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SAT0102 Stem Cell Augmentation for Cardiovascular Risk in Rheumatoid Arthritis with Olmesartan: Star-O Study
  1. A. Syngle1,
  2. N. Garg2,
  3. P. Krishan2
  1. 1Cardio Rheuma, Healing Touch City Clinic, Chandigarh and Rheumatologist Fortis Multi Speciality Hospital, Mohali, India., Chandigarh
  2. 2Department of Pharmaceutical Sciences & Drug Research, Punjabi University, Patiala, India

Abstract

Background Cardiovascular disease remains the leading cause of mortality in rheumatoid arthritis (RA). Endothelial progenitor cells (EPCs) are depleted and contribute to increased cardiovascular (CV) risk in RA.1 Olmesartan exerts a protective cardiovascular effect in diabetes by augmenting EPCs.2 However, this vasculoprotective effect of olmesartan has not yet been investigated in RA.

Objectives To investigate the impact of olmesartan on circulating endothelial progenitor cell population in RA.

Methods Forty RA patients fulfilling the 2010 Rheumatoid Arthritis classification criteria were randomized to receive 24 weeks of treatment with olmesartan (10mg/day, n=20) or placebo (n=20) as an adjunct to existing stable antirheumatic drugs. EPCs (CD34+/CD133+) were quantified by Flow cytometry. Flow mediated dilatation (FMD) was assessed by AngioDefender™ (Everest Genomic Ann Arbor, United States). Inflammatory measures included DAS28, CRP, ESR, pro-inflammatory cytokines (TNF-α, IL-6 and IL-1), serum nitrite and adhesion molecules (ICAM-1 and VCAM-1) at baseline and after 24 weeks treatment.

Results At baseline, inflammatory measures, pro-inflammatory cytokines, adhesion molecules and nitrite levels were elevated and EPCs and endothelial function were impaired among both groups. EPCs significantly 0.018±0.001 to 0.031±0.001 increased p<0.01 after treatment with olmesartan but did not show significant change with placebo 0.019±0.001 to 0.022±0.001, p=0.14. After 24 weeks of treatment, FMD improved significantly from (5.2±1.4 to 9.0±1.10, p=0.01) as compared to placebo (p=0.47) group. Olmesartan significantly decreased systolic/diastolic blood pressure (mean difference, -7.5/-1.6, p=0.01) as compared with placebo (mean difference, -4.1/-1.2, p>0.05). After 24 weeks: inflammatory measures DAS28, ESR, CRP (All p=0.01) and nitrite (p=0.03) were significantly reduced after treatment with olmesartan. Proinflammatory cytokines TNF-α, IL-6 and VCAM-1 significantly (p=0.38, p=0.02 and 0.01 respectively) reduced in olmesartan group. Significant negative correlation was observed between EPCs and CRP (Fig. 1A), TNF- α (Fig. 1B), IL-6, VCAM-1 (Fig. 1D) and FMD (Fig. 1C) after treatment with olmesartan.

Conclusions First study to show that olmesartan improves inflammation, EPC biology and endothelial dysfunction in RA possibly through its anti-inflammatory effect via inhibition of proinflammatory cytokines. This anti-inflammatory effect may be of therapeutic relevance in RA.

References

  1. Grisar J et al. Circulation. 2005;111:204-211.

  2. Bahlmann FH et al. Hypertension. 2005;45:526-29

Acknowledgements This study was supported by Research Grant from Universal Grant Commission, New Delhi [F. No.41-725/2012 (SR)].

Disclosure of Interest None declared

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