title: Increased preoperative serum apoptosis marker fas ligand correlates with histopathology and new-onset of atrial fibrillation in patients after cardiac surgery.
abstract: BACKGROUND
  We evaluated if preoperative serum apoptosis markers correlate with atrial histological remodeling and postoperative atrial fibrillation (POAF) after cardiac surgery.
  
  
  RESULTS
  A total of 33 patients with sinus rhythm (SR) and without history of atrial fibrillation (AF) undergoing cardiac surgery were prospectively enrolled. Serum concentrations of Fas (apoptosis-stimulating fragment ligand) and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) were measured preoperatively. Right atrial appendage (RAA) tissue was obtained during surgery. Atrial apoptosis was assessed via TUNEL assay and degree of atrial fibrosis was categorized histologically by visual quantification. Continuous ECG-Monitoring was used to screen for POAF throughout 10 days after cardiac surgery. POAF occurred in 15 patients (45%). Atrial apoptosis was higher in patients with POAF as compared to those without (35.9 ± 9.8% vs 14.5 ± 7.5%; P < 0.0001) and correlated with the degree of atrial fibrosis (r = 0.69; P < 0.0001). In contrast to TRAIL (87.0 ± 8.2 pg/mL vs 83.3 ± 9.4 pg/mL; P = 0.77), preoperative Fas serum concentration was significantly higher in patients with POAF compared to patients in stable SR (91.3 ± 7.2 pg/mL vs 66.7 ± 3.0 pg/mL; P < 0.01). Serum Fas concentration correlated with the degree of atrial apoptosis (r = 0.63; P < 0.001) and the degree of atrial fibrosis (r = 0.39; P < 0.05).
  
  
  CONCLUSIONS
  Preoperative evaluation of serum apoptosis marker Fas is useful to identify patients at risk for POAF undergoing cardiac surgery. Fas but not TRAIL correlates with the documented degree of atrial apoptosis and atrial fibrosis in RAA tissue. Further studies need to identify the prospective role of Fas in predicting POAF events.
authors.affiliation: Division of Cardiology & Angiology.
authors.forename: Patrick
authors.initials: P
authors.lastname: Müller
authors.forename: Thomas
authors.initials: T
authors.lastname: Deneke
authors.forename: Fabian
authors.initials: F
authors.lastname: Schiedat
authors.forename: Leif
authors.initials: L
authors.lastname: Bösche
authors.forename: Justus
authors.initials: J
authors.lastname: Strauch
authors.forename: Johannes Wolfgang
authors.initials: JW
authors.lastname: Dietrich
authors.forename: Markus
authors.initials: M
authors.lastname: Vogt
authors.forename: Andrea
authors.initials: A
authors.lastname: Tannapfel
authors.forename: Hugo
authors.initials: H
authors.lastname: Stiegler
authors.forename: Andreas
authors.initials: A
authors.lastname: Mügge
authors.forename: Aydan
authors.initials: A
authors.lastname: Ewers
mesh_terms: D000368:Aged; D017209:Apoptosis; D001281:Atrial Fibrillation / Q000097:blood / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D064752:Atrial Remodeling; D015415:Biomarkers / Q000097:blood; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D015716:Electrocardiography, Ambulatory; D053222:Fas Ligand Protein / Q000097:blood*; D005260:Female; D005355:Fibrosis; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012307:Risk Factors; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human
keywords: apoptosis-stimulating fragment ligand; atrial apoptosis; atrial fibrillation; atrial remodeling; cardiac surgery; tumor necrosis factor