title: Intracardiac measurement of pre-ejection myocardial velocities estimates the transmural extent of viable myocardium early after reperfusion in acute myocardial infarction.
abstract: OBJECTIVE
  We hypothesized that wall motion velocity during pre-ejection is proportional to the regional content of viable myocardium after reperfusion for acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Pre-ejection wall motion consists of short and fast inward and outward movement towards and away from the center of the left ventricle (LV) and is altered during regional ischemia. This short-lived event can be accurately quantified by Doppler myocardial imaging (DMI).
  
  
  METHODS
  Fourteen open-chest pigs underwent 60 to 120 min of left anterior descending coronary artery occlusion followed by 30 min of reperfusion. The DMI data were collected using a phased-array intracardiac catheter (LV cavity) from ischemic and nonischemic myocardium encompassed within a plane passing through two epicardial bead markers. Peak tissue velocities during isovolumic contraction (IVC) (peak positive and peak negative), ejection (S) and early filling (E) were measured. The cardiac specimen was sliced through the epicardial markers in a plane approximating the ultrasound imaging plane. The transmural extent of necrosis (TEN) (%) was measured by triphenyltetrazolium chloride staining.
  
  
  RESULTS
  During ischemia, positive IVC velocity was zero in ischemic walls with TEN >20%. At reperfusion, positive IVC velocity correlated better with TEN (r = -0.94, p < 0.0001) than it did S (r = -0.70, p < 0.01) and E (r = -0.81, p < 0.01). Differential IVC (the difference between peak positive and peak negative velocity) highly correlated with TEN, during ischemia (r = -0.78, p < 0.001) and during reperfusion (r = -0.93, p < 0.0001).
  
  
  CONCLUSIONS
  Pre-ejection tissue velocity, as measured by intracardiac ultrasound, allows rapid estimation of the transmural extent of viable myocardium after reperfusion for AMI.
authors.affiliation: Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. Pislaru.Cristina@mayo.edu
authors.forename: C
authors.initials: C
authors.lastname: Pislaru
authors.forename: C J
authors.initials: CJ
authors.lastname: Bruce
authors.forename: M
authors.initials: M
authors.lastname: Belohlavek
authors.forename: J B
authors.initials: JB
authors.lastname: Seward
authors.forename: J F
authors.initials: JF
authors.lastname: Greenleaf
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D015150:Echocardiography, Doppler; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D012039:Regional Blood Flow / Q000502:physiology; D012044:Regression Analysis; D013318:Stroke Volume; D013552:Swine