Nerve sprouting, defibrillation and calcium waves

Mitsunori Maruyama, Shengmei Zhou, Gyo Seung Hwang, Su Kiat Chua, Po Cheng Chang, Shien-Fong Lin, Lan S. Chen, Tomohiko Ai, Peng Sheng Chen*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Zoll et al. first reported the successful termination of ventricular fibrillation (VF) by externally applied electrical countershocks. In the same seminal report, the authors also discovered that recurrent VF may occur shortly after successful ventricular de fibrillation. Due to the general availability of the implantable cardioverter-de fibrillator (ICD), patients may survive the initial VF episodes but suffer from multiple recurrent VF and de fibrillation shocks within a short period of time. The clustering of recurrent VF episodes (electrical storm) after initial successful de fibrillation suggests that the first episode of VF begets subsequent episodes of VF. The mechanisms by which VF begets VF remains poorly understood. In this chapter we will discuss the mechanisms of neural remodeling after myocardial infarction (MI). We propose that nerve sprouting and sympathetic hyperinnervation occur after MI. The increased sympathetic nerve densities in the heart is highly heterogeneous, with portions of the heart showing increased nerve densities while the remaining portions of the heart showing denervation. During sympathetic nerve activation, there is increased heart rate and augmented intracellular calcium (Ca i) concentration. In addition, we found that the action potential duration (APD) is abbreviated after a fibrillation-de fibrillation episode in failing ventricles. The shortened APD and the elevated Ca i promotes late phase 3 early afterdepolarization (EAD) and Ca 2+-transient triggered firing (CTTF), leading to recurrent cardiac fibrillation. We also propose that the mechanisms of APD shortening after fibrillation-de fibrillation episodes in the failing (but not in the normal) ventricles are due to the upregulation of small conductance Ca 2+ activated potassium (SK) currents. We hope that these discussions will help the readers better understand the relevance of cardiac neural remodeling and electrical remodeling in the mechanisms of arrhythmogenesis.

Original languageEnglish
Title of host publicationElectrical Diseases of the Heart
Subtitle of host publicationVolume 1: Basic Foundations and Primary Electrical Diseases
PublisherSpringer-Verlag London Ltd
Pages219-232
Number of pages14
ISBN (Electronic)9781447148814
ISBN (Print)9781447148807
DOIs
StatePublished - 1 Jan 2013

Keywords

  • Afterdepolarization
  • Apamin
  • Calcium dynamics
  • Defibrillation
  • Heart failure
  • Optical mapping
  • Small conductance calcium activated potassium channels
  • Sudden death
  • Triggered activity
  • Ventricular fibrillation

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  • Cite this

    Maruyama, M., Zhou, S., Hwang, G. S., Chua, S. K., Chang, P. C., Lin, S-F., Chen, L. S., Ai, T., & Chen, P. S. (2013). Nerve sprouting, defibrillation and calcium waves. In Electrical Diseases of the Heart: Volume 1: Basic Foundations and Primary Electrical Diseases (pp. 219-232). Springer-Verlag London Ltd. https://doi.org/10.1007/978-1-4471-4881-4_13