New Paper about Sympathetic Compensatory Mechanisms for Hypocalcaemia-Induced Bradycardia

In this work, we explored interspecies differences between the extended Severi (rabbit) and Fabbri (human) sinoatrial node cell models to elucidate the pathophysiological mechanisms of the elevated prevalence of sudden cardiac death in haemodialysis patients.

- We extended the sinoatrial node cell models of Severi et al. (rabbit) and Fabbri et al. (human) using the β-adrenergic receptor signalling cascade Behar et al. described.
- Simulations were conducted across various extracellular calcium (0.6–1.8 mM) and isoprenaline concentrations [ISO] (0–1000 nM) to reflect conditions in haemodialysis patients.
- An exponential-like increase in [ISO] compensated for hypocalcaemia-induced bradycardia in both models, whereas interspecies differences increased the sensitivity of the extended Fabbri model towards hypocalcaemia and increased sympathetic tone.
- The extended models may help to further understand the pathomechanisms of several cardiovascular diseases affecting pacemaking, such as the high occurrence of sudden cardiac death in chronic kidney disease patients.

This achievement would not have been possible without the invaluable contributions of the authors: Moritz Linder, Tomas Stary, Gergő Bitay, Norbert Nagy, and Axel Loewe.

We also extend our gratitude to all members of the CaMo KIT for their support and contributions. For those interested in exploring this work further, the paper is available at this link.

We look forward to further discussions and collaborations in advancing the field of cardiac electrophysiology.