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Cardiovascular Research Advance Access originally published online on September 13, 2007
Cardiovascular Research 2008 77(2):285-292; doi:10.1093/cvr/cvm009
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

The sarcoplasmic reticulum and arrhythmogenic calcium release

Luigi A. Venetucci, Andrew W. Trafford, Stephen C. O'Neill and David A. Eisner*

Unit of Cardiac Physiology, University of Manchester, Core Technology Facility, 46 Grafton St, Manchester M13 9NT, UK

* Corresponding author. Tel: +44 161 275 2702; fax: +44 161 275 2703. E-mail address: eisner{at}man.ac.uk

There is much evidence showing that some lethal ventricular arrhythmias arise from waves of Ca2+ release from the sarcoplasmic reticulum (SR) that propagate along cardiac cells. The purpose of this review is to discuss the mechanism of production of these waves and how they depend on the properties of the SR Ca2+ release channel or ryanodine receptor (RyR). The best-known method of producing Ca2+ waves is by increasing the Ca2+ content of the cell by either increasing Ca2+ influx or decreasing efflux. Once SR Ca2+ content reaches a threshold level a Ca2+ wave is produced. Altering the properties of the RyR affects the threshold level of Ca2+ required to produce a wave. Patients with a mutation in the RyR suffer from catecholaminergic polymorphic ventricular tachycardia, and this may be due to a decrease in the SR Ca2+ threshold for wave production. Heart failure has also been suggested to result in Ca2+ waves due to a leak of Ca2+ through the RyR. We review the finding that these changes in RyR function will only result in Ca2+ waves in the steady state if some other mechanism maintains the SR Ca2+ content. The review concludes with a description of potential mechanisms for treating arrhythmias produced by Ca2+ waves.

KEYWORDS Calcium; Wave; Delayed afterdepolarization; Arrhythmia

Time for primary review: 26 days


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