title: Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction.
abstract: OBJECTIVE
  We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations.
  
  
  BACKGROUND
  The nature of the reentrant circuit that underlies VT during acute MI is not well understood.
  
  
  METHODS
  Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI.
  
  
  RESULTS
  Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P < .01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P < .05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P < .05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P < .05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT.
  
  
  CONCLUSIONS
  The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.
authors.affiliation: Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, 46202, USA.
authors.forename: Tamana
authors.initials: T
authors.lastname: Takahashi
authors.forename: Pascal
authors.initials: P
authors.lastname: van Dessel
authors.forename: John C
authors.initials: JC
authors.lastname: Lopshire
authors.forename: William J
authors.initials: WJ
authors.lastname: Groh
authors.forename: John
authors.initials: J
authors.lastname: Miller
authors.forename: Jianyi
authors.initials: J
authors.lastname: Wu
authors.forename: Douglas P
authors.initials: DP
authors.lastname: Zipes
mesh_terms: D000208:Acute Disease; D000818:Animals; D004285:Dogs; D022062:Electrophysiologic Techniques, Cardiac; D006352:Heart Ventricles / Q000503:physiopathology; D007090:Image Interpretation, Computer-Assisted; D023421:Models, Animal; D009203:Myocardial Infarction / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000503:physiopathology*; D041622:Tomography, Optical; D014693:Ventricular Fibrillation / Q000503:physiopathology