Objective: To characterize myocardial metabolism by positron emission tomography (PET) of ventricular fibrillation cardiac arrest (VFCA) and asphyxiation cardiac arrest (ACA) porcine models after postresuscitation.Design and Method: Thirty-two healthy miniature pigs were randomized into two groups.The VFCA group (n=16) were subject to programmed electric stimulation, and the ACA group (n=16) underwent endotracheal tube clamping, to induce CA.Once induced, CA remained untreated for a period of 8 min.Two minutes following initiation of cardiopulmonary resuscitation (CPR), defibrillation was attempted until return spontaneous circulation (ROSC) was achieved or animals died.To assess myocardial metabolism, PET was performed at baseline, 4 hrs and 24hrs after return of spontaneous circulation (ROSC) ROSC.To analyze 18F-FDG myocardial uptake in PET, the maximum standardized uptake value (SUVmax) was measured.Results: ROSC was 100% successful in VFCA and only 62.5% successful in ACA.The average survival time of VFCA was however significantly longer than ACA (22.50±1.10 vs 11.16±2.66h, P=0.005).Myocardial metabolism imaging using PET demonstrated that myocardial metabolism injuries after ACA were more severe and widespread than after VFCA at 4 hrs and 24hrs after ROSC.SUVmax was higher in VFCA group than in ACA group (4 hrs after ROSC: 1.95±0.13 vs 1.00-±-0.17, P<0.01; 24 hrs after ROSC: 2.51±-0.22 vs 1.21±0.08, P<0.01).In VFCA group, SUVmax of left ventricular at 24 hrs after ROSC was increased to the level of baseline.Conclusions: Compared with VFCA, ACA causes more severe cardiac metabolism dysfunction associated with less successful resuscitation and shorter survival time.Myocardial stunning does occur with VFCA but maybe not with ACA.