Abstract
BackgroundThe aim was to estimate the impact of individual risk factors and treatment with various disease-modifying antirheumatic drugs (DMARDs) on the incidence of myocardial infarction (MI) in patients with rheumatoid arthritis (RA).MethodsWe analysed data from 11,285 patients with RA, enrolled in the prospective cohort study RABBIT, at the start of biologic (b) or conventional synthetic (cs) DMARDs. A nested case–control study was conducted, defining patients with MI during follow-up as cases. Cases were matched 1:1 to control patients based on age, sex, year of enrolment and five cardiovascular (CV) comorbidities. Generalized linear models were applied (Poisson regression with a random component, conditional logistic regression).ResultsIn total, 112 patients developed an MI during follow-up. At baseline, during the first 6 months of follow-up and prior to the MI, inflammation markers (erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)) but not 28-joint-count disease activity score (DAS28) were significantly higher in MI cases compared to matched controls and the remaining cohort. Baseline treatment with DMARDs was similar across all groups. During follow-up bDMARD treatment was significantly more often discontinued or switched in MI cases. CV comorbidities were significantly less often treated in MI cases vs. matched controls (36 % vs. 17 %, p < 0.01). In the adjusted regression model, we found a strong association between higher CRP and MI (OR for log-transformed CRP at follow-up: 1.47, 95 % CI 1.00; 2.16). Furthermore, treatment with prednisone ≥10 mg/day (OR 1.93, 95 % CI 0.57; 5.85), TNF inhibitors (OR 0.91, 95 % CI 0.40; 2.10) or other bDMARDs (OR 0.85, 95 % CI 0.27; 2.72) was not associated with higher MI risk.ConclusionsCRP was associated with risk of MI. Our results underline the importance of tight disease control taking not only global disease activity, but also CRP as an individual marker into account. It seems irrelevant with which class of (biologic or conventional) DMARD effective control of disease activity is achieved. However, in some patients the available treatment options were insufficient or insufficiently used - regarding DMARDs to treat RA as well as regarding the treatment of CV comorbidities.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1077-z) contains supplementary material, which is available to authorized users.
Highlights
The aim was to estimate the impact of individual risk factors and treatment with various diseasemodifying antirheumatic drugs (DMARDs) on the incidence of myocardial infarction (MI) in patients with rheumatoid arthritis (RA)
Between 1 May 2001 and 31 October 2013, a total of 11,285 patients were enrolled into the Rheumatoid Arthritis: Observation of Biologic Therapy (RABBIT) register (Fig. 1)
They were matched to controls with heart failure but were allowed to differ from their corresponding case in no more than two comorbidities
Summary
The aim was to estimate the impact of individual risk factors and treatment with various diseasemodifying antirheumatic drugs (DMARDs) on the incidence of myocardial infarction (MI) in patients with rheumatoid arthritis (RA). In rheumatoid arthritis (RA), increased morbidity and mortality due to myocardial infarctions (MI) cannot entirely explained by traditional cardiovascular (CV) risk factors [1,2,3]. A recent meta-analysis of studies investigating single nucleotide polymorphisms (SNPs) hypothesized a causal role of the IL6R-gene signalling via the inflammatory markers CRP and fibrinogen in the development of coronary heart disease (CHD) [10]. Global disease activity might not be sensitive enough in patients at increased risk of MI. Observational studies, on the other hand, should be suitable to investigate risk factors for MI. Comparisons between patients with RA who develop MI and the rest of the cohort are difficult to interpret in observational studies, due to significant differences in age, sex and CV comorbidities [12, 19]
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