title: Mechanisms of ventricular arrhythmias induced by myocardial contusion: a high-resolution mapping study in left ventricular rabbit heart.
abstract: BACKGROUND
  The aims of the Langendorff-perfused rabbit heart study were to evaluate the arrhythmogenic consequences of myocardial contusion and to determine the mechanism of arrhythmia.
  
  
  METHODS
  Six hearts were in the control group, and 24 hearts (intact heart protocol) were submitted to one of four different contusion kinetic energies (75, 100, 150, or 200 millijoules [mJ]; n = 6). Occurrence of arrhythmia, of an electrically silent area (i.e., area with no electrical activity), and of line of fixed conduction block were reported before and for 1 h after contusion. In 16 hearts (frozen hearts) submitted to cryoprocedure and contusion impact of 100 or 200 mJ, ventricular conduction velocities, anisotropic ratio, wavelengths, ventricular effective refractory period, and its dispersion were measured before and for 1 h after contusion. Using high-resolution mapping, arrhythmias were recorded and analyzed.
  
  
  RESULTS
  The intact heart study showed that the number and seriousness of contusion-induced arrhythmias increased with increasing contusion kinetic energy, as did the number of electrically silent areas (five of six ventricular fibrillations and five of six electrically silent areas at 200 mJ). In the frozen heart study, immediately after contusion ventricular effective refractory periods were shortened and dispersed, and wavelengths were also shortened. The arrhythmia analysis showed that all ventricular tachycardias but one were based on reentry developed around an electrically silent area or a line of fixed conduction block.
  
  
  CONCLUSIONS
  Myocardial contusion has direct arrhythmogenic effects, and the seriousness of arrhythmia increases with the level of contusion kinetic energy. The mechanism of arrhythmia was mainly based on reentrant circuit around a fixed obstacle.
authors.affiliation: Laboratory of Anesthesiology and Cardiovascular Physiology, Medical School of Montpellier-Nîmes, France.
authors.forename: E
authors.initials: E
authors.lastname: Robert
authors.forename: J E
authors.initials: JE
authors.lastname: de La Coussaye
authors.forename: A G
authors.initials: AG
authors.lastname: Aya
authors.forename: J P
authors.initials: JP
authors.lastname: Bertinchant
authors.forename: A
authors.initials: A
authors.lastname: Polge
authors.forename: P
authors.initials: P
authors.lastname: Fabbro-Pèray
authors.forename: C
authors.initials: C
authors.lastname: Pignodel
authors.forename: J J
authors.initials: JJ
authors.lastname: Eledjam
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D003288:Contusions / Q000150:complications / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D004594:Electrophysiology; D005615:Freezing; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology; D006352:Heart Ventricles / Q000503:physiopathology; D066298:In Vitro Techniques; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D010496:Pericardium / Q000502:physiology; D011817:Rabbits; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D013610:Tachycardia / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D003402:Creatine Kinase