Volume 1108, Issue 1 p. 349-358

Accelerated Atherosclerosis in Rheumatoid Arthritis

ZOLTÁN SZEKANECZ

ZOLTÁN SZEKANECZ

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

Dr. Szekanecz and Dr. Kerekes have equal contribution to this study so they are co-first authors.

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GYÖRGY KEREKES

GYÖRGY KEREKES

Cardiovascular Unit, Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

Dr. Szekanecz and Dr. Kerekes have equal contribution to this study so they are co-first authors.

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HENRIETT DÉR

HENRIETT DÉR

Cardiovascular Unit, Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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ZSUZSA SÁNDOR

ZSUZSA SÁNDOR

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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ZOLTÁN SZABÓ

ZOLTÁN SZABÓ

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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ANIKÓ VÉGVÁRI

ANIKÓ VÉGVÁRI

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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ENIKÖ SIMKOVICS

ENIKÖ SIMKOVICS

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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LILLA SOÓS

LILLA SOÓS

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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ÁGNES SZENTPÉTERY

ÁGNES SZENTPÉTERY

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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TIMEA BESENYEI

TIMEA BESENYEI

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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GABRIELLA SZÜCS

GABRIELLA SZÜCS

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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SÁNDOR SZÁNTÓ

SÁNDOR SZÁNTÓ

Division of Rheumatology, and Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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LÁSZLÓ TAMÁSI

LÁSZLÓ TAMÁSI

Department of Rheumatology, Szent Ferenc Hospital, Miskolc, Hungary

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GYULA SZEGEDI

GYULA SZEGEDI

Research Center for Autoimmune Diseases, Hungarian Academy of Sciences, Debrecen, Hungary

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YEHUDA SHOENFELD

YEHUDA SHOENFELD

Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel

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PÁL SOLTÉSZ

PÁL SOLTÉSZ

Cardiovascular Unit, Third Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary

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First published: 29 August 2007
Citations: 82
Address for correspondence: Zoltán Szekanecz, M.D., Ph.D., Third Department of Internal Medicine, Rheumatology Division, University of Debrecen, Medical and Health Science Center, Móricz Zs krt. 22., H-4004 Debrecen, Hungary. Voice: +36-52-314-091; fax: +36-52-414-489.
[email protected]

Abstract

Abstract: Cardiovascular disease is a leading cause of mortality in rheumatoid arthritis (RA). Endothelial dysfunction often precedes manifest atherosclerosis. Both traditional, Framingham risk factors and inflammation-associated factors are involved in RA-associated atherosclerosis. Among imaging techniques, the early determination of common carotid intima-media thickness (ccIMT), flow-mediated vasodilation (FMD), and nitroglycerine-mediated vasodilation (NMD) may be useful to determine atherosclerosis and endothelial dysfunction. We and others found increased ccIMT and impaired FMD in RA patients. Among immunological and metabolic laboratory markers, anticyclic citrullinated peptide (anti-CCP) antibodies, IgM rheumatoid factor, circulating immune complexes, pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), Th0/Th1 T cells, homocysteine, dyslipidemia, decreased folate and vitamin B12 production, and impaired paraoxonase activity may all be involved in the development of vascular disease in RA. The early diagnosis of endothelial dysfunction and atherosclerosis, active immunosuppressive treatment, the use of drugs that control atherosclerosis, changes in sedentary lifestyle, and the close follow-up of RA patients may help to minimize cardiovascular risk in these individuals.