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High-grade C-Reactive Protein Elevation Correlates with Accelerated Atherogenesis in
Patients with Rheumatoid Arthritis
MIGUEL A. GONZALEZ-GAY, CARLOS GONZALEZ-JUANATEY, ANGELA PIÑEIRO, CARLOS GARCIA-PORRUA, ANA TESTA, and JAVIER LLORCA ABSTRACT. Objective. Patients with rheumatoid arthritis (RA) are at greater risk of developing cardiovascular events compared with individuals without RA. Increased risk for cardiovascular disease in these patients is a consequence of atherosclerosis. Case-control studies have shown that increased intima-media thickness (IMT) of the common carotid artery is an indicator of generalized atherosclerosis. Some investigators have suggested that the development of atherosclerosis in RA may be related to the magnitude and chronicity of the systemic inflammation. We examined the relationship between carotid IMT to C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), which are the most commonly assessed markers of inflammatory response in patients with RA. Methods. Retrospective review of CRP and ESR values in 47 patients with longterm actively treated (at least 5 years) RA without clinically evident atherosclerosis or its complications, who had been studied for carotid IMT with high resolution B-mode ultrasound. Results. No correlation between ESR and carotid IMT was observed. However, a correlation was found between the maximum CRP values and the carotid IMT (p = 0.009). The distribution of patients in 4 quartiles according to the average CRP values showed significant differences in the carotid IMT (p = 0.03). Those exhibiting the highest mean CRP values (quartile 4) had greater carotid IMT. There was no correlation between CRP at the time of disease diagnosis or at the time of the ultrasound study and the carotid IMT. Conclusion. Our study confirms that the magnitude and chronicity of the inflammatory response measured by CRP correlates directly with the presence of atherosclerosis in patients with RA. (J Rheumatol 2005;32:1219–23) Key Indexing Terms: RHEUMATOID ARTHRITIS From the Divisions of Rheumatology and Cardiology, Hospital Xeral-Calde, Lugo; and Department of Preventive Medicine and Public Health, School of Medicine, University of Cantabria, Santander, Spain. M.A. Gonzalez-Gay, MD, PhD; A. Piñeiro, MD; C. Garcia-Porrua, MD, PhD, Division of Rheumatology; C. Gonzalez-Juanatey, MD; A. Testa, MD, Division of Cardiology, Hospital Xeral-Calde; J. Llorca, MD, PhD, Department of Preventive Medicine and Public Health, School of Medicine, University of Cantabria. Dr. Gonzalez-Gay and Dr. Llorca share senior authorship in this report. Address reprint requests to Dr. M.A. Gonzalez-Gay, Rheumatology Division, Hospital Xeral-Calde, c) Dr. Ochoa s/n, 27004 Lugo, Spain. E-mail: miguelaggay@hotmail.com Accepted for publication January 24, 2005. |