Abstract

This editorial refers to ‘KATP channel opening accelerates and stabilizes rotors in a swine heart model of ventricular fibrillation’ by J.G. Quintanilla et al ., pp. 576–585, this issue. Ventricular fibrillation (VF) is a remarkably complex and seemingly disorganized cardiac excitation, in which propagating electrical waves fail dismally to activate the ventricles synchronously, with the consequent loss of contractile function. Despite its declining incidence, VF is still a major cause of sudden cardiac death in industrialized nations, which accounts for nearly 300 000 annual fatalities in the USA alone.1,2 Clinically, VF can be observed on the electrocardiogram (ECG) as the sudden transition from the highly ordered and rhythmic pattern generated by sinuatrial activation into an irregular and aperiodic pattern, with undulating and variable morphology of the QRS complex. Traditionally, the highly aperiodic and irregular ECG traces associated with VF have been thought to be the result of a totally random excitation of the ventricles.3,4 However, over the last 20 years,5 numerous advances in high-resolution spatiotemporal imaging, computer simulations, molecular, and genetic techniques have led to the gradual emergence of a new concept of VF, which turns out to be much more organized than the ECG would first suggest.6,7 Such new advances have allowed investigation into the dynamics of fibrillatory behaviour and, just as important, the mechanisms underlying such dynamics in the structurally normal heart. Our technology has progressed to the point where we can now integrate multiple levels of organization, from the molecule to the organ level, as an aid to generate a cohesive understanding of the mechanisms that underlie the generation and maintenance of VF even in the structurally abnormal, diseased heart. With such efforts, we might be able to improve patient outcomes through the development of better designed and …

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