BackgroundThere is accumulating evidence for an increased cardiovascular burden in inflammatory arthritis, but the true magnitude of this cardiovascular burden is still debated. We sought to determine the prevalence rate of non-fatal cardiovascular disease (CVD) in inflammatory arthritis, diabetes mellitus and osteoarthritis (non-systemic inflammatory comparator) compared to controls, in primary care.MethodsData on CVD morbidity (ICPC codes K75 (myocardial infarction), K89 (transient ischemic attack), and/or K90 (stroke/cerebrovascular accident)) from patients with inflammatory arthritis (n = 1,518), diabetes mellitus (n = 11,959), osteoarthritis (n = 4,040) and controls (n = 158,439) were used from the Netherlands Information Network of General Practice (LINH), a large nationally representative primary care based cohort. Data were analyzed using multi-level logistic regression analyses and corrected for age, gender, hypercholesterolemia and hypertension.ResultsCVD prevalence rates were significantly higher in inflammatory arthritis, diabetes mellitus and osteoarthritis compared with controls. These results attenuated - especially in diabetes mellitus - but remained statistically significant after adjustment for age, gender, hypertension and hypercholesterolemia for inflammatory arthritis (OR = 1.5 (1.2-1.9)) and diabetes mellitus (OR = 1.3 (1.2-1.4)). The association between osteoarthritis and CVD reversed after adjustment (OR = 0.8 (0.7-1.0)).ConclusionsThese results confirm an increased prevalence rate of CVD in inflammatory arthritis to levels resembling diabetes mellitus. By contrast, lack of excess CVD in osteoarthritis further suggests that the systemic inflammatory load is critical to the CVD burden in inflammatory arthritis.
ObjectiveTo evaluate the risk of cardiovascular disease in patients with rheumatoid arthritis exposed to glucocorticoids.MethodsRetrospective analysis of exposure to glucocorticoids in a prospective cohort of 353 patients with rheumatoid arthritis followed from June 2001 up to November 2011 for incident cardiovascular disease in a hospital-based outpatient cohort in the Netherlands. Hazard ratios with 95%-confidence intervals were calculated for the association between different types of exposure to glucocorticoids and incident cardiovascular disease. Associations were adjusted for demographics, cardiovascular risk factors and disease related parameters.ResultsRecent and current exposure to glucocorticoids were associated with incident cardiovascular disease, as was a longer duration of exposure and cumulative exposure to glucocorticoids. Adjustment for disease activity and severity negated the association.ConclusionIn observational studies the finding of incident cardiovascular disease in patients with rheumatoid arthritis exposed to glucocorticoids is strongly confounded by indication due to high disease activity. The adverse cardiovascular effects of glucocorticoids might be balanced by positive effects working through inflammation control.
Background Ankylosing spondylitis (AS) is associated with an increased cardiovascular risk that might be due to the chronic underlying inflammatory process. We investigated whether subclinical atherosclerosis of the carotid artery in patients with AS was reduced after antiinflammatory treatment with tumour necrosis factor (TNF) inhibitors in a prospective observational cohort study. Methods 67 out of 81 AS patients who used TNF inhibitors and underwent ultrasonography at baseline returned for follow-up after 4.9 years. Of all patients, 12 (15%) discontinued the use of TNF inhibitors. Assessments of medication use, AS-related factors and cardiovascular risk factors were measured at baseline and repeated at follow-up. B-mode carotid ultrasonography was used to investigate arterial wall parameters, including carotid intima-media thickness (cIMT) and Young's elastic modulus (YEM).Results After a median 4.9 years of follow-up, cIMT did not change significantly (paired t test +0.011 mm, p=0.561) in those who continued the use of TNF inhibitors, while cIMT increased substantially (+0.057 mm, p=0.069) in those who did not continue their use of TNF inhibitors. The effect of TNF inhibitors was mainly mediated by a subsequent decrease in AS disease activity. Vascular elasticity (as measured with YEM) did not change significantly in patients who discontinued TNF inhibitors or those who continued TNF inhibitors. Conclusions The use of TNF inhibitors might stabilise or slow down the progression of subclinical atherosclerosis in AS patients, reflecting a decreased cardiovascular risk in these patients.
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