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Objective.Cardiovascular (CV) risk estimation calculators for the general population do not perform well in patients with rheumatoid arthritis (RA). An RA-specific risk calculator has been developed, but did not perform better than a risk calculator for the general population when validated in a heterogeneous multinational cohort.Methods.In a cohort of patients with new-onset RA from northern Sweden (n = 665), the risk of CV disease was estimated by the Expanded Cardiovascular Risk Prediction Score for Rheumatoid Arthritis (ERS-RA) and the American College of Cardiology/American Heart Association algorithm (ACC/AHA). The ACC/AHA estimation was analyzed, both as crude data and when adjusted according to the recommendations by the European League Against Rheumatism (ACC/AHA × 1.5). ERS-RA was calculated using 2 variants: 1 from patient and physician reports of hypertension (HTN) and hyperlipidemia [ERS-RA (reported)] and 1 from assessments of blood pressure (BP) and blood lipids [ERS-RA (measured)]. The estimations were compared with observed CV events.Results.All variants of risk calculators underestimated the CV risk. Discrimination was good for all risk calculators studied. Performance of all risk calculators was poorer in patients with a high grade of inflammation, whereas ACC/AHA × 1.5 performed best in the high-inflammatory patients. In those patients with an estimated risk of 5–15%, no risk calculator performed well.Conclusion.ERS-RA underestimated the risk of a CV event in our cohort of patients, especially when risk estimations were based on patient or physician reports of HTN and hyperlipidemia instead of assessment of BP and blood lipids. The performance of ERS-RA was no better than that of ACC/AHA × 1.5, and neither performed well in high-inflammatory patients.

Objective.This prospective followup study investigated subclinical atherosclerosis in relation to traditional cardiovascular disease (CVD) risk factors and inflammation in patients with rheumatoid arthritis (RA) recruited at diagnosis compared with controls.Methods.Patients diagnosed with early RA were consecutively recruited into a prospective study. From these, a subgroup aged ≤ 60 years (n = 71) was consecutively included for ultrasound measurement of intima-media thickness (IMT) and flow-mediated dilation (FMD) at inclusion (T0) and after 5 years (T5). Age- and sex-matched controls (n = 40) were also included.Results.In the Wilcoxon signed-rank test, both IMT and FMD were significantly aggravated at T5 compared to baseline in patients with RA, whereas only IMT was significantly increased in controls. In univariate linear regression analyses among patients with RA, the IMT at T5 was significantly associated with age, systolic blood pressure (BP), cholesterol, triglycerides, Systematic Coronary Risk Evaluation (SCORE), and Reynolds Risk Score at baseline (p < 0.05). Similarly, FMD at T5 was significantly inversely associated with age, smoking, systolic BP, SCORE, and Reynolds Risk Score (p < 0.05). A model with standardized predictive value from multiple linear regression models including age, smoking, BP, and blood lipids at baseline significantly predicted the observed value of IMT after 5 years. When also including the area under the curve for the 28-joint Disease Activity Score over 5 years, the observed value of IMT was predicted to a large extent.Conclusion.This prospective study identified an increased subclinical atherosclerosis in patients with RA. In the patients with RA, several traditional CVD risk factors at baseline significantly predicted the extent of subclinical atherosclerosis 5 years later. The inflammatory load over time augmented this prediction.

Background Patients with rheumatoid arthritis (RA) have an increased mortality and morbidity due to cardiovascular disease (CVD). Objectives In this prospective follow up over eleven years, we investigated the progression of atherosclerosis measured by intima media thickness (IMT), in relation to traditional CVD risk factors and inflammation, in patients with early RA compared to controls. Methods Patients from northern Sweden diagnosed with early RA are consecutively recruited into an ongoing prospective study. A subgroup aged ≤60 years (n=54) was consecutively included for ultrasound measurements of IMT of a. Carotis communis at inclusion (T0), and after 11 years (T11). 31 age-sex-matched controls were included. The patients were clinically assessed, SCORE, Reynolds Risk Score and Larsen score were calculated and blood samples drawn from all individuals at T0 and T11. Data and results presented in this abstract are preliminary. Results Patients with RA as well as controls had a significant aggravation in IMT over 11 years (0.52 at T0 and 0.68 at T11 in RA: p 0.05). The patients with RA had a significantly higher progression in IMT from T0 until T11 (0.16 vs 0.08, p Conclusions In this prospective study, the progression of sub-clinical atherosclerosis over 11 years was significantly higher in patients with RA than in controls. The IMT at T11 was associated with several traditional cardiovascular risk factors, as well as disease severity, at time of diagnosis. Disclosure of Interest None declared

ObjectivesPatients with rheumatoid arthritis (RA) have an increased mortality and morbidity due to cardiovascular disease (CVD). In this prospective 5-year follow up of patients with RA, we analysed several biomarkers, known to be associated with atherosclerosis and/or inflammation in the general population. The aim of this study was to find out whether the RA-disease per se affect these biomarkers and if those could be associated with the progression of atherosclerosis, as measured by intima media thickness (IMT) among patients with early RA.MethodsPatients from northern Sweden diagnosed with early RA, are consecutively recruited into an ongoing prospective study on CVD comorbidity. A subgroup of patients, aged ≤60 years (n = 71) was included for ultrasound measurements of IMT at inclusion (T0) and after 5 years (T5) together with age-sex-matched controls (n = 40). The patients were clinically assessed. Blood was analysed for lipids, ESR and CRP and several biomarkers known to be associated with atherosclerosis in the general population.ResultsAt T0, the patients with RA had significantly lower levels of MIF and significantly higher levels of interleukin (IL)-18 and MIC-1 compared with controls. At T5, the patients with RA had significantly higher levels of pentraxin3, MIC-1, TNF-R2, ICAM-1, VCAM-1 and endostatin compared with controls. At T0 the levels of MPO correlated with DAS28, sCD40L with CRP and IL-18 with systolic blood pressure and Reynolds risk score. Using PLSR on a CVD-panel analysed with multiplex immunoassay, the patients with RA could be correctly classified into those who had a worsening in their IMT over the five years or not. Here, MMP3 was identified as influential.ConclusionsThis study indicates that the RA disease itself could affect several of the biomarkers in this study, and possibly also the processes involved in the development of atherosclerosis.

Background: Patients with rheumatoid arthritis (RA) suffer from co-morbidities that contribute to a shortened lifespan. Inflammation is important for the development of cardiovascular disease, but little is known on its relationship with other co-morbidities. We investigated the role of inflammation for the development of new comorbidities in early RA. Methods: Since 1995, all patients with early RA in Northern Sweden are included in a prospective study on comorbidities, with a total of 950 patients being included. At the time for this study, 726 had been ill for >= 5 years. Data on co-morbidities, clinical and laboratory disease activity and pharmacological therapy were collected from patient records and further validated using a questionnaire at RA onset (T0) and after 5 years (T5). Results: Of the patients, 53.2 % of the patients had one or more co-morbidity at onset, the commonest being: hypertension (27.3 %), obstructive pulmonary disease (13.9 %), diabetes (8.0 %), hypothyroidism (6.3 %) and malignancy (5.0 %). After 5 years, 41.0 % had developed at least one new co-morbidity, the most common being: hypertension (15.1 %), malignancy (7.6 %), stroke/transient ischemic accident (5.1 %), myocardial infarction (4.3 %) and osteoporosis (3.7 %). Age at disease onset, a raised erythrocyte sedimentation rate (ESR) at inclusion, previous treatment with glucocorticoids (GC; p < 0.001 for all), extra-articular RA (Ex-RA; p < 0.01), DAS28 (area under the curve) at 24 months (p < 0.05), previous smoking at inclusion (p = 0.058) and male gender (p < 0.01) were associated with a new co-morbidity overall at T5. Treatment with biologics (p < 0.05) reduced the risk. In multiple logistic regression modelling, ESR (p = 0.036) at inclusion was associated with a new co-morbidity after 5 years, adjusted for age, sex, smoking and GC treatment. In a similar model, Ex-RA (p < 0.05) was associated with a new co-morbidity at T5. In a third model, adjusted for age and sex, a new pulmonary co-morbidity was associated with a smoking history at inclusion (p < 0.01), but not with ESR. Conclusion: There was substantial co-morbidity among early RA patients already at disease onset, with considerable new co-morbidity being added during the first five years. Measures of disease activity were associated with the occurrence of a new co-morbidity indicating that the inflammation is of importance in this context.

Systemic lupus erythematosus (SLE) is a chronic disease which can affect any organ, and the impact of the condition will affect each person differently. There are few qualitative studies including the experiences of both women and men with a diagnosis of SLE corresponding to the American College of Rheumatology (ACR) criteria where both negative and positive impacts of the disease have been presented. Purpose The aim was to describe how patients with established SLE experience their illness in everyday life, including both negative and positive aspects. Method Four focus group interviews were conducted with 16 women and three men with SLE according to ACR criteria, with varied disease activity and no or little organ damage. The interviews were tape recorded, transcribed verbatim and analysed using qualitative content analysis. Results Two themes emerged: multifaceted uncertainty contained the categories ‘an unreliable body’, ‘obtrusive pain and incomprehensible fatigue’, ‘mood changes and worries’, ‘reliance on medication and health care’; Focus on health and opportunities included ‘learning process implying personal strength’, ‘limitations and possibilities in activities and work’, ‘a challenge to explain and receive support’ and ‘living an ordinary life incorporating meaningful occupations’. Conclusions While we expected to find a mainly negative impact, positive aspects were also described. Our findings were complex and showed that patients with established SLE can experience both uncertainty and opportunities. This highlights the importance for healthcare professionals of gaining a better understanding of patients' uncertainty, to enable them to support patients, allowing them to focus on health and opportunities. Measurement instruments that capture different aspects of uncertainty and opportunities needs to be developed. Copyright © 2011 John Wiley & Sons, Ltd.

Objective. Lipoprotein-associated phospholipase A2 (Lp-PLA2), a marker of vascular inflammation, is associated with cardiovascular disease. This prospective study of an inception cohort aimed to investigate whether the level of Lp-PLA2 is associated with subclinical atherosclerosis in patients with rheumatoid arthritis (RA).Methods. Patients from northern Sweden diagnosed with early RA were consecutively recruited into an ongoing prospective study. From these, all patients ≤60 years (n=71) were included for measurements of subclinical atherosclerosis at inclusion (T0) and five years later (T5). Forty age- and sex-matched controls were included. The patients were clinically assessed, SCORE, Reynolds Risk Score, and Larsen score were calculated, and blood samples were drawn from all individuals at T0 and T5.Results. There was no significant difference in the level of Lp-PLA2 between patients with RA and controls (p>0.05). In simple linear regression models among patients with RA, Lp-PLA2 at T0 was significantly associated with intima media thickness (IMT) at T0 and T5, flow mediated dilation (FMD) at T0 and T5, ever smoking, male sex, HDL-cholesterol (inversely), non-HDL-cholesterol, SCORE, Reynolds Risk Score, and Larsen score (p<0.05).Conclusion. In this cohort of patients with early RA, the concentration of Lp-PLA2 was associated with both subclinical atherosclerosis and disease severity.

Objective: To analyse associations of two oestrogen receptor α (ORα) gene polymorphisms in 260 patients with SLE from northern Sweden. The two polymorphisms, PvuII T/C and the XbaI A/G, are located in the first intron of the ORα gene. Methods: All patients fulfilling at least four of the ACR criteria for SLE were consecutively recruited during one year. The SLEDAI score and SLICC damage index were recorded. 670 individuals from the same geographical area served as controls. DNA from the patients and controls was extracted and genotyped using the 5′ nuclease assay with an ABI PRISM 7900HT instrument. The genotype/phenotype relationships were calculated using SPSS. Results: The unusual PvuII C allele was associated with malar rash and the unusual XbaI G allele with photosensitivity (p = 0.001, OR = 2.53, 95% CI = 1.43 to 4.47 and p = 0.007, OR = 2.12, 95% CI = 1.22 to 3.66, respectively). The common XbaI AA genotype was associated with serositis (p = 0.013, OR = 1.92, 95% CI = 1.15 to 3.22). Based on the SLICC damage index associations of the common TT genotype and AA genotype with cognitive impairment were identified (p = 0.018, OR = 2.47, 95% CI = 1.17 to 5.25 and p = 0.018, OR = 2.75, 95% CI = 1.19 to 6.38 respectively). There was also an association of the XbaI AA genotype with the angina/coronary artery bypass variable (p = 0.042, OR = 2.58, 95% CI = 1.03 to 6.43). Of the variables describing disease severity and duration it was found that carriers of the unusual PvuII C allele showed a later onset of SLE (p = 0.02) and carriers of the unusual XbaI G allele a lower SLICC damage index. Conclusions: The unusual PvuII C and XbaI G alleles were associated with a milder form of SLE characterised by skin manifestations, later onset, and less organ damage.

The aim was to translate, test, and describe aspects of reliability and validity of the Fatigue Severity Scale (FSS) in Swedish (FSS-Swe) in patients with systemic lupus erythematosus (SLE).Patients with stable SLE, low or moderate disease activity, and low organ damage were included. Forward and back translations of the FSS were performed. Construct validity was tested with 32 women using a first Swedish translation. Feasibility, ceiling and floor effects, internal consistency, test-retest reliability, and content validity were tested on a slightly modified final version of the FSS-Swe in a non-selected group of patients (n = 23).There were correlations (por =0.05) between the FSS-Swe and overall disease activity according to the Systemic Lupus Activity Measure (SLAM) (r(s) = 0.48) and the SLAM Visual Analogue Scale (SLAM-VAS) (r(s) = 0.46); between the FSS-Swe and eight subscales of the Swedish 36-Item Medical Outcomes Study Short-Form Health Survey (SF-36) (r(s) = -0.41 to -0.65) and between the FSS-Swe and age (r(s) = -0.35). All patients answered all FSS-Swe questions at both test and retest. There was one ceiling effect in one question on one occasion. The Kolmogorov-Smirnov test indicated normal distribution. Cronbach's alpha was 0.94 and corrected item-to-total correlation exceeded 0.3. There were no significant systematic test-retest differences, and the median-weighted kappa coefficient was 0.75. Twenty patients understood the questions in FSS-Swe, 18 considered they were relevant, reflected their fatigue, and that none should be excluded. Five items were suggested to be included.The FSS-Swe supports construct validity, is feasible, has no important ceiling or floor effects, has satisfactory internal consistency, substantial test-retest reliability, and satisfactory content validity in the SLE patients studied. However, its sensitivity to change needs to be tested.

To analyze the association of the PD-1.3 polymorphism within the PDCD1 gene in patients with systemic lupus erythematosus (SLE) from the homogeneous population in northern Sweden. The PD-1.3A allele was analyzed in relation to disease manifestations and severity representing various phenotypes of SLE.The study group comprised 260 patients fulfilling at least 4 of the American College of Rheumatology (ACR) criteria for SLE during 1 year. The Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and the Systemic Lupus International Collaborating Clinics/ACR damage index scores were recorded. Population-based, randomly selected individuals (n = 670) from the same geographic area served as controls. DNA was extracted from blood samples from both patients and controls and was genotyped for the PD-1.3 A/G polymorphism, using an ABI Prism 7900HT Sequence Detection System.The frequency distribution of alleles, carriers, or genotypes did not differ between patients and controls. The PD-1.3A allele and carriage of the A allele were highly associated with renal disorder (ACR criterion 7) (P = 0.005, odds ratio [OR] 2.71 [95% confidence interval (95% CI) 1.32-5.55] and P = 0.012, OR 2.62 [95% CI 1.28-5.35], respectively). In regression analysis adjusted for sex and age at disease onset, carriage of the A allele remained significantly associated with renal disorder (P = 0.002, OR 3.54 [95% CI 1.56-8.01]). The presence of proteinuria, as measured by the SLEDAI score, and the presence of renal damage were also significantly associated with carriage of the A allele (P = 0.007, OR 3.88 [95% CI 1.44-10.47] and P = 0.021, OR 2.98 [95% CI 1.18-7.54], respectively).The PD-1.3A allele is associated with renal manifestations in SLE patients from northern Sweden but not with susceptibility to SLE per se.

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease caused by both genetic and environmental factors. Genome scans in families with SLE point to multiple potential chromosomal regions that harbor SLE susceptibility genes, and association studies in different populations have suggested several susceptibility alleles for SLE. Increased production of type I interferon (IFN) and expression of IFN-inducible genes is commonly observed in SLE and may be pivotal in the molecular pathogenesis of the disease. We analyzed 44 single-nucleotide polymorphisms (SNPs) in 13 genes from the type I IFN pathway in 679 Swedish, Finnish, and Icelandic patients with SLE, in 798 unaffected family members, and in 438 unrelated control individuals for joint linkage and association with SLE. In two of the genes--the tyrosine kinase 2 (TYK2) and IFN regulatory factor 5 (IRF5) genes--we identified SNPs that displayed strong signals in joint analysis of linkage and association (unadjusted P10(-7)) with SLE. TYK2 binds to the type I IFN receptor complex and IRF5 is a regulator of type I IFN gene expression. Thus, our results support a disease mechanism in SLE that involves key components of the type I IFN system.

Background Patients with rheumatoid arthritis (RA) suffer from comorbidities that contribute to a shortened lifespan. Inflammation is of importance for the development of cardiovascular disease, but little is known on its relationship with other comorbidities in RA. Objectives To examine the prevalence of comorbidities in early RA and the role of inflammation in this context. Methods All patients with early RA (symptom duration Results 53% had one or more comorbidities at RA onset. By then, the most common comorbidities were hypertension (26.3%), obstructive pulmonary disease (13.9%), diabetes (8.0%), hypothyroidism (6.3%) and malignancy (5.0%). After 5 years, 41% had developed at least one new comorbidity; most common were hypertension (15.1%), malignancy (7.8%), stroke/TIA (5.1%), myocardial infarction (4.3%) and osteoporosis (3.7%). Univariate regression analyses showed that age (p Conclusions There was substantial comorbidity among RA patients already at disease onset and considerable new comorbidity during the first five years of disease. Measures of disease activity were associated with occurrence of comorbidity. References Innala et al. Arthritis Res Ther 2011; 13: R131, Charlson et al. J Chron Dis, 1987; 40: 373-383, 25: 469-483, Norton et al. Rheumatol. 2013;52:99-110. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4651

Introduction: Disease activity, severity and comorbidity contribute to increased mortality in patients with rheumatoid arthritis (RA). We evaluated the impact of age at disease onset on prognostic risk factors and treatment in patients with early disease. Methods: In this study, 950 RA patients were followed regularly from the time of inclusion (

Background Patients with rheumatoid arthritis (RA) have an increased mortality and morbidity due to cardiovascular disease (CVD). Premature atherosclerosis can be measured by ultrasound of intima media thickness (IMT) and of flow-mediated dilation (FMD). In patients with RA of recent onset, we have found IMT and FMD to be similar as in controls at diagnosis. Objectives In this prospective 5-year follow up, we aimed to investigate for increased progression of atherosclerosis in the patients with early RA compared to the controls. We also aimed to analyze the relationship between IMT and FMD and traditional CVD risk factors as well as markers of inflammation. Methods Patients from northern Sweden diagnosed with early RA are consecutively recruited into a ongoing prospective study of co-morbidity. From these patients, a subgroup aged ≤60 years (n=71), was consecutively included for measurements of IMT of a. carotis communis and FMD of a. brachialis. The ultrasound measurements were taken at inclusion (T0) and after 5 years (T5). 40 age-sex matched controls were included. The patients were clinically assessed (DAS28, TJC, SJC, DMARDs) and blood was analysed for cholesterol, HDL-cholesterol, triglycerides, ESR and CRP. SCORE and Reynolds Risk Score were calculated at T0 and T5. Results Patients with RA had a significant aggravation in both IMT (0.52 at T0 and 0.58 at T5, p Conclusions After five years, the increase in subclinical atherosclerosis tended to be more evident among patients with early RA compared to the controls. Both traditional CVD risk factors as well as inflammatory load over time seems to contribute to this increased atherosclerotic findings among patients with RA. Disclosure of Interest None Declared

Background In the general population several inflammatory cytokines, for example pentraxin3 (ptx3), monocyte chemoattractant protein 1 (MCP-1), interleukin 6 (IL-6), TNF-receptor 1 (TNFR1), TNFR2, endoglin, VCAM and ICAM, have been found to be associated with an increased risk of cardiovascular disease (CVD). In most studies these biomarkers are elevated in patients with rheumatoid arthritis (RA), however they are not well studied with regard of the development of atherosclerosis among patients with RA. After five years of follow-up in patients with a recent onset of RA, we have found sub-clinical atherosclerosis, when measured as intima media thickness (IMT) and flow-mediated dilation (FMD), to be more progressive than in controls. Objectives The aim of the present study was to investigate whether this sub-clinical atherosclerosis in the patients with RA could be associated with cytokines associated with an increased risk of CVD. Methods Patients from northern Sweden diagnosed with early RA are followed in an ongoing prospective study of co-morbidity. From these patients a subgroup aged ≤60 years (n=71), was consecutively included for measurements of IMT of a. carotis communis and FMD of a. brachialis. 40 age/sex matched controls were included. The ultrasound measurements were taken at inclusion (T0) and after 5 years (T5). The patients were clinically assessed (DAS28, TJC, SJC, DMARDs, ESR and CRP) and blood was drawn from all individuals at T0 and T5 for analysis of cholesterol, HDL-cholesterol, triglycerides, ptx3, MCP-1, IL-6. At T5 also s-VCAM, s-ICAM, TNFR1, TNFR2 and endoglin were analysed. SCORE and Reynolds Risk Score were calculated at T0 and T5. Results At the follow up at 5 years, i.e. at T5, patients with RA had significantly higher levels of ptx3 (0.996 vs 0.69, p Conclusions The extent of atherosclerosis among patients with RA after 5 years follow-up was associated with the adhesion molecule s-ICAM. Moreover, several of the inflammatory cytokines associated with an increased risk of CVD in the general population were associated with conventional markers of disease activity among the patients with RA. Again, this emphasise the necessity of an optimal treatment of these patients, also for the prevention of co-morbidities like CVD. Disclosure of Interest None Declared

Background In the general population several serological biomarkers, for example phospholipase A2 group 7 (PLA2G7), macrophage inhibitory cytokine 1 (MIC-1), soluble CD40 ligand (sCD40L), myeloperoxidase (MPO) and interleukin 18 (IL-18), have been found to be associated with unstable atherosclerotic plaques and hence with an increased risk of cardiovascular disease (CVD). These biomarkers are not well studied among patients with rheumatoid arthritis (RA). After five years of follow-up in patients with a recent onset of RA, we have found sub-clinical atherosclerosis, when measured as intima media thickness (IMT) and flow-mediated dilation (FMD), to be more progressive than in controls. Objectives The aim of the present study was to investigate whether this sub-clinical atherosclerosis could be associated with serological biomarkers of unstable plaques. Methods Patients from northern Sweden diagnosed with early RA are followed in an ongoing prospective study of co-morbidity. From these patients a subgroup aged ≤60 years (n=71), was consecutively included for measurements of IMT of a. carotis communis and FMD of a. brachialis. The ultrasound measurements were taken at inclusion (T0) and after 5 years (T5). 40 age/sex matched controls were included. The patients were clinically assessed (DAS28, TJC, SJC, DMARDs, ESR and CRP) and blood was drawn from all individuals at T0 and T5 for analysis of cholesterol, HDL-cholesterol, triglycerides, PLA2G7, MIC-1, sCD40L, MPO and IL-18. SCORE and Reynolds Risk Score were calculated at T0 and T5. Larsen score was calculated on x-rays taken at inclusion. Results At inclusion as well after 5 years, i.e. at T0 and T5, patients with RA had significantly higher levels of MIC-1 (1773 vs. 1216 at T0 and 1941 vs 1331 at T5, p In the same simple regression models but after 5 years of follow up the biomarkers were significantly associated with other variables at T5: PLA2G7 with cholesterol, HDL-cholestrol (inversely), BMI and Reynolds Risk score at T5 (p Conclusions Among patients with RA, followed prospectively over 5 years, biomarkers of unstable plaques were associated with sub-clinical atherosclerosis as well as with traditional CVD risk factors and inflammation. This might, in part, clarify the increased risk of CVD among patients with RA. Disclosure of Interest None Declared

Introduction: Co-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. Methods: All 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). Results: Among 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. Conclusions: The 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.