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THU0090 Cardiovascular Morbidity in Patients with Ankylosing Spondylitis: A Population-Based Cohort Study
  1. I. Essers1,2,3,
  2. C. Stolwijk1,2,3,
  3. A. van Tubergen1,2,
  4. A. Boonen1,2,
  5. M.L. De Bruin3,
  6. M. Bazelier3,
  7. F. de Vries2,3,4,5
  1. 1Rheumatology, Maastricht University Medical Center
  2. 2School for Care and Public Health Research Institute (CAPHRI), Maastricht University, Maastricht
  3. 3Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, Netherlands
  4. 4MRC Lifecourse Epidemiology Unit, Southampton General Hospital, Southampton, United Kingdom
  5. 5Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Center, Maastricht, Netherlands


Background It is well recognized that rheumatoid arthritis is an independent risk factor for cardiovascular (CV) disease. For ankylosing spondylitis (AS), the literature on this risk is relatively scarce, and shows conflicting results. Furthermore, these studies did not explore the role of non-steroidal anti-inflammatory drugs (NSAIDs) use.

Objectives To examine the incidence and risk of ischemic heart disease (IHD) and acute myocardial infarction (AMI) in patients with AS compared with population-based controls, and explore the role of recent NSAID use.

Methods All incident patients with AS from the UK Clinical Practice Research Datalink (1987-2012) were matched with up to 7 persons without AS by year of birth, sex and practice. Incidence rates, cumulative incidence rates and hazard ratios (HR) for the development of IHD and AMI were calculated, with time-varying adjustments for age, sex, comorbidity and drug use. When further exploring the role of NSAIDs on the risk of IHD, patients with AS were stratified according to the use of coxibs, naproxen or other traditional NSAIDs in the previous 3 months.

Results In total, 3,809 patients with AS (mean age at index date 43.7 years, 70.5% male, median duration of follow-up 6.6 years) were matched with 26,197 control subjects. At baseline, 4.3% of the patients had IHD compared with 3.4% of the controls (p-value<0.01), and 1.8% of the patients had AMI compared with 1.4% of the controls (p-value=0.02). After excluding patients with IHD and/or AMI at baseline, the incidence rates were 1.2/1000 person years (pys) and 0.9/1000 pys for IHD and AMI, respectively. The age-gender adjusted (adj.) HR of developing IHD was 1.2 (95% Confidence interval [CI] 1.0-1.5), and for AMI 0.9 (95% CI 0.7-1.3). After statistical adjustment for recent use of NSAIDs, the increased risk of IHD disappeared (adj. HR 1.1 95% CI 0.9-1.3). In the fully adjusted model, the risk remained almost unchanged (adj. HR 1.0, 95% CI 0.8-1.3). In patients with AS, stratification according to the use of coxibs, naproxen or other NSAIDs, showed that exposure to NSAIDs other than naproxen or coxibs increased the risk of IHD to 1.5 (95% CI 1.1-2.1) compared with controls irrespective of their NSAID use. However, within patients with AS this risk was not different from AS patients who did not use NSAIDs other than naproxen or coxibs (p=0.17).

Conclusions Patients with AS seemed at increased risk of developing IHD, but this effect could be attributed to their recent NSAID use. Although it cannot be excluded that NSAID use is (partly) a reflection of disease activity, rheumatologists should carefully balance the beneficial effects of NSAIDs and the increased risk of IHD.

Disclosure of Interest : None declared

DOI 10.1136/annrheumdis-2014-eular.1853

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