Killing the primary heart pacemaker

Abstract

This editorial refers to ‘Insights into sick sinus syndrome from an inducible mouse model’ by S. Herrmann et al. , pp. 38–48, this issue. The most aggressive reviewer I have ever experienced is my barber. When I first came into his shop, conviviality naturally drove the conversation towards my job. Once asked about my research field I proudly replied: ‘I work on the mechanisms underlying the genesis and regulation of the heartbeat'. He looked surprised that such an important and apparently self-evident physiological function was still enveloped by some kind of uncertainty. ‘I am amazed that we are still paying researchers with public money to work on such an obvious thing'. To demonstrate that we still deserve our salaries, I explained that, while potentially counterintuitive, cardiac pacemaking is a complex function and several aspects of how heart rate is determined at the cellular and tissue level are not completely understood. Hermann et al .1 will further fuel the current debate on cardiac automaticity (and accessorily my personal debate with the barber). Heart pacemaker activity is generated in the sino-atrial node (SAN) by a relatively small population of specialized automatic myocytes. Beside the SAN, the atrioventricular node (AVN) and the Purkinje fibres network also contain spontaneously active myocytes. However, since the SAN possesses the highest intrinsic rate of pacing, it determines the heart rate under physiological conditions and constitutes the ‘primary’ cardiac rhythmogenic centre. …