title: Electromechanical characterization of acute experimental myocardial infarction.
abstract: OBJECTIVE
  A new cardiac mapping system combines harmless magnetic field energy and tip-deflecting catheters (equipped with location sensors) to obtain real-time 3-dimensional electromechanical maps of the left ventricle endocardial surface without using x-ray fluoroscopy. This experimental study assessed electromechanical changes during acute coronary occlusion and reperfusion in a canine model.
  
  
  METHODS
  Group 1 (n = 10) underwent coronary occlusion for 45 minutes followed by reperfusion (n = 6) and group 2 (n = 11) underwent coronary occlusion for 90 minutes. Endocardial peak-to-peak voltage amplitudes and local endocardial shortening values were measured in ischemic and non-ischemic zones at baseline, following coronary occlusion and reperfusion.
  
  
  RESULTS
  In ischemic zones, local shortening was significantly reduced during coronary occlusion compared to baseline (Group 1: 4.7 +/- 2.0% at 45 minutes vs. 15.5 +/- 3.4%, p < 0.001, 6.2 +/- 2.1% at 90 minutes vs. 15.5 +/- 3.4%, p < 0.001; Group 2: 5.0 +/- 2.9% at 90 minutes vs. 13.9 +/- 3.3%, p = 0.007). Coronary occlusion caused a significant reduction in voltage potentials in the ischemic area (unipolar voltage at 45 minutes: 32.2 +/- 7.3 mV vs. 36.2 +/- 8.5 mV at baseline, p = 0.03; unipolar voltage at 90 minutes: 30.5 +/- 11.3 mV vs. 38.3 +/- 14.2 mV, p = 0.003; bipolar voltage at 45 minutes: 7.6 +/- 5.5 mV vs. 10.1 +/- 6.0 mV, p < 0.04; bipolar voltage at 90 minutes: 7.6 +/- 4.4 mV vs. 9.8 +/- 6.2 mV, p < 0.02). Voltage amplitudes were no longer reduced during reperfusion (unipolar voltage: 34.3 +/- 10.5 mV vs. 36.2 +/- 8.5 mV, p = 0.26; bipolar voltage: 9.1 +/- 4.5 mV vs. 10.1 +/- 6.0 mV at baseline, p = 0.37), or in non-ischemic regions during either coronary occlusion or reperfusion.
  
  
  CONCLUSIONS
  Electromechanical mapping study provides unique insights into acute myocardial infarction and stunning by detection and localization of early electromechanical changes during coronary occlusion and/or reperfusion.
authors.affiliation: Cardiology Research Foundation, Department of Cardiology and Medlantic Research Institute, Washington Hospital Center, 110 Irving Street, N.W., 4B-1, Washington, D.C. 20010, USA. rxk3@mhg.edu
authors.forename: R
authors.initials: R
authors.lastname: Kornowski
authors.forename: M K
authors.initials: MK
authors.lastname: Hong
authors.forename: A
authors.initials: A
authors.lastname: Shiran
authors.forename: S
authors.initials: S
authors.lastname: Fuchs
authors.forename: A
authors.initials: A
authors.lastname: Pierre
authors.forename: S D
authors.initials: SD
authors.lastname: Collins
authors.forename: S
authors.initials: S
authors.lastname: Elahham
authors.forename: M B
authors.initials: MB
authors.lastname: Leon
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology; D004285:Dogs; D004594:Electrophysiology; D004699:Endocardium / Q000503:physiopathology; D021621:Imaging, Three-Dimensional; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000175:diagnosis / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D017682:Myocardial Stunning / Q000503:physiopathology; D016277:Ventricular Function, Left