title: Electrocardiographic factors playing a role in ischemic ventricular fibrillation in ST elevation myocardial infarction are related to the culprit artery.
abstract: BACKGROUND
  Sudden cardiac death caused by ischemic ventricular fibrillation (VF) associated with ST elevation myocardial infarction (STEMI) is one of the most frequent causes of death.
  
  
  OBJECTIVE
  We hypothesized that electrocardiographic (ECG) characteristics differ between STEMI patients with and without ischemic VF.
  
  
  METHODS
  Fifty-five first STEMI patients with at least one 12-lead ECG recorded before ischemic VF were compared with 110 first STEMI patients without ischemic VF. Patients with bundle branch blocks or high-degree atrioventricular blocks with escape rhythms were not included. ECG measurements were performed manually after scanning the ECG with the most prominent ST deviation into a software environment and magnifying it 4 times.
  
  
  RESULTS
  Mean age was 57 +/- 12 years, and 126 patients were male. No differences were present between the VF and control group regarding baseline, enzymatic, and angiographic data. In left circumflex artery and right coronary artery myocardial infarction, a longer QRS interval (109 +/- 23 ms vs. 91 +/- 16 ms, P = .02 and 107 +/- 24 ms vs. 93 +/- 19, P = .02) was present. In the latter the PR interval (211 +/- 64 ms vs. 160 +/- 36 ms, P <.001) and ST deviation score (3.6 +/- 1.0 mV vs. 1.7 +/- 1.5 mV, P <.001) were also increased. In the left anterior descending artery group no differences in conduction intervals and ST deviation score were present.
  
  
  CONCLUSIONS
  Longer PR and QRS intervals in right coronary artery and left circumflex artery MI fit with the perfusion and activation pattern of the atrioventricular node and the ventricular myocardium. Myocardium perfused by the left anterior descending artery is activated earliest, hiding any intraventricular conduction delay within the QRS complex. Intramural slowed conduction could be a substrate for ischemic VF.
authors.affiliation: Department of Cardiology, University Hospital Maastricht, Maastricht, The Netherlands. m.lemmert@cardio.azm.nl
authors.forename: Miguel E
authors.initials: ME
authors.lastname: Lemmert
authors.forename: Jonas S S G
authors.initials: JS
authors.lastname: de Jong
authors.forename: Antonius M W
authors.initials: AM
authors.lastname: van Stipdonk
authors.forename: Harry J G M
authors.initials: HJ
authors.lastname: Crijns
authors.forename: Hein J J
authors.initials: HJ
authors.lastname: Wellens
authors.forename: Mitchell W
authors.initials: MW
authors.lastname: Krucoff
authors.forename: Lukas R
authors.initials: LR
authors.lastname: Dekker
authors.forename: Arthur A M
authors.initials: AA
authors.lastname: Wilde
authors.forename: Anton P M
authors.initials: AP
authors.lastname: Gorgels
mesh_terms: D016022:Case-Control Studies; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D004562:Electrocardiography; D006329:Heart Conduction System / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000150:complications* / Q000503:physiopathology; D012189:Retrospective Studies; D013610:Tachycardia / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000503:physiopathology