title: Combining monophasic action potential recordings with pacing to demonstrate delayed afterdepolarizations and triggered arrhythmias in the intact heart. Value of diastolic slope.
abstract: BACKGROUND
  In the intact heart, methodological difficulties hamper the direct visualization of delayed afterdepolarizations (DADs) responsible for triggered arrhythmias. Therefore, we tested the hypothesis that a combination of pacing and the recording of a monophasic action potential (MAP) could facilitate the recognition of ouabain-induced DADs and triggered arrhythmias by demonstrating an increase in the diastolic baseline slope (dV/dT) of the MAP recording at the end of a pacing train.
  
  
  RESULTS
  In anesthetized dogs with chronic atrioventricular block, a right ventricular endocardial MAP was recorded during (1) control (n = 11), (2) 15 to 45 minutes after administration of ouabain (45 +/- 10 micrograms/kg, n = 11), (3) 10 minutes after administration of lidocaine (3 mg/kg, n = 5), and (4) during lidocaine washout (n = 3). Pacing was performed with the MAP catheter. Also, the protocol was performed in 3 dogs with conducted sinus rhythm during control and ouabain circumstances. During control, the slope value was 2 +/- 2 mV/s (mean +/- SD), the incidence of DADs after the stimulation train was 6%, and no ventricular tachycardias (VTs) were induced in dogs with atrioventricular block. During ouabain administration, the slope and DAD incidences increased to, respectively, 26 +/- 14 mV/s and 74% (P < .05 for both). VTs were induced frequently. Lidocaine prevented VT induction by decreasing the slope and the incidence of DADs. This effect disappeared after lidocaine washout. During conducted sinus rhythm, similar results were found.
  
  
  CONCLUSIONS
  By combining pacing and MAP recordings, the diastolic slope observed on MAP recordings in ouabain-intoxicated hearts can be used as a marker for DADs and triggered arrhythmias. This finding may be helpful in identifying triggered activity in the intact heart.
authors.affiliation: Department of Cardiology, Cardiovascular Research Institute Maastricht, University Hospital, The Netherlands.
authors.forename: S H
authors.initials: SH
authors.lastname: de Groot
authors.forename: M A
authors.initials: MA
authors.lastname: Vos
authors.forename: A P
authors.initials: AP
authors.lastname: Gorgels
authors.forename: J D
authors.initials: JD
authors.lastname: Leunissen
authors.forename: B J
authors.initials: BJ
authors.lastname: van der Steld
authors.forename: H J
authors.initials: HJ
authors.lastname: Wellens
mesh_terms: D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D003971:Diastole; D004285:Dogs; D004594:Electrophysiology; D005260:Female; D008297:Male; D010042:Ouabain
chemical_list: D010042:Ouabain