title: Ventricular repolarization dynamicity and arrhythmic disturbances after beating-heart and arrested-heart revascularization.
abstract: BACKGROUND
  Arrhythmias attributable to altered autonomic modulation of the heart, with elevated sympathetic and depressed vagal modulation, occur to a similar extent after surgery performed on beating or arrested hearts. Coronary artery bypass grafting (CABG) with cardiopulmonary bypass has been associated with more frequent occurrence of arrhythmic events than surgery performed without CABG, even with comparable levels of postoperative cardiac autonomic (dis) regulation after arrested- and beating-heart revascularization. We explored the effects of arrested- and beating-heart revascularization procedures on the dynamics of ventricular repolarization and on increased postoperative arrhythmic events.
  
  
  METHODS
  Study participants included 57 CABG patients; 28 underwent on-pump and 29 underwent off-pump procedures. The 2 groups were comparable regarding clinical and postoperative characteristics. With high-quality 15-minute digital electrocardiograms, we assessed ventricular repolarization dynamics using RR and QT intervals and analyzed QT variability (QTV) and QT-RR interdependence. RR and QT intervals were determined from stationary 5-minute segments. QT-interval variability was determined by a T-wave template-matching algorithm. We used linear regression to compute the slope/correlation of the QT/RR interval. The Fisher exact test, nonpaired t-test, and ANOVA were applied to test the results; P <.05 was considered significant.
  
  
  RESULTS
  Postoperative arrhythmic events were significantly more frequent in both groups. One week postoperatively these events were significantly more frequent in the on-pump group. In both groups, the RR interval was shorter after CABG (P <.001). The QT variability index increased from -1.2 + or - 0.6 to -0.8 + or - 0.4 after off-pump CABG and from -1.3 + or - 0.5 to -0.5 + or - 0.6 on day 4 after surgery (P <.05), further deteriorating to -0.2 + or - 0.6 one week after CABG in the on-pump group only (P <.05). QT-RR correlations decreased from 0.39 to 0.24 in the off-pump vs 0.34 to 0.17 in the on-pump group (P <.05), and in both groups they remained significantly reduced for as long as 4 weeks after CABG.
  
  
  CONCLUSIONS
  For both on- and off-pump CABG, beat-to-beat heart-rate changes and rate-dependent ventricular repolarization adaptation showed disparities that worsened after surgery. The observed repolarization lability after CABG procedures seems to be transient but more pronounced after on-pump CABG. The association of arrhythmic events with ventricular repolarization lability changes in the setting of faster heart rates offers novel insights into the mechanisms of perioperative proarrhythmia after beating- and arrested-heart revascularization.
authors.affiliation: Department of Cardiovascular Surgery, University Medical Center, Ljubljana, Slovenia. jurij-matija.kalisnik@mf.uni-lj.si
authors.forename: Jurij M
authors.initials: JM
authors.lastname: Kalisnik
authors.forename: Viktor
authors.initials: V
authors.lastname: Avbelj
authors.forename: Roman
authors.initials: R
authors.lastname: Trobec
authors.forename: Gaj
authors.initials: G
authors.lastname: Vidmar
authors.forename: Giovanni
authors.initials: G
authors.lastname: Troise
authors.forename: Borut
authors.initials: B
authors.lastname: Gersak
mesh_terms: D000368:Aged; D000465:Algorithms; D001145:Arrhythmias, Cardiac / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D001026:Coronary Artery Bypass / Q000009:adverse effects* / Q000379:methods; D047549:Coronary Artery Bypass, Off-Pump / Q000009:adverse effects*; D003936:Diagnosis, Computer-Assisted; D004562:Electrocardiography / Q000379:methods; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006339:Heart Rate; D006352:Heart Ventricles; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology