 |
|
|
 |
Influence of Nonclassical Cardiovascular Risk Factors on the Accuracy of Predicting Subclinical Atherosclerosis in Rheumatoid Arthritis
PATRICK H. DESSEIN, GAVIN R. NORTON, ANGELA J. WOODIWISS, BARRY I. JOFFE, and FRED WOLFE ABSTRACT. Objective. To determine whether nontraditional risk factors increase the accuracy of predicting the presence of carotid artery plaque based on traditional cardiovascular risk factors only in patients with rheumatoid arthritis (RA). Methods. We identified risk factors that were independently associated with ultrasonographically located plaque. In predicting carotid artery plaque, the area under the curve (AUC) of the receiver-operating characteristic (ROC) curve for the combination of traditional and nontraditional risk factors was compared to the AUC of the ROC curve for traditional risk factors and nontraditional risk factors considered separately in 91 patients with RA. Results. Thirty-one (34%) patients had carotid artery plaque. The 3 traditional risk factors of age > 55 years, hypertension, and ever-smoking, and the 3 nontraditional risk factors of a disease duration > 8 years, polymorphonuclear cell count > 4.5 ´ 106/l, and hypothyroidism were each independently associated with the presence of plaque (odds ratios 2.08–8.78; p = 0.001–0.02). The percentage of patients with plaque was 0, 10%, 50%, and 83% in patients with 0–1, 2, 3, and 4–6 of these risk factors, respectively. In predicting plaque, the AUC of the ROC curve for the combination of traditional and nontraditional risk factors (0.90 ± 0.03) was greater than that for either traditional (0.80 ± 0.05; p = 0.006) or nontraditional (0.80 ± 0.04; p = 0.005) risk factors considered separately. Conclusion. The combination of disease duration, polymorphonuclear cell counts, and thyroid status increased the accuracy of predicting subclinical atheroma in patients with RA. We believe that our findings merit external validation. (First Release April 15 2007; J Rheumatol 2007;34:943–51) Key Indexing Terms:
RHEUMATOID ARTHRITIS From the Department of Rheumatology, Johannesburg Hospital and Milpark Hospital, Parktown, University of the Witwatersrand, Johannesburg, South Africa; Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand; Centre for Diabetes and Endocrinology, Houghton, University of the Witwatersrand; and the National Data Bank for Rheumatic Diseases, University of Kansas School of Medicine, Wichita, Kansas, USA. P.H. Dessein, MD, FCP(SA), PhD, Department of Rheumatology, Johannesburg Hospital and Milpark Hospital, University of the Witwatersrand; G.R. Norton, MBBCh, PhD; A.J. Woodiwiss, PhD, Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand; B.I. Joffe, DSc, Centre for Diabetes and Endocrinology, University of the Witwatersrand; F. Wolfe, MD, National Data Bank for Rheumatic Diseases, University of Kansas School of Medicine. Address reprint requests to Dr. P.H. Dessein, PO Box 1012, Melville 2109, Johannesburg, South Africa. E-mail: Dessein@telkomsa.net Accepted for publication January 12, 2007.
|
