Systemic inflammatory changes after pulmonary vein radiofrequency ablation do not alter stem cell mobilization.
OBJECTIVE
Aim of this study was to investigate the number of circulating progenitor cells, systemic inflammatory mediators, and myocardial necrosis in patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation by radiofrequency (RF) ablation. Radiofrequency ablation generates a localized myocardial necrosis that might result in a release of inflammatory mediators enhancing progenitor cell mobilization and improving tissue repair.


RESULTS
Blood samples were collected in patients with paroxysmal AF before and after PV isolation. Interleukin (IL)-6, IL-1beta, TNF-alpha, IL-8, IL-10, and IL-12, and stromal derived factor (SDF)-1 were measured by immunoassay. CD34+CD133+, CD117+, and endothelial progenitor cells (EPCs) were analysed by flow cytometry and culture assay. After ablation procedure, a rise in creatine kinase and troponin T levels indicated myocardial necrosis. Leukocyte counts and C-reactive protein and IL-6 levels increased significantly. Myocardial necrosis and inflammatory response correlated with an increase in IL-6 (P = 0.007). In contrast, SDF-1 levels decreased after RF ablation (P = 0.004). Yet, no significant changes were observed in IL-1beta, TNF-alpha, IL-8, IL 10, and IL-12 plasma levels or in the number of circulating CD34+CD133+ and CD117+ progenitor cells, whereas EPCs decreased by trend.


CONCLUSIONS
Although PV isolation by RF ablation in patients with paroxysmal AF induces a systemic inflammatory response associated with myocardial necrosis, no alterations in circulating progenitor cells were observed. Thus, isolated myocardial necrosis may not be sufficient to account for progenitor cell mobilization.
Stein
Andreas
A
Deutsches Herzzentrum und 1, Medizinische Klinik der Technischen Universität München, 80636 München, Germany.
Wessling
Gabi
G
Deisenhofer
Isabel
I
Busch
Gabriele
G
Steppich
Birgit
B
Estner
Heidi
H
Zrenner
Bernhard
B
Schmitt
Claus
C
Braun
Siegmund
S
Schömig
Albert
A
Ott
Ilka
I
D000071916:AC133 Antigen; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D018952:Antigens, CD34 / Q000378:metabolism; D001281:Atrial Fibrillation / Q000473:pathology / Q000601:surgery*; D017115:Catheter Ablation; D054377:Chemokine CXCL12 / Q000378:metabolism; D022062:Electrophysiologic Techniques, Cardiac; D042783:Endothelial Cells / Q000166:cytology* / Q000276:immunology; D005260:Female; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D010455:Peptides / Q000378:metabolism; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D011667:Pulmonary Veins / Q000601:surgery*; D013234:Stem Cells / Q000166:cytology* / Q000276:immunology
D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D054377:Chemokine CXCL12; D006023:Glycoproteins; D015850:Interleukin-6; C000606023:PROM1 protein, human; D010455:Peptides; D019009:Proto-Oncogene Proteins c-kit