Disease Markers

Disease Markers / 2010 / Article

Open Access

Volume 28 |Article ID 212509 | 14 pages | https://doi.org/10.3233/DMA-2010-0690

Coincidence of Moderately Elevated N-Terminal Pro–B-Type Natriuretic Peptide, Endothelial Progenitor Cells Deficiency and Propensity to Exercise-Induced Myocardial Ischemia in Stable Angina

Received25 Mar 2010
Accepted25 Mar 2010

Abstract

Aim: To assess endothelial progenitor cells (EPC) counts, a novel prognostic marker, in relation to classical adverse outcome predictors–N-terminal pro–B-type natriuretic peptide (NT-proBNP), impaired left ventricular (LV) relaxation and exercise-induced ischemia–in stable coronary artery disease (CAD) with preserved LV systolic function.Methods: We studied 30 non-diabetic men with one-vessel CAD, LV ejection fraction ≥ 60% and normal LV diastolic function (n = 16) or impaired LV relaxation (by ultrasound including tissue Doppler) (n = 14), and 14 non-CAD controls matched for risk profile and medication. CD34+/kinase-insert domain receptor (KDR)+ cells (CD34+/KDR+ cells), a leukocytes subpopulation enriched for EPC, were enumerated by flow cytometry.Results: CAD patients with abnormal LV relaxation exhibited significantly elevated NT-proBNP and decreased CD34+/KDR+ cells vs. CAD with regular diastolic function and non-CAD controls. An inverse NT-proBNP–CD34+/KDR+ cells relationship was precipitated by the clustering of high resting NT-proBNP and low CD34+/KDR+ cells in the subjects with a lower Duke treadmill score.Conclusions: Propensity to symptomatic exertional ischemia may underlie the coincidence of moderately elevated NT-proBNP and EPC deficiency in stable angina. Additionally, chronic subclinical ischemia can also be involved in these associations. These might result from BNP overexpression in the ischemic myocardium and a hypothetical exhaustion of the bone marrow capacity to mobilize EPC at multiple ischemic episodes, thus contributing to NT-proBNP prognostic effect irrespective of hemodynamic factors.

Copyright © 2010 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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