Home Page - About the Arthritis Center -Hopkins Rheumatology - Myositis Center - Vasculitis Center - Scleroderma Center
Search for:




















Cardiovascular Disease
OP0013 Prevalence, Clinical Expression and Causes of Ischaemic Heart Disease in Rheumatoid Arthritis
MJ Banks, EJ Flint, PA Bacon, GD Kitas

There is increased cardiovascular mortality in patients with rheumatoid arthritis (RA). Banks, et al assessed the prevalence, clinical presentation, and risk factors of ischaemic heart disease (IHD).

67 patients with RA were compared to 37 patients with osteoarthritis (OA) after being matched for all IHD risk factors. IHD detection methods included the Rose questionnaire, ECG, and adenosine-stressed myocardial perfusion SPECT imaging. Other assessments performed were as follows: demographics, BMI, disease and drug history, HAQ, ESR, CRP, joint count, RF, vWF, ACE, lipids, fibrinogen, homocysteine, H. pylori, CMV and C. pneumoniae titers.

IHD in RA patients was ~2x the incidence of IHD in the control patients, 49% and 27% (p=0.03), respectively. ESR, CRP, fibrinogen, vWF, and ACE were significantly higher in the patients with RA when compared to control patients (p<0.001). RA patients with IHD had higher BMI, H. Pylori titers, triglycerides, blood pressure, steroid use, age and male gender compared to those without IHD (p<0.05). Using logistic regression analysis, age, male sex, RA and BMI were found to be independent predictors of IHD among these study patients. These data demonstrate that RA is an independent risk factor for IHD.

Editorial Comment: This study confirms others in showing the association of RA with increasing risk of IHD. The etiology of this association is unknown. Recent studies in non-RA patients showing the association of elevated c-reactive protein levels with increased cardiovascular disease has raised the possibility that systemic inflammation may play a role. However, it is difficult to sort out the relevant risk factors as RA patients may differ from controls in many aspects. Changes in body mass composition, lipid changes from steroid use, and deconditioning resulting from chronic joint disease may all play a role in the increased cardiovascular risk. This study is limited by its small size and cross-sectional design. Further work needs to be done with larger prospectively followed cohorts. From a practical clinical perspective, alterable cardiovascular risk factors need to be aggressively managed.

((top of page))

OP0014 The acute phase response does not fully explain dyslipidemia and insulin resistance in inflammatory arthritis
P.H. Dressein, B.I. Joffee, A.E. Stanwix, Z. Zoomal

Objectives: To evaluate insulin resistance (IR) and lipid metabolism in patients with inflammatory arthritis.

Methods: 87 patients (38 rheumatoid arthritis, 29 spondyloarthropathy, 20 undifferentiated inflammatory arthritis ) with inflammatory arthropathy (IA) and 30 race matched healthy controls were evaluated. No glucocorticoids were allowed. Evaluations include body mass index (BMI), ESR, plasma glucose, serum insulin, cholesterol (chol) and lipid profiles were measured. IR was estimated by the homeostasis model.

Results: HDL-chol was lower (p<0.002) and total chol/HDL-chol was higher (P<0.001in the IA group than in controls. This difference was maintained after controlling for BMI, ESR and IR. IR could be attributed to excess weight and acute phase reactants.

Editorial Comment: Cardiovascular events are a significant cause of mortality in rheumatoid arthritis (RA) and, thus, cardiovascular risk factors should be recognized and treated as part of management of RA and other inflammatory arthropathies. This study demonstrates that crude measures of inflammation (ESR) do correlate with the decrease in HDL-chol seen in patients with IR. Their conclusion that dyslipidemia may be risk factor for IA is clearly premature. More work needs to be done including the effects of inflammatory cytokines on the hormonal axes and the effect on body composition and fat metabolism.

((top of page)) (next page)

All information contained within the Johns Hopkins Arthritis Center website is intended for educational purposes only. Physicians and other health care professionals are encouraged to consult other sources and confirm the information contained within this site. Consumers should never disregard medical advice or delay in seeking it because of something they may have read on this website.