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Serum uric Acid predicts declining of circulating proangiogenic mononuclear progenitor cells in chronic heart failure patients.

Berezin AE, Kremzer AA, Samura TA, Berezina TA, Martovitskaya YV - J Cardiovasc Thorac Res (2014)

Bottom Line: 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.We suggest that even mild elevations of SUA might be used to predict of relative depletion of proangiogenic MPCs among chronic HF patients.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Medical University, Internal Medicine 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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Mentions: The predictive value of SUA level with respect to the MPCs with phenotypes CD14+CD309+ and CD14+CD309+Tie2+in the patients with CHF was performed using ROC-analysis, the results of which are presented in Figure 1. SUA demonstrated a high predictive value for declining both MPC phenotypes (CD14+CD309+ and CD14+CD309+Tie2+)in CHF patients. The estimated areas under the curves (AUC) were 0.631 (sensitivity= 63.9%; specificity= 56.2%) for CD14+CD309+ cells and 0.687 (sensitivity= 72.2%; specificity= 52.9%) for CD14+CD309+Tie2+ cell population. The cut-off value for the SUA level that predicted the cell loss best in both models was 31.5 mmol/L. Of all the variables (SUA, eGFR, BMI, LVEF, NYHA, diuretics, and T2DM) included in our multivariate model, SUA was the strongest predictor of proangiogenic MPCs depletion. However, the addition of SUA over cut-off point 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 (Table 5). For category-free NRI, 16% of events (P=0.001) and 19% of non-events (P=0.0001) were correctly reclassified by the addition of SUA to the ABC model for depletion of CD14+CD309+ cells (Table 6). When we added Q4 SUA to the ABC model, 18% of events (P=0.001) and 24% of non-events (P=0.0012) were reclassified for depletion of CD14+CD309+Tie2+cells. Thus, these data suggest that elevation of SUA might be considered a predictor of proangiogenic MPCs loss in patients with CHF.


Serum uric Acid predicts declining of circulating proangiogenic mononuclear progenitor cells in chronic heart failure patients.

Berezin AE, Kremzer AA, Samura TA, Berezina TA, Martovitskaya YV - J Cardiovasc Thorac Res (2014)

© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4195965&req=5

Mentions: The predictive value of SUA level with respect to the MPCs with phenotypes CD14+CD309+ and CD14+CD309+Tie2+in the patients with CHF was performed using ROC-analysis, the results of which are presented in Figure 1. SUA demonstrated a high predictive value for declining both MPC phenotypes (CD14+CD309+ and CD14+CD309+Tie2+)in CHF patients. The estimated areas under the curves (AUC) were 0.631 (sensitivity= 63.9%; specificity= 56.2%) for CD14+CD309+ cells and 0.687 (sensitivity= 72.2%; specificity= 52.9%) for CD14+CD309+Tie2+ cell population. The cut-off value for the SUA level that predicted the cell loss best in both models was 31.5 mmol/L. Of all the variables (SUA, eGFR, BMI, LVEF, NYHA, diuretics, and T2DM) included in our multivariate model, SUA was the strongest predictor of proangiogenic MPCs depletion. However, the addition of SUA over cut-off point 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 (Table 5). For category-free NRI, 16% of events (P=0.001) and 19% of non-events (P=0.0001) were correctly reclassified by the addition of SUA to the ABC model for depletion of CD14+CD309+ cells (Table 6). When we added Q4 SUA to the ABC model, 18% of events (P=0.001) and 24% of non-events (P=0.0012) were reclassified for depletion of CD14+CD309+Tie2+cells. Thus, these data suggest that elevation of SUA might be considered a predictor of proangiogenic MPCs loss in patients with CHF.

Bottom Line: 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.We suggest that even mild elevations of SUA might be used to predict of relative depletion of proangiogenic MPCs among chronic HF patients.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Medical University, Internal Medicine 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.

No MeSH data available.


Related in: MedlinePlus