Endocardial focal activation originating from Purkinje fibers plays a role in the maintenance of long duration ventricular fibrillation.

Sudden cardiac death (SCD), commonly caused by ventricular fibrillation (VF), is responsible in China for at least 500 000 deaths per year (1). Typically, patients with SCD due to VF are not defibrillated for several minutes, even in areas with the shortest first response times. After 10 minutes of VF, few patients are successfully resuscitated (2). However, after 5 minutes of VF, cardiopulmonary resuscitation (CPR) for 3 minutes prior to the first shock resulted in 22% survival to hospital discharge and 4% survival when the defibrillation shock was given before CPR (3). Thus, survival after more than 5 minutes of VF is possible. Furthermore, different treatment algorithms may be preferable during different durations of long duration ventricular fibrillation (LDVF). As such, it is important to understand the mechanisms of LDVF maintenance. However, despite our understanding of VF initiation and early VF, the electrophysiological mechanism by which LDVF is maintained remains largely unknown (4). Early VF is characterized by rapid, chaotic activation, after which a more organized pattern is observed (5,6). Although the primary VF maintenance mechanism regardless of VF duration is considered to be reentry into the working ventricular myocardium (WVM) (4,7), the mechanisms for short duration VF (SDVF, VF<1 minute) and LDVF may differ (4,7,8). While in SDVF the dominant driving force is reentrant activity, in LDVF it may be Purkinje fiber (PF) activation (4,7,8). For example, Tabereaux et al (9) reported highly active PFs throughout the first 10 minutes of VF using an isolated canine heart model of repetitive endocardial focal activations during LDVF. Furthermore, these PF were associated with the genesis of repetitive endocardial focal activations. Thus, the aim of the present study was to test whether repetitive endocardial focal activations played a role in the maintenance of LDVF, and to determine the role of PF in LDVF maintenance in canine hearts in vivo.