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Arthritis Research and Therapy

, 13:R131

First Online: 15 August 2011Received: 22 December 2010Revised: 18 May 2011Accepted: 15 August 2011


IntroductionCo-morbidity and mortality due to cardiovascular disease CVD are increased in patients with rheumatoid arthritis RA. Most published studies in this field are retrospective or cross sectional. We investigated the presence of traditional and disease related risk factors for CVD at the onset of RA and during the first five years following diagnosis. We also evaluated their potential for predicting a new cardiovascular event CVE during the five-year follow-up period and the modulatory effect of pharmacological treatment.

MethodsAll patients from the four northern-most counties of Sweden with early RA are, since December 1995, consecutively recruited at diagnosis T0 into a large survey on the progress of the disease. Information regarding cardiovascular co-morbidity and related predictors was collected from clinical records and supplemented with questionnaires. By April 2008, 700 patients had been included of whom 442 patients had reached the five-year follow-up T5.

ResultsAmong the 442 patients who reached T5 during the follow-up period, treatment for hypertension increased from 24.5 to 37.4% P < 0.001, diagnosis of diabetes mellitus DM from 7.1 to 9.5% P < 0.01 whilst smoking decreased from 29.8 to 22.4% P < 0.001 and the BMI from 26.3 to 25.8 P < 0.05, respectively. By T5, 48 patients had suffered a new CVE of which 12 were fatal. A total of 23 patients died during the follow-up period. Age at disease onset, male sex, a previous CVE, DM, treatment for hypertension, triglyceride level, cumulative disease activity area under the curve AUC disease activity score DAS28, extra-articular disease, corticosteroid use, shorter duration of treatment with disease modifying anti-rheumatic drugs DMARDs and use of COX-2 inhibitors increased the hazard rate for a new CVE. A raised erythrocyte sedimentation rate ESR at inclusion and AUC DAS28 at six months increased the hazard rate of CVE independently whilst DMARD treatment was protective in multiple Cox extended models adjusted for sex and CV risk factors. The risk of a CVE due to inflammation was potentiated by traditional CV risk factors.

ConclusionsThe occurrence of new CV events in very early RA was explained by traditional CV risk factors and was potentiated by high disease activity. Treatment with DMARDs decreased the risk. The results may have implications for cardio-protective strategies in RA.

AbbreviationsACPAantibodies against cyclic citrullinated peptides-proteins

anti-CCPanti-cyclic citrullinated peptid

ANAanti-nuclear antibodies

AUCarea under the curve

BMIbody mass index

CABGcoronary artery bypass grafting


CRPC-reactive protein


CVDcardiovascular disease

CVEcardiovascular event

DAS28disease activity score

DMdiabetes mellitus

DMARDdisease-modifying anti-rheumatic drug

DVTdeep vein thrombosis

EADextra-articular disease

ELISAenzyme-linked immunoassays

ESRerythrocyte sedimentation rate

HAQHealth Assessment Questionnaire

HDLhigh-density lipoprotein

HLAhuman leucocyte antigen

HRhazard ratio

MImyocardial infarction

NSAIDnon-steroidal anti-inflammatory drugs

PEpulmonary embolism

PTPN22protein tyrosine phosphatise nonreceptor type 22

RArheumatoid arthritis

RFrheumatoid factor

SEshared epitope

TIAtransient ischaemic attack

VASvisual analogous scale

WHOWorld Health Organization.

Electronic supplementary materialThe online version of this article doi:10.1186-ar3442 contains supplementary material, which is available to authorized users.

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Autor: Lena Innala - Bozena Möller - Lotta Ljung - Staffan Magnusson - Torgny Smedby - Anna Södergren - Marie-Louise Öhman - So


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