title: Three distinct phases of VF during global ischemia in the isolated blood-perfused pig heart.
abstract: Changes in ventricular fibrillation (VF) organization occurring after the onset of global ischemia are relevant to defibrillation and survival but remain poorly understood. We hypothesized that ischemia-specific dynamic instability of the action potential (AP) causes a loss of spatiotemporal periodicity of propagation and broadening of the electrocardiogram (ECG) frequency spectrum during VF in the ischemic myocardium. We recorded voltage-sensitive fluorescence of di-4-ANEPPS (anterior left ventricle, 35 x 35 mm, 64 x 64 pixels) and the volume-conducted ECG in six blood-perfused hearts during 10 min of VF and global ischemia. We used coefficient of variation (CV) to estimate variability of AP amplitude, AP duration, and diastolic interval (CV-APA, CV-APD, and CV-DI, respectively). We computed excitation median frequency (Median_F), spectral width of the AP and ECG (SpW-AP and SpW-ECG, respectively), wavebreak incidence (WBI), and recurrence of propagation direction (RPD). We found three distinct phases of local VF dynamics: "relatively periodic" (<or=1 min, high Median_F, moderate AP variability, high WBI, low RPD), "highly periodic" (1-2 min, reduced Median_F, low AP variability, low WBI, high RPD), and "aperiodic" (3-10 min, low Median_F, high AP variability, high WBI, low RPD). In one experiment, spontaneous conversion from the aperiodic to the highly periodic phase occurred after 5 min of ischemia. The SpW-ECG was correlated with SpW-AP, CV-APD, and CV-APA. We conclude that 1) at least three distinct phases of VF dynamics are present in our model, and 2) the newly described aperiodic phase is related to ischemia-specific dynamic instability of the AP shape, which underlies broadening of the ECG spectrum during VF evolution.
authors.affiliation: Institute for Cardiovascular Research, State University of New York Upstate Medical University, Syracuse, New York, USA.
authors.forename: Jose F
authors.initials: JF
authors.lastname: Huizar
authors.forename: Mark D
authors.initials: MD
authors.lastname: Warren
authors.forename: Alexander G
authors.initials: AG
authors.lastname: Shvedko
authors.forename: Jérôme
authors.initials: J
authors.lastname: Kalifa
authors.forename: Javier
authors.initials: J
authors.lastname: Moreno
authors.forename: Sergey
authors.initials: S
authors.lastname: Mironov
authors.forename: José
authors.initials: J
authors.lastname: Jalife
authors.forename: Alexey V
authors.initials: AV
authors.lastname: Zaitsev
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D013552:Swine; D014693:Ventricular Fibrillation / Q000503:physiopathology*