title: Extent of myocardial viability predicts response to biventricular pacing in ischemic cardiomyopathy.
abstract: BACKGROUND
  The clinical response to biventricular pacing is unpredictable, especially in patients with ischemic cardiomyopathy.
  
  
  OBJECTIVE
  The purpose of this study was to prospectively examine the relationship between the extent of myocardial viability and the response to cardiac resynchronization therapy.
  
  
  METHODS
  Twenty-one patients with ischemic left ventricular (LV) dysfunction (left ventricular ejection fraction [LVEF] 21 +/- 5%), New York Heart Association (NYHA) functional class III-IV, and QRS >120 ms received biventricular devices. Myocardial viability was assessed by myocardial contrast echocardiography, and a perfusion score index (PSI) was calculated from summed segmental perfusion scores. LV performance was assessed by echocardiography on the day after implantation and at 6 months.
  
  
  RESULTS
  PSI was closely correlated with acute improvement in LVEF (P = .003, r = 0.65), stroke volume (P = .02, r = 0.54), and end-systolic volume (P = .05, r = -0.49). PSI also correlated with early diastolic LV relaxation (E', P < .05, r = 0.50) and global myocardial performance or Tei index (P = .003, r = 0.63). By multiple linear regression analysis, PSI provided incremental predictive value to the degree of dyssynchrony, measured by tissue Doppler imaging, for predicting improvement in LVEF. At 6 months, PSI remained positively correlated with improvement in ventricular performance and with reduction in LV end-diastolic dimension (P = .003, r = -0.68). PSI also influenced the clinical variables of NYHA class, 6-minute walk distance, quality-of-life score, and number of hospitalizations for heart failure.
  
  
  CONCLUSIONS
  In patients with ischemic cardiomyopathy, the extent of myocardial viability predicts acute and long-term improvement in LV performance, exercise tolerance, and reduction in LV end-diastolic dimension with biventricular pacing.
authors.affiliation: Cardiovascular Division, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. jph4b@virginia.edu
authors.forename: James P
authors.initials: JP
authors.lastname: Hummel
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Lindner
authors.forename: J Todd
authors.initials: JT
authors.lastname: Belcik
authors.forename: John D
authors.initials: JD
authors.lastname: Ferguson
authors.forename: J Michael
authors.initials: JM
authors.lastname: Mangrum
authors.forename: James D
authors.initials: JD
authors.lastname: Bergin
authors.forename: David E
authors.initials: DE
authors.lastname: Haines
authors.forename: Douglas E
authors.initials: DE
authors.lastname: Lake
authors.forename: John P
authors.initials: JP
authors.lastname: DiMarco
authors.forename: J Paul
authors.initials: JP
authors.lastname: Mounsey
mesh_terms: D000368:Aged; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D015150:Echocardiography, Doppler; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy; D011379:Prognosis; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology; D014022:Tissue Survival / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*