Following an acute myocardial infarction (AMI), bone-marrow derived endothelial progenitor cells (EPC) are mobilised into the peripheral blood. Our aim was to examine the factors influencing this spontaneous cell mobilisation.
In this study we analysed 47 patients with extensive AMI (left ventricular ejection fraction [LVEF] < 50 % by echocardiography during the first week post-AMI); we studied the peripheral blood EPC populations expressing CD133+, CD34+, KDR+, CXCR4+, as well as the cytokines VEGF (vascular endothelial growth factor), SDF-1 (stromal cell-derived factor 1) and TSP-1 (thrombospondin 1), measured on day 5 ¡À 2.5 after AMI.
The extension of AMI (CPK peak) correlated with the number of CD133+ mobilised cells: (r = 0.40; P = .011). Patients who did not receive perfusion during the acute phase (34 % ) had more CD34+CXCR4+ cells with a median (interquartile ranges) of 2,401 (498-7,004) vs. 999 (100-1,600), P = .048, and strong correlations between VEGF and CD133+CD34+KDR+ (r = .84; P < .01) and SDF-1 and CD34+CXCR4+ (r = .67; P < .01), and between these 2 cytokines (r = .57; P = .01). In the reperfused patients, the correlation between VEGF and CD133+CD34+KDR+ was lower (r = .38; P = .03) and the correlation between SDF-1 and CD34+CXCR4+ and VEGF disappeared. Multivariate analysis showed that a VEGF >7 pg/mL (P < .01) predicted the mobilisation of CD133+CD34+KDR+, whereas hypertension showed a trend (P = .055). Diabetes (P = .045) predicted the number of CD34+CXCR4+, with reperfusion treatment showing a trend in this subpopulation (P = .054).
Mobilisation of progenitor cells after AMI is influenced by factors such as diabetes and the cytokine VEGF. Hypertension and reperfusion therapy during the acute phase also tend to influence the cell response.