TY - JOUR
T1 - Endothelial progenitor cell mobilization and increased intravascular nitric oxide in patients undergoing cardiac rehabilitation
AU - Paul, Jonathan D.
AU - Powell, Tiffany M.
AU - Thompson, Michael
AU - Benjamin, Moshe
AU - Rodrigo, Maria
AU - Carlow, Andrea
AU - Annavajjhala, Vidhya
AU - Shiva, Sruti
AU - Dejam, Andre
AU - Gladwin, Mark T.
AU - McCoy, J. Philip
AU - Zalos, Gloria
AU - Press, Beverly
AU - Murphy, Mandy
AU - Hill, Jonathan M.
AU - Csako, Gyorgy
AU - Waclawiw, Myron A.
AU - Cannon, Richard O.
PY - 2007/3
Y1 - 2007/3
N2 - PURPOSE: We investigated whether cardiac rehabilitation participation increases circulating endothelial progenitor cells (EPCs) and benefits vasculature in patients already on stable therapy previously shown to augment EPCs and improve endothelial function. METHODS: Forty-six of 50 patients with coronary artery disease completed a 36-session cardiac rehabilitation program: 45 were treated with HMG-CoA reductase inhibitor (statin) therapy ≥1 month (average baseline low-density lipoprotein cholesterol = 81 mg/dL). Mononuclear cells isolated from blood were quantified for EPCs by flow cytometry (CD133/VEGFR-2 cells) and assayed in culture for EPC colony-forming units (CFUs). In 23 patients, EPCs were stained for annexin-V as a marker of apoptosis, and nitrite was measured in blood as an indicator of intravascular nitric oxide. RESULTS: Endothelial progenitor cells increased from 35 ± 5 to 63 ± 10 cells/mL, and EPC-CFUs increased from 0.9 ± 0.2 to 3.1 ± 0.6 per well (both P < .01), but 11 patients had no increase in either measure. Those patients whose EPCs increased from baseline showed significant increases in nitrite and reduction in annexin-V staining (both P < .01) versus no change in patients without increase in EPCs. Over the course of the program, EPCs increased prior to increase in nitrite in the blood. CONCLUSIONS: Cardiac rehabilitation in patients receiving stable statin therapy and with low-density lipoprotein cholesterol at goal increases EPC number, EPC survival, and endothelial differentiation potential, associated with increased nitric oxide in the blood. Although this response was observed in most patients, a significant minority showed neither EPC mobilization nor increased nitric oxide in the blood.
AB - PURPOSE: We investigated whether cardiac rehabilitation participation increases circulating endothelial progenitor cells (EPCs) and benefits vasculature in patients already on stable therapy previously shown to augment EPCs and improve endothelial function. METHODS: Forty-six of 50 patients with coronary artery disease completed a 36-session cardiac rehabilitation program: 45 were treated with HMG-CoA reductase inhibitor (statin) therapy ≥1 month (average baseline low-density lipoprotein cholesterol = 81 mg/dL). Mononuclear cells isolated from blood were quantified for EPCs by flow cytometry (CD133/VEGFR-2 cells) and assayed in culture for EPC colony-forming units (CFUs). In 23 patients, EPCs were stained for annexin-V as a marker of apoptosis, and nitrite was measured in blood as an indicator of intravascular nitric oxide. RESULTS: Endothelial progenitor cells increased from 35 ± 5 to 63 ± 10 cells/mL, and EPC-CFUs increased from 0.9 ± 0.2 to 3.1 ± 0.6 per well (both P < .01), but 11 patients had no increase in either measure. Those patients whose EPCs increased from baseline showed significant increases in nitrite and reduction in annexin-V staining (both P < .01) versus no change in patients without increase in EPCs. Over the course of the program, EPCs increased prior to increase in nitrite in the blood. CONCLUSIONS: Cardiac rehabilitation in patients receiving stable statin therapy and with low-density lipoprotein cholesterol at goal increases EPC number, EPC survival, and endothelial differentiation potential, associated with increased nitric oxide in the blood. Although this response was observed in most patients, a significant minority showed neither EPC mobilization nor increased nitric oxide in the blood.
KW - Cardiac rehabilitation
KW - EPCs
KW - Nitric oxide
UR - http://www.scopus.com/inward/record.url?scp=34247593808&partnerID=8YFLogxK
U2 - 10.1097/01.HCR.0000265031.10145.50
DO - 10.1097/01.HCR.0000265031.10145.50
M3 - Article
C2 - 17558240
AN - SCOPUS:34247593808
SN - 1932-7501
VL - 27
SP - 65
EP - 73
JO - Journal of Cardiopulmonary Rehabilitation and Prevention
JF - Journal of Cardiopulmonary Rehabilitation and Prevention
IS - 2
ER -