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Extended report
Systemic inflammation in patients with inflammatory joint diseases does not influence statin dose needed to obtain LDL cholesterol goal in cardiovascular prevention
  1. S Rollefstad1,
  2. E Ikdahl1,
  3. J Hisdal2,
  4. T K Kvien1,3,
  5. T R Pedersen3,4,
  6. I Holme5,
  7. A G Semb1
  1. 1Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway
  2. 2Section of Vascular Investigations, Oslo Vascular Centre, Oslo University Hospital Aker, Oslo, Norway
  3. 3Faculty of Medicine, University of Oslo, Oslo, Norway
  4. 4Centre of Preventive Medicine, Oslo University Hospital, Ullevaal, Oslo, Norway
  5. 5Department of Biostatistics, Epidemiology and Health Economics, Oslo University Hospital, Ullevaal, Oslo, Norway
  1. Correspondence to Dr S Rollefstad, Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet Hospital, P.O. Box 23 Vinderen, Oslo NO-0319, Norway; s-rollef{at}diakonsyk.no, s.c.h.rollefstad{at}medisin.uio.no

Abstract

Objectives There is a lipid paradox in rheumatoid arthritis describing that despite low lipids related to systemic inflammation, there is an increased cardiovascular (CV) risk. Our aim was to evaluate if baseline lipid levels or baseline systemic inflammation were associated with the statin dose sufficient to achieve lipid targets in patients with inflammatory joint diseases.

Methods In this longitudinal, short-term follow-up observational report, we evaluated 197 patients who did and 36 patients who did not reach the recommended low density lipoprotein cholesterol (LDL-c) target. The patients were, after CV risk evaluation, classified to either primary or secondary CV prevention with lipid lowering treatment (LLT). LLT was initiated with statins and adjusted until at least two lipid targets were achieved. Intensive LLT was defined as rosuvastatin ≥20 mg, atorvastatin and simvastatin at the highest dose (80 mg), and conventional LLT were defined as all lower doses.

Results In an independent sample t test, systemic inflammation or lipid levels at baseline were not associated with the statin dose (intensive or conventional) needed to achieve recommended LDL-c target (C reactive protein/erythrocyte sedimentation rate: p=0.10 and p=0.11, and LDL-c/total cholesterol: p=0.17 and p=0.34, respectively). The baseline inflammatory status and lipid levels in patients who did and did not obtain LDL-c goal were comparable (C reactive protein/erythrocyte sedimentation rate: p=0.32 and p=0.64, and LDL-c/total cholesterol: p=0.20 and p=0.83, respectively).

Conclusions Systemic inflammation or lipid levels did not influence the intensity of statin treatment needed to obtain guideline recommended lipid targets in CV prevention. Whether the background inflammation in patients with inflammatory joint diseases over time influences the CV risk reduction related to statins is yet unknown.

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