Related Experiment Video
Updated: Sep 19, 2026

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
Published on: February 17, 2023
Ventricular Fibrillation Mapping in a Large-Animal Model Using Dual Mechanical Circulatory Support: Electroanatomic
Karol Quelal Analuisa1, Jason A Tri1, Ikram U Haq1
1Department of Cardiovascular Medicine, Mayo Clinic, Rochester (K.Q.A., J.A.T., I.U.H., A.W., H.N., A.B., S.Y., R.W., F.E., N.Y.T., F.D.-C.M., S.A., C.V.D.).
Background:
Ventricular fibrillation (VF) remains a leading cause of sudden cardiac death with an incompletely characterized electrophysiological substrate. Traditional large-animal VF models are limited by hemodynamic collapse and myocardial ischemia. This study establishes a reproducible swine model using dual mechanical circulatory devices to enable high-density electroanatomic mapping under nonischemic conditions.
Methods:
Five Yorkshire swine (55-65 kg) underwent sustained VF supported by venoarterial extracorporeal membrane oxygenation (2.5-3.0 L/min) and percutaneous left ventricular unloading (Impella CP, P-2-P-4). High-density electroanatomic mapping using CARTO 7 was performed at baseline and after defibrillation. Bipolar voltage was acquired from 7 predefined ventricular regions (21 measurements per animal per time point; n=210 paired observations). Unipolar voltage mapping and continuous surface ECG monitoring were used to assess acute ischemic injury. Systemic perfusion was maintained at systolic arterial pressure ≥80 mm Hg. Linear mixed-effects modeling was used to analyze voltage changes from pre-VF to post-VF.
Results:
Sustained VF (10±1 minutes) was reproducibly induced and maintained with consistent hemodynamics (systolic arterial pressure, 90±5 mm Hg; extracorporeal membrane oxygenation flow, 2.5±0.5 L/min). All animals were successfully defibrillated. High-density mapping was feasible in all experiments (1000±300 points per chamber). Bipolar voltage showed no change from pre-VF (5.86±2.56 mV) to post-VF (6.53±2.22 mV; mean difference, 0.67 mV [95% CI, -0.31 to 1.65]; P=0.15). Both left (P=0.17) and right ventricles (P=0.08) demonstrated voltage preservation. Regional analysis showed no significant changes (all P>0.05); post-VF voltages remained above viability thresholds (>1.5 mV). Unipolar voltage maps recovered toward baseline, with no ECG injury pattern identified after defibrillation.
Conclusions:
Dual mechanical circulatory support with venoarterial extracorporeal membrane oxygenation and Impella CP enables reproducible, high-fidelity electroanatomic mapping and preserves myocardial substrate after sustained VF in a large-animal model. This platform overcomes key technical barriers in VF research, providing a nonischemic foundation for future mechanistic and translational studies.

