title: Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences.
abstract: BACKGROUND
  ST-Segment elevation is a common electrocardiogram (ECG) manifestation of acute transmural myocardial ischemia in leads facing the injury. Acute myocardial ischemia involving the right-ventricular (RV) outflow tract is known to induce a Brugada-like ECG. In this paper, we examined the electrophysiological bases for the similarities between the ECG characteristics of the Brugada syndrome model induced by terfenadine (5 mumol/L) and the ECG manifestations of the acute transmural no-flow ischemia model.
  
  
  METHODS
  For both experimental simulations, we used isolated arterially perfused canine RV wedge preparations to record transmembrane action potentials (AP) from endocardium and epicardium together with a transmural pseudo-ECG (ECG); basic cycle length=400 to 2000 ms.
  
  
  RESULTS
  In the presence of a prominent Ito-mediated AP notch, no-flow ischemia causes true ST-segment elevation because of selective depression and loss of the AP dome at some epicardial sites. In the absence of a prominent AP notch, ischemia ultimately produces an apparent ST-segment elevation, which is secondary to a prolongation of the R wave caused by marked transmural conduction delays. Similarly, in the Brugada syndrome model generated in preparations displaying a large epicardial Ito, ST-segment elevation was due to loss of the epicardial AP dome at some sites but not at others. Transmural conduction delay giving the appearance of ST-segment elevation is also observed in the Brugada model in preparations exhibiting smaller AP notch. In both models, propagation of the dome from the site at which it is maintained to a site at which it is lost may result in closely coupled phase 2 reentrant extrasystoles.
  
  
  CONCLUSIONS
  Our results suggest that Ito can modulate the electrocardiographic manifestation of acute ischemia as well as that of the Brugada syndrome, and that both clinical entities are the result of a similar electrophysiological substrate.
authors.affiliation: Experimental Cardiology Department, Masonic Medical Research Laboratory, Utica, NY 13501-1787, USA. didiego@mmrl.edu
authors.forename: José M
authors.initials: JM
authors.lastname: Di Diego
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Fish
authors.forename: Charles
authors.initials: C
authors.lastname: Antzelevitch
mesh_terms: D000200:Action Potentials; D000818:Animals; D002037:Bundle-Branch Block / Q000503:physiopathology*; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D004699:Endocardium / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D010496:Pericardium / Q000503:physiopathology; D013577:Syndrome