title: Infarct artery patency predicts outcome of serial electropharmacological studies in patients with malignant ventricular tachyarrhythmias.
abstract: BACKGROUND
  Surviving myocardial cells near the infarct border zone form the arrhythmogenic substrate for sustained ventricular tachycardia (VT) in humans. Infarct-related artery (IRA) patency may modulate the electrophysiological function of this arrhythmogenic substrate and its response to antiarrhythmic drug therapy. We postulated that effective antiarrhythmic drug therapy selected during serial electrophysiological studies in patients with VT after a myocardial infarction would be identified more frequently when the IRA is patent than when chronically occluded.
  
  
  RESULTS
  Consecutive patients (n = 64) with documented coronary artery disease and remote myocardial infarction presenting with spontaneous sustained VT or ventricular fibrillation (VF) were studied. These patients underwent 4 +/- 2 electropharmacological studies identifying effective antiarrhythmic drug therapy in 16 (25%) patients. Drug responders did not differ significantly from nonresponders in demographic, electrocardiographic, angiographic, or hemodynamic measurements. A patent IRA was associated with antiarrhythmic drug response significantly more frequently than was an occluded IRA (45% versus 9%, p = 0.001). Patency of the IRA was the only independent predictor of response to antiarrhythmic drug therapy in this study population. The sensitivity and specificity of using a patent IRA to predict successful drug testing were 81% and 67%, respectively.
  
  
  CONCLUSIONS
  The outcome of electropharmacological studies was predicted by the patency of the IRA. A patent IRA was associated with a greater probability of finding effective drug therapy.
authors.affiliation: Department of Medicine, Foothills Medical Centre, Calgary, Alberta, Canada.
authors.forename: J T
authors.initials: JT
authors.lastname: Hii
authors.forename: M
authors.initials: M
authors.lastname: Traboulsi
authors.forename: L B
authors.initials: LB
authors.lastname: Mitchell
authors.forename: D G
authors.initials: DG
authors.lastname: Wyse
authors.forename: H J
authors.initials: HJ
authors.lastname: Duff
authors.forename: A M
authors.initials: AM
authors.lastname: Gillis
mesh_terms: D000368:Aged; D001158:Arteries; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D004594:Electrophysiology; D005260:Female; D005544:Forecasting; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D013599:Systole; D017180:Tachycardia, Ventricular / Q000188:drug therapy* / Q000503:physiopathology; D016896:Treatment Outcome; D014654:Vascular Patency; D016277:Ventricular Function, Left