Endothelial progenitor cells in patients with coronary artery disease and left ventricular dysfunction.
OBJECTIVE
Endothelial progenitor cells (EPCs) play a key role in maintenance of endothelial integrity and postnatal neovascularization. We verified whether the number of subpopulations of EPCs is different in patients with coronary artery disease (CAD) and normal or impaired left ventricular (LV) function.


METHODS
Sixty-eight consecutive patients (37 men, age 60+/-18 years) with CAD were studied. All patients underwent quantitative coronary angiography and flow cytometric analysis.


RESULTS
Patients with LV ejection fraction <45% (n=22) were compared with those with normal function (n=46). The two groups had similar age, sex, cardiovascular risk factors, medical therapy, LV dimension, and number of diseased vessels. Patients with LV dysfunction, by study design, were more symptomatic and had a lower LV ejection fraction. The two groups had similar white cell count and mononuclear cells. The absolute number of CD34 and CD133 cells was significantly (P<0.05) higher in patients with LV dysfunction as compared with patients with normal function or healthy participants. In contrast, CD14 cells were significantly (P=0.005) lower in the former patients than in the latter, whereas no significant difference was noted in the number of cells positive for CD105 among groups.


CONCLUSIONS
Subpopulations of EPCs have a discordant behavior in CAD patients with or without LV dysfunction, with cells positive for the endothelial markers CD34 and CD133 being increased and cells that promote vasculogenesis and microvascular development being significantly reduced.
Pelliccia
Francesco
F
Department of Cardiology, San Filippo Neri Hospital, University of Cagliari, Cagliari, Italy. f.pelliccia@mclink.it
Pasceri
Vincenzo
V
Cianfrocca
Cinzia
C
Vitale
Cristiana
C
Pristipino
Christian
C
Speciale
Giulio
G
Mercuro
Giuseppe
G
Rosano
Giuseppe
G
D000071916:AC133 Antigen; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D018952:Antigens, CD34 / Q000032:analysis; D002452:Cell Count; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D004452:Echocardiography; D000071063:Endoglin; D042783:Endothelial Cells / Q000276:immunology / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006023:Glycoproteins / Q000032:analysis; D006801:Humans; D016014:Linear Models; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000032:analysis; D010865:Pilot Projects; D011956:Receptors, Cell Surface / Q000032:analysis; D013234:Stem Cells / Q000276:immunology / Q000473:pathology*; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000473:pathology* / Q000503:physiopathology
D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; C064206:ENG protein, human; D000071063:Endoglin; D006023:Glycoproteins; D018950:Lipopolysaccharide Receptors; C000606023:PROM1 protein, human; D010455:Peptides; D011956:Receptors, Cell Surface