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Subclinical Atherosclerosis in Patients with Psoriatic Arthritis To the Editor: In the May 2008 issue, Eder, et al reported the presence of subclinical atherosclerosis, determined by high-resolution carotid ultrasonography, in 40 unselected patients diagnosed with psoriatic arthritis (PsA)1. The authors concluded that subclinical atherosclerosis in PsA may not be attributed solely to the presence of traditional cardiovascular (CV) risk factors1. We entirely agree with this assumption. In this regard, in 2007 we described the presence of endothelial dysfunction, considered as an early development in the atherogenesis process2, in patients with PsA without previous history of CV events or traditional CV risk factors3. More important, using high-resolution carotid ultrasonography, in the same year we found evidence of subclinical atherosclerosis, manifested by increased carotid intima-media thickness, in 59 PsA patients without history of CV events or traditional CV risk factors compared to matched controls4. Although it is now clear that rheumatoid arthritis (RA) is associated with accelerated atherosclerosis and increased CV mortality5, information about PsA is still limited. However, epidemiologic studies performed by highly experienced investigators support that CV is one of the leading causes of death in PsA patients6,7. A remaining question regards the increased incidence of subclinical atherosclerosis observed in PsA patients without traditional CV risk factors3,4. In RA this may be explained by the persistence of a chronic inflammatory status. An association between the mean values of C-reactive protein in patients with longstanding RA without classic CV risk factors and the presence of subclinical atherosclerosis was found8. Pathogenic mechanisms similar to those leading to accelerated atherosclerosis in RA, in particular the presence of chronic inflammation, may possibly account for the development of subclinical atherosclerosis in PsA. In keeping with that, we also observed a positive association between the duration of PsA and the presence of subclinical atherosclerosis4. Based on these considerations, we feel that patients with PsA must now be considered as individuals who are at high risk for CV events. MIGUEL A. GONZALEZ-GAY, MD, PhD; TOMAS R. VAZQUEZ-RODRIGUEZ, MD, Rheumatology Division; CARLOS GONZALEZ-JUANATEY, MD, PhD, Cardiology Division, Hospital Xeral-Calde, Lugo; JAVIER LLORCA, MD, PhD, Division of Preventive Medicine and Public Health, School of Medicine, University of Cantabria, Santander, Spain. Address reprint requests to Dr. Gonzalez-Gay. E-mail: miguelaggay@hotmail.com 2. Gonzalez-Gay MA, Gonzalez-Juanatey C, Martin J. Inflammation and endothelial dysfunction in rheumatoid arthritis. Clin Exp Rheumatol 2006;24:115-7. [MEDLINE] 3. Gonzalez-Juanatey C, Llorca J, Miranda-Filloy JA, et al. Endothelial dysfunction in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:287-93. [MEDLINE] 4. Gonzalez-Juanatey C, Llorca J, Amigo-Diaz E, Dierssen T, Martin J, Gonzalez-Gay MA. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum 2007;57:1074-80. [MEDLINE] 5. Gonzalez-Gay MA, Gonzalez-Juanatey C, Martin J. Rheumatoid arthritis: a disease associated with accelerated atherogenesis. Semin Arthritis Rheum 2005;35:8-17. [MEDLINE] 6. Wong K, Gladman DD, Husted J, Long JA, Farewell VT. Mortality studies in psoriatic arthritis: results from a single outpatient clinic. I. Causes and risk of death. Arthritis Rheum 1997;40:1868-72. [MEDLINE] 7. Gladman DD, Farewell VT, Wong K, Husted J. Mortality studies in psoriatic arthritis: results from a single outpatient center. II. Prognostic indicators for death. Arthritis Rheum 1998;41:1103-10. [MEDLINE] 8. Gonzalez-Gay MA, Gonzalez-Juanatey C, Pineiro A, Garcia-Porrua C, Testa A, Llorca J. High-grade C-reactive protein elevation correlates with accelerated atherogenesis in patients with rheumatoid arthritis. J Rheumatol 2005;32:1219-23. [MEDLINE]
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