Cardiac uptake of progenitor cells in patients with moderate-to-severe left ventricular failure scheduled for cardiac resynchronization therapy.
OBJECTIVE
Injury to the heart causes haematopoietic and endothelial progenitor cells (PCs) to migrate to the site of damage and to undergo PC differentiation, which may contribute to angiogenesis and myocardial tissue repair. We sought to determine the cardiac uptake of PC in patients with moderate-to-severe congestive heart failure (CHF) scheduled for cardiac resynchronization therapy.


RESULTS
A total of 28 patients was included in the study. Fourteen patients had moderate-to-severe CHF with a mean left ventricular ejection fraction (LVEF) of 20 +/- 9%. The remaining patients had a normal LVEF and served as controls. PCs (CD34(+) and CD34(+)/CD117(+)) were quantified using a fluorescence-activated cell sorter. In CHF patients, PCs were determined from whole blood samples taken from the aorta, the coronary sinus (CS), and the superior vena cava (SVC) during right and left heart catheterization. Cardiac PC uptake was determined as the difference in PC levels between the aorta and the CS. Differences in CD34(+)PC counts (Delta0.11 +/- 0.98 x 10(3) mL(-1)) and relative amount of CD34(+)/CD117(+)PC (Delta0.08 +/- 0.31%) between the aorta and the CS were not significant. PC levels were comparable between the SVC, CS, and aorta. CD34(+) and PC levels did not correlate with New York Heart Association class (r(2) = 0.22), LVEF (r(2) = 0.01), LV diameter (r(2) = 0.05), QRS complex duration (r(2) = 0.1), or maximal O(2) uptake during exercise (r(2) = 0.08). There was no difference between patients with ischaemic cardiomyopathy (ICM) and non-ICM. Systemic PC levels were not different compared with age-matched controls without LV failure (CD34(+): 4.61 +/- 1.83 x 10(3) mL(-1) vs. control: 5.25 +/- 1.67 x 10(3) mL(-1); P = n.s.).


CONCLUSIONS
Moderate-to-severe chronic CHF is not associated with elevated PC levels in the systemic circulation. A measurable cardiac uptake of CD34(+) and CD34(+)/CD117(+)PC cannot be demonstrated by FACS analysis in this cohort of patients.
Goette
Andreas
A
Division of Cardiology, University Hospital Magdeburg, Leipziger Street 44, 39120 Magdeburg Germany. andreas.goette@medizin.uni-magdeburg.de
Jentsch-Ullrich
Kathleen
K
Hammwöhner
Matthias
M
Trautmann
Silke
S
Franke
Astrid
A
Klein
Helmut U
HU
Auricchio
Angelo
A
D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis; D002304:Cardiac Pacing, Artificial; D002465:Cell Movement; D004562:Electrocardiography; D042783:Endothelial Cells / Q000166:cytology / Q000276:immunology / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D005434:Flow Cytometry; D006333:Heart Failure / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000166:cytology*; D019009:Proto-Oncogene Proteins c-kit / Q000032:analysis; D013234:Stem Cells / Q000166:cytology / Q000276:immunology / Q000502:physiology*
D018952:Antigens, CD34; D019009:Proto-Oncogene Proteins c-kit