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Subclinical Coronary Artery Calcification and Relationship to Disease Duration in Women with Rheumatoid Arthritis
AMY H. KAO, SHANTHI KRISHNASWAMI, AMYLYNN CUNNINGHAM, DANIEL EDMUNDOWICZ, PENELOPE A. MOREL, LEWIS H. KULLER, and MARY CHESTER M. WASKO
ABSTRACT. Methods. In this cross-sectional study, 185 women with RA duration of at least 2 years and no clinical cardiovascular disease completed electron-beam tomography (EBT) scans and risk factor assessment. Multivariable logistic regression was used to associate RA duration quartiles with subclinical CAC and extent of CAC. Results. Age was similar across the quartiles of RA duration. Patients with RA > 23 years had significant increased odds (unadjusted OR 2.60, 95% CI 1.21–5.53) of having more extensive CAC compared to the referent group, those with RA for 2–7 years. This association remained significant after adjustment for traditional coronary heart disease (CHD) risk factors and RA-related covariates. Patients with intermediate RA duration (8–13 yrs) were more likely to have presence of any CAC (OR 3.03, 95% CI 1.06–8.66) compared to the referent group only after adjusting for age, race, and traditional CHD risk factors. Patients with longer RA duration were more likely to have cumulative joint damage, manifested as prior joint surgery, joint deformity, and greater functional disability. Lower body mass index also was associated with longer RA duration. Conclusion. Patients with longstanding RA have more extensive subclinical atherosclerosis or CAC compared to patients of the same age, independent of other CHD risk factors. RA duration may be a surrogate for factors related to the disease process or its treatment that may promote coronary atherogenesis. (First Release Nov 15 2007; J Rheumatol 2008;35:61-9) Key Indexing Terms:
RHEUMATOID ARTHRITIS
From the Division of Rheumatology and Clinical Immunology, Department of Medicine, and Department of Immunology, University of Pittsburgh; University of Pittsburgh Cardiovascular Institute; Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania; the Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, Tennessee; and the Department of Psychology, LaSalle University, Philadelphia, Pennsylvania, USA. Supported by NIH/NCRR/GCRC Grant MO1-RR000056, American Heart Association Established Investigator Award 0040149N, Arthritis Foundation, Western PA Chapter, NIH K23 AR47571, American College of Rheumatology/REF Physician Scientist Development Award, NIH K23 AR051044, and NIH/NCRR/GCRC Grant M01 RR000056. A.H. Kao, MD, MPH; M.C.M. Wasko, MD, MSc, Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh; S. Krishnaswami, MBBS, MPH, Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University; A. Cunningham, BS, Department of Psychology, LaSalle University; D. Edmundowicz, MS, MD, University of Pittsburgh Cardiovascular Institute; P.A. Morel, MD, Division of Rheumatology and Clinical Immunology; L.H. Kuller, MD, DrPH, Department of Epidemiology, University of Pittsburgh Graduate School of Public Health. Address reprint requests to Dr. A.H. Kao, S721 Biomedical Science Tower, 3500 Terrace Street, Pittsburgh, PA 15261. E-mail: ahk7@pitt.edu Accepted for publication September 10, 2007. |