Key result
VF mechanism theories shift over ~160 years from neurogenic origins to myogenic and propagation disturbances.
A historical review of the theories surrounding the mechanisms of ventricular fibrillation, tracing the debate between neurogenic and myogenic origins.
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Historical context on VF mechanisms informs current models without guiding therapy; leaves open need for targeted mechanistic trials.
The mechanisms of initiation and maintenance of ventricular fibrillation (VF) we have been hotly debated since Hoffa and Ludwig first observed and documented the bizarre chaotic action of ventricles after exposure to electrical current.1 During this initial period of inquiry the majority of prominent physiologists favored a neurogenic origin of arrhythmogenesis with abnormal impulse formation within a specialized network of nerve cells, which were considered the primary culprit of arrhythmogenesis. Vulpian, in his work Note sur les effets de la faradisation directe des ventricules du coeur le chien in 1874, however, was the first to suggest a myogenic origin of arrhythmogenesis, postulating that the cardiac muscle fibers themselves and not a specialized nerve network were responsible for initiating and sustaining abnormal cardiac rhythms.2 In line with this observation he coined the term “mouvement fibrillaire ” or fibrillation to emphasize the myogenic nature of the process that he had observed. A former student of Ludwig, John McWilliam of Scotland presented similar observations supporting the myogenic nature of fibrillation and was the first to suggest in his work titled Fibrillar contraction of the heart in 1887 that disturbances in impulse propagation were responsible for the onset of fibrillation.3 In addition to the
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Kurian et al. (2010) conducted a review in Ventricular fibrillation. The mechanisms of ventricular fibrillation have been debated for over 160 years, evolving from early theories of a neurogenic origin to the recognition of a myogenic origin and impulse propagation disturbances.
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