title: Fundamental differences in electrophysiologic and electroanatomic substrate between ischemic cardiomyopathy patients with and without clinical ventricular tachycardia.
abstract: OBJECTIVE
  The aim of this study was to compare the electrophysiologic substrate in ischemic cardiomyopathy (ICM) patients with and without sustained monomorphic ventricular tachycardia (SMVT).
  
  
  BACKGROUND
  Despite the universal presence of potentially arrhythmogenic left ventricular (LV) scarring, it is not clear why the majority of ICM patients never develop SMVT.
  
  
  METHODS
  Detailed electroanatomic mapping of the LV endocardium was performed in 17 stable control ICM patients (16 males) without clinical SMVT. They were compared with 17 ICM patients (15 males) with spontaneous SMVT. Standard definitions of low-voltage zones and fractionated, isolated, and very late potentials were used.
  
  
  RESULTS
  There were no significant baseline differences between the groups in terms of LV diameter, ejection fraction (27% vs. 28%), infarct territory, or time from infarction. However, control patients had smaller total low-voltage area < or =1.5 mv (30% of surface area vs. 55%, p < 0.001); smaller very low-voltage area <0.5 mv (7.3% vs. 29%, p < 0.001); higher mean voltage of low-voltage zones; fewer fractionated, isolated, and very late potentials with lower density of these scar-related electrograms per unit low-voltage area; and less SMVT inducibility. Potential conducting channels within dense scar and adjacent to the mitral annulus were more frequent in SMVT patients.
  
  
  CONCLUSIONS
  Compared with ICM patients with SMVT, an otherwise similar control group demonstrated markedly smaller endocardial low-voltage zones, lower scar-related electrogram density, and fewer conducting channels with faster conduction velocity. These findings may explain why some ICM patients develop SMVT and others do not.
authors: Department of Cardiology, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria, Australia.
authors: Haris M
authors: HM
authors: Haqqani
authors: Jonathan M
authors: JM
authors: Kalman
authors: Kurt C
authors: KC
authors: Roberts-Thomson
authors: Richard N
authors: RN
authors: Balasubramaniam
authors: Raphael
authors: R
authors: Rosso
authors: Richard L
authors: RL
authors: Snowdon
authors: Paul B
authors: PB
authors: Sparks
authors: Jitendra K
authors: JK
authors: Vohra
authors: Joseph B
authors: JB
authors: Morton
mesh_terms: D000368:Aged; D018780:Body Surface Potential Mapping / Q000379:methods*; D009202:Cardiomyopathies / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D003937:Diagnosis, Differential; D004554:Electric Countershock / Q000379:methods; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D011379:Prognosis; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology