Abstract 3327: Mechanism of Ventricular Fibrillation in Diseased Human Hearts In-Vivo: Insights from Intra-Operative Multi-electrode Mapping
Purpose Ventricular fibrillation (VF), a chaotic cardiac rhythm, is an important cause of sudden cardiac death and cardiovascular mortality. In spite of the fact that VF is a common cause of demise in cardiomyopathic patients, the mechanism of human VF is unknown. VF in humans is generally thought to be due to small wandering re-entrant wavefronts that change paths cycle to cycle.
Methods We studied early VF in-vivo in myopathic patients using multi-electrode arrays intra-operatively; simultaneously on the epicardium and endocardium in left ventricular cardiomyopathy (n=3) and the endocardium in right ventricular myopathy (n=2) patients.
Results The total duration mapped was 7±4 s. Rotors were identified in all 5 of the myopathic heart studied during VF. Commonly 2 rotors were present on the mapping surface with opposite chirality. For each surface mapped 3.6±2.9 rotors were identified. The rotors lasted mean of 48±29% of the VF segments analyzed. The mean duration of the rotors was 200±32 ms. The average number of cycles completed by these rotors was 4.9±4.9. Longest rotor lasted 10.2±6.2 rotation and lasted 2.0±1.2 s. When these rotors are spatially clustered, they give rise to domains that activate at faster rates with evidence of conduction block at the border between the slower domains. There is evidence of centrifugal activation away from these rotors. When the rotors are multiple and short lived or meandering they do not give rise to domains.
Conclusions These findings are consistent with the mechanistic notion that dominant sources that exhibit conduction block that give rise to a pattern of fibrillatory conduction underlie early VF in myopathic human hearts.