Submitted: 23 Jun 2014
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J Cardiovasc Thorac Res. 2014;6(3):153-162.
doi: 10.15171/jcvtr.2014.004
PMID: 25320662
PMCID: PMC4195965
  Abstract View: 771
  PDF Download: 1353

Original Article

Serum Uric Acid Predicts Declining of Circulating Proangiogenic Mononuclear Progenitor Cells in Chronic Heart Failure Patients

Alexander E. Berezin 1 * , Alexander A. Kremzer 2, Tatyana A. Samura 2, Tatyana A. Berezina 3, Yulia V. Martovitskaya 4

1 State Medical University, Internal Medicine Department, Zaporozhye, Ukraine
2 State Medical University, Clinical Pharmacology Department, Zaporozhye, Ukraine
3 Privat Medical center “Vitacenter”, Zaporozhye, Ukraine
4 State Medical University, Pathology Department, Zaporozhye, Ukraine

Abstract

Introduction: Serum uric acid (SUA) is considered a marker for natural progression of chronic heart failure (CHF) mediated cardiovascular remodelling. CHF associates with declining of circulating mononuclear progenitor cells (MPCs). The objective of this study was to evaluate the interrelationship between SUA concentrations and proangiogenic MPCs in ischemic CHF patients. Methods: The study population was structured retrospectively after determining the coronary artery disease (CAD) by contrast-enhanced spiral computed tomography angiography in 126 subjects with symptomatic ischemic mild-to-severe CHF and 128 CAD subjects without CHF. Baseline biomarkers were measured in all patients. Cox proportional multivariate hazard ratio was calculated for predictors of MPCs declining in both CHF and non-CHF patient population predictors of MPCs declining in CHF subjects were examined in stepwise logistic regression. C-statistics, integrated discrimination indices (IDI) and net-reclassification improvement were utilized for prediction performance analyses. Results: Cox proportional adjusted hazard ratio analyses for CD14+CD309+ and CD14+CD309+Tie2+ MPCs by SUA has shown that the higher quartiles (Q3 and Q4) of SUA compared to the lower quartiles (Q1 and Q2) are associated with increased risks of depletion of both CD14+CD309+ and CD14+CD309+Tie2+ MPCs. The addition of Q4 SUA to the ABC model improved the relative IDI by 13.8% for depletion of CD14+CD309+ MPCs and by 14.5% for depletion of CD14+CD309+Tie2+ MPCs. Conclusion: Circulating levels of proangiogenic MPCs are declined progressively depending on the levels of SUA in the HF subjects with CHF. We suggest that even mild elevations of SUA might be used to predict of relative depletion of proangiogenic MPCs among chronic HF patients.
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