Effect of atrial fibrillation on hematopoietic progenitor cells: a novel pathophysiological role of the atrial natriuretic peptide?
BACKGROUND
Injury to the heart causes hematopoietic progenitor cells (HPCs) to migrate to the site of damage and to undergo cell differentiation. Studies suggest that myocardial progenitor cells invade atrial tissue. So far it is unclear, however, whether an atrial disease per se affects circulating HPCs.


RESULTS
Seventeen patients with persistent atrial fibrillation (persistAF), 12 with paroxysmal AF (paroxAF), and 17 matched patients with sinus rhythm (SR) were studied. HPCs (CD34+ and CD34+/CD117+) were quantified with the use of a fluorescence-activated cell sorter; stromal cell-derived factor-1alpha (SDF-1alpha), vascular endothelium growth factor (VEGF), and atrial natriuretic peptide (ANP) were determined by immunoassays. In patients with persistAF, blood samples were obtained before as well as 10 minutes, 24 hours, and 48 hours after electrical cardioversion. CD34+HPCs (AF, 7.0+/-2.3x10(3)/mL versus SR, 5.0+/-1.6x10(3)/mL; P<0.01) were increased during persistAF only. Highest SDF-1alpha levels were also observed during persistAF. Successful and unsuccessful cardioversion decreased CD34+HPCs temporarily (7.0+/-2.3x10(3)/mL versus 24 hours: 5.0+/-1.5x10(3)/mL; P<0.05). Forty-eight hours after successful cardioversion, SDF-1alpha and CD34+HPC levels started to decline, reaching control levels after 59+/-19 days. CD34+/CD117+ and VEGF levels, however, were increased by DC energy but not by AF. ANP levels correlated with CD34+HPC (r=0.76; P<0.01) and SDF-1alpha (r=0.56; P<0.01). HPCs from patients with AF had a greater tendency to differentiate into cells expressing (cardio)myocyte markers ANP and myocyte enhancer factor-2.


CONCLUSIONS
PersistAF appears to increase the potential of HPCs for (cardio)myogenesis. Restitution of CD34+HPC levels, mediated by SDF-1alpha and possibly ANP, occurs within several weeks after successful cardioversion.
Goette
Andreas
A
University Hospital Magdeburg, Division of Cardiology, Leipziger Str 44, 39120 Magdeburg, Germany. andreas.goette@medizin.uni-magdeburg.de
Jentsch-Ullrich
Kathleen
K
Lendeckel
Uwe
U
Röcken
Christoph
C
Agbaria
Mahmood
M
Auricchio
Angelo
A
Mohren
Martin
M
Franke
Astrid
A
Klein
Helmut U
HU
D018952:Antigens, CD34 / Q000096:biosynthesis; D001281:Atrial Fibrillation / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis* / Q000097:blood; D002452:Cell Count; D002478:Cells, Cultured; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000097:blood; D004268:DNA-Binding Proteins / Q000096:biosynthesis; D004554:Electric Countershock; D005260:Female; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D064326:MEF2 Transcription Factors; D008297:Male; D008875:Middle Aged; D018006:Myogenic Regulatory Factors; D019009:Proto-Oncogene Proteins c-kit / Q000096:biosynthesis; D014157:Transcription Factors / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
D018952:Antigens, CD34; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D004268:DNA-Binding Proteins; D015850:Interleukin-6; D064326:MEF2 Transcription Factors; D018006:Myogenic Regulatory Factors; D014157:Transcription Factors; D042461:Vascular Endothelial Growth Factor A; D016753:Interleukin-10; D009320:Atrial Natriuretic Factor; D019009:Proto-Oncogene Proteins c-kit