Current limitations in the management of cardiovascular risk in rheumatoid arthritis.
ABSTRACT Rheumatoid arthritis (RA) is associated with excess cardiovascular (CV) disease. Many studies have shown subclinical atherosclerosis in RA is associated with CV risk factors and inflammation. Their relationship with CV events has however received less attention. Furthermore, except for hypertension CV risk factor management has not been examined in a UK RA population. We therefore evaluated the contribution of RA specific and CV risk factors to CV events alongside the management of CV risk factors in RA patients.
We assessed the prevalence, screening and treatment of CV risk factors in a cross-sectional survey of RA patients consecutively attending specialist clinics. We used binary logistic regression to examine relationships between CV events and RA and CV risk factors.
We enrolled 309 patients (81% female; median age 60 years; median disease duration 8 years). 27 (9%) had previous CV events. 56% had hypertension, 42% hyperlipidaemia, 11% diabetes, 52% were ex/current smokers and 26% obese. Lipid status was unknown in one third. 47% of patients on anti-hypertensive agents were undertreated. CV events were associated with hyperlipidaemia (OR 13.5; 95% CI 3.9, 45.9), hypertension (OR 6.4; 95% CI 1.9, 21.9), having ever smoked (OR 2.7; 95% CI 1.1, 6.5), RA duration (OR 1.09; 95% CI 1.06, 1.13) and erosions (OR 2.9; 95% CI 1.1, 8.2).
CV events are prevalent in RA. They are associated with CV risks and RA factors. Despite this burden we found CV risk factors were inadequately managed. A robust system to identify and treat CV risks in RA is required.
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ABSTRACT: Rheumatic diseases are associated with an increased risk of cardiovascular (CV) mortality attributed to a higher incidence of heart failure (HF) and ischemic heart disease. Although traditional CV risk factors contribute to the increased incidence seen in this population, by themselves they do not account for the increased risk; in fact, obesity and hyperlipidemia may play a paradoxic role. Immune-mediated mechanisms and chronic inflammation likely play a role in the pathogenesis of CV disease in patients with rheumatic diseases. The usual clinical features of ischemic heart disease and HF are less likely to be seen in this patient population.Heart Failure Clinics 04/2014; 10(2):339-352. · 1.41 Impact Factor
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ABSTRACT: BACKGROUND: Rheumatoid arthritis (RA) is a systemic inflammatory condition associated with increased cardiovascular risk. This is not fully explained by traditional risk factors, but direct vascular inflammation and aortic stiffening may play a role. We hypothesised that patients with RA exhibit aortic inflammation, which can be reversed with anti-tumour necrosis factor alpha (TNF-α) therapy, and correlates with aortic stiffness reduction. METHODS AND RESULTS: Aortic inflammation was quantified in 17 patients with RA, before and after eight weeks of anti-TNF-α therapy, using (18)F-fluoro-deoxyglucose positron emission tomography ((18)F-FDG-PET) with CT co-registration. Concomitantly, 34 patients with stable cardiovascular disease (CVD) were imaged as positive controls at baseline. Aortic FDG target to background ratios (TBR) and aortic pulse wave velocity (aPWV) were assessed. RA patients had higher baseline aortic TBR compared to CVD patients (2.02±0.22 v. 1.74±0.22, P=0.0001). Following therapy, aortic TBR fell to 1.90±0.29, P=0.03 and the proportion of inflamed aortic slices (defined as TBR>2.0) decreased from 50±33% to 33±27%, P=0.03. Also, TBR in the most diseased segment of the aorta fell from 2.51±0.33 to 2.05±0.29, P<0.0001. Treatment also reduced aPWV significantly (from 9.09±1.77 to 8.63±1.42 m/s, P=0.04), which correlated with the reduction of aortic TBR (R=0.60, P=0.01). CONCLUSIONS: This study demonstrates, that RA patients have increased aortic 18F-FDG uptake in comparison to stable CVD patients. Anti-TNF-α therapy reduces aortic inflammation in patients with RA, and this effect correlates with the fall in aortic stiffness. These results suggest that RA patients exhibit a sub-clinical vasculitis, which provides a mechanism for the increased CVD risk seen in RA.Circulation 10/2012; · 14.95 Impact Factor