence rates was apparent, with evidence of 6 peak periods. Survival among individuals with GCA was not significantly different from that expected in the population (P = 0.80). CONCLUSIONS: The incidence of GCA increased over the first 3 decades of the study, then remained stable over the last 20 years. The previously observed cyclic pattern of annual incidence rates was still apparent over a 50-year period. Overall survival in GCA was similar to that in the population.
Age Distribution↗
A prospective clinical practice intervention to improve osteoporosis management following distal forearm fracture.
Secondary prevention of osteoporosis after fracture is underutilized, despite cost-effective therapies. This clinical practice intervention aimed to improve osteoporosis care of the postfracture patient. Residents of Olmsted County, Minnesota, USA, > or = age 45 who sustained a moderate trauma distal forearm fracture were identified, and participants received educational materials, referral for bone densitometry and physician consultation to address osteoporosis in January 1999 through October 2000. Osteoporosis educational materials were provided to patients at the time of recruitment, and primary care physicians provided osteoporosis practice guidelines. Outcomes included: completion of bone densitometry, acceptance of interventions at the first postfracture primary care physician visit, and adherence to advice at 6 months. There were 105 patients identified (80% women), but only 58 agreed to participate (88% women). Women with lower T-scores (< -1.5) had an 89% initial treatment rate, and 67% were adherent to treatment at 6 months. All women with normal bone density (T-score above -1.5) were advised by their primary care physicians about antiresorptive treatment, and 100% adhered to these recommendations, even though they were not eligible for such treatment based on the National Osteoporosis Foundation (NOF) guidelines. None of the men accepted the treatments offered, despite T-scores that fell at or below the NOF treatment threshold. Bone densitometry and consultation improved osteoporosis interventions after index fracture from a 16% baseline rate in the population (1993-1997) to a 45% overall rate for the study population. In summary, while referral for bone densitometry and discussion by a physician about postfracture osteoporosis preventive treatments did increase treatment rate, the majority of patients at highest risk did not accept interventions. Further initiatives are needed to overcome both system and patient barriers.
Absorptiometry, Photon↗
Prognostic importance of low body mass index in relation to cardiovascular mortality in rheumatoid arthritis.
OBJECTIVE: Various etiologic mechanisms have been implicated in the observed increase in cardiovascular mortality in rheumatoid arthritis (RA). Body mass index (BMI) is associated with cardiovascular mortality in the general population. This study compared the effect of BMI on cardiovascular mortality in a population-based cohort of subjects with RA with that in a cohort of individuals without RA from the same population. METHODS: The RA cohort comprised all members of an incidence cohort of Rochester, Minnesota residents ages > or =18 years who were first diagnosed with RA (by the American College of Rheumatology 1987 criteria) from 1955 through 1994. An age- and sex-matched comparison cohort of subjects without RA was assembled. Both cohorts were followed up longitudinally through their complete (inpatient, outpatient) medical records beginning at age 18 years and continuing until death, migration, or January 1, 2001, and the details of weight and height changes during this period were recorded. High BMI was defined as a BMI >30 kg/m(2) and low BMI as <20 kg/m(2). Cox regression models were used to estimate the effect of BMI on cardiovascular mortality after accounting for traditional cardiac risk factors and malignancies. RESULTS: RA subjects with low BMI at incidence had a significantly higher risk of cardiovascular death (hazard ratio [HR] 3.34, 95% confidence interval [95% CI] 2.23-4.99) compared with non-RA subjects with normal BMI, after adjusting for age, sex, personal cardiac history, smoking status, and presence of diabetes, hypertension, and malignancies. RA subjects with normal BMI at incidence who experienced low BMI during followup also had a higher risk of cardiovascular death (HR 2.09, 95% CI 1.50-2.92) when compared with non-RA subjects who maintained normal BMI throughout followup. CONCLUSION: Among patients with RA, low BMI is associated with a significantly increased risk of cardiovascular death.
Aged↗
Rochester Epidemiology Project: a unique resource for research in the rheumatic diseases.
Olmsted County, Minnesota is one of the few places in the world to conduct comprehensive population-based studies of disease etiology, natural history, and outcomes because of a unique resource, the Rochester Epidemiology Project (REP). This article describes the REP and highlights its research capabilities in the context of the rheumatic diseases.
Epidemiologic Studies↗
The effect of oral contraceptives and estrogen replacement therapy on the risk of rheumatoid arthritis: a population based study.
OBJECTIVE: Epidemiologic evidence for a protective effect of exogenous female sex hormones on the development of rheumatoid arthritis (RA) is contradictory. We examined whether exposure to either oral contraceptives (OC) or postmenopausal estrogen replacement therapy (ERT) is associated with the development of RA in women. METHODS: We separately examined the relationship between use of OC and ERT on the risk of RA in a population based case-control study. Case patients, including all female residents of Rochester, Minnesota, > or = 18 years of age, who first fulfilled 1987 American College of Rheumatology criteria for RA between 1955 and 1994 (n = 445), were compared with age matched female controls from the community. Multivariable conditional logistic regression models were used to determine whether OC or ERT exposure had an effect on RA development after controlling for potential confounders. RESULTS: We observed an inverse association between ever-use of OC and the risk of RA, which persisted after adjusting for potential confounders in multivariate analyses (OR 0.56, 95% CI 0.34, 0.92). Earlier calendar-year of first exposure to OC was associated with lower OR for RA. We found no evidence of a significant association of ERT with RA risk (adjusted OR 1.11, 95% CI 0.69, 1.78). CONCLUSION: Exposure to OC, but not ERT, significantly reduces the risk of development of RA. The risk of developing RA is lower when OC exposure occurred in earlier years, which suggests that the higher doses of estrogens and progestins contained in earlier OC preparations may have a stronger protective effect against developing RA. While this protective effect is strong, it only explains a small portion of the observed decrease in RA incidence over the past few decades because the proportion of Rochester women exposed to OC is quite small.
Adult↗