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Electrical storm and calcium signaling: a review
1Department of Cardiovascular Research, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan. y-tsuji@hh.iij4u.or.jp
Journal of Electrocardiology
|October 25, 2011
Summary
Electrical storm (ES) involves recurrent arrhythmias and heart failure. Our animal model reveals CaMKII activation and altered calcium handling, offering insights into ES pathophysiology and potential treatments.
Area of Science:
- Cardiology
- Molecular Biology
- Electrophysiology
Background:
- Electrical storm (ES) is a critical condition in patients with implantable cardioverter-defibrillators, often leading to progressive heart failure.
- The molecular mechanisms driving ES and its associated heart failure remain poorly understood.
Purpose of the Study:
- To describe the pathophysiology of electrical storm.
- To explore potential therapeutic strategies for electrical storm.
- To present a novel animal model of electrical storm.
Main Methods:
- Creation of an animal model simulating electrical storm with repetitive implantable cardioverter-defibrillator firing.
- Analysis of molecular changes, including Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activation and Ca(2+)-handling protein phosphorylation.
Main Results:
- Electrical storm events in the animal model induced significant CaMKII activation.
- Prominent alterations in Ca(2+)-handling protein phosphorylation were observed during electrical storm.
- These molecular changes may explain mechanical dysfunction and arrhythmia promotion in ES.
Conclusions:
- The developed animal model provides a platform for studying electrical storm.
- CaMKII activation and altered calcium handling are key molecular events in ES pathophysiology.
- Understanding these mechanisms can guide the development of novel therapeutic strategies for electrical storm.
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