title: The effect of lesion size and tissue remodeling on ST deviation in partial-thickness ischemia.
abstract: BACKGROUND
  Myocardial ischemia causes ST segment elevation or depression in electrocardiograms and epicardial leads. ST depression in epicardium overlying the ischemic zone indicates that the ischemia is nontransmural. However, nontransmural ischemia does not always cause ST depression. Especially in animal models, ST depression is hard to reproduce.
  
  
  OBJECTIVE
  The purpose of this study was to determine the circumstances in which ST depression could be expected.
  
  
  METHODS
  We studied ischemia in a large-scale computer model of the human heart. A realistic representation of the ischemia-induced changes in resting membrane potential was used, which was based on diffusion of extracellular potassium. Ischemia diameter, transmural extent, and tissue conductivity were varied.
  
  
  RESULTS
  Our simulations confirm earlier work showing that partial-thickness ischemia, like full-thickness ischemia, typically causes ST elevation in an anisotropic model of the ventricles. However, we identified three situations in which ST depression can occur in overlying leads. The first is a reduced anisotropy ratio of the intracellular conductivity, which may result from hypertrophy and gap-junctional remodeling, circumstances that are likely to accompany ischemia. Second, an increase of the extracellular anisotropy has the same effect. Third, ST depression was found, independent of the anisotropy ratios, in very large and thin ischemic regions, resembling those that may occur in left-main or multivessel disease.
  
  
  CONCLUSIONS
  Both tissue remodeling and geometric factors can explain ST depression in overlying epicardial leads. We note at the same time that ST elevation is found in most circumstances, while depression occurs as a reciprocal effect, even in partial-thickness ischemia.
authors.affiliation: Research Center, Sacré-Coeur Hospital, Montréal, Québec, Canada. mark.potse.nl
authors.forename: Mark
authors.initials: M
authors.lastname: Potse
authors.forename: Ruben
authors.initials: R
authors.lastname: Coronel
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Falcao
authors.forename: A-Robert
authors.initials: AR
authors.lastname: LeBlanc
authors.forename: Alain
authors.initials: A
authors.lastname: Vinet
mesh_terms: D000200:Action Potentials; D016880:Anisotropy; D003198:Computer Simulation; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology*