Cardiac contraction is activated by an increase of intracellular calcium concentration ([Ca²⁺]_i), most of which comes from the sarcoplasmic reticulum (SR) where it is released, via the ryanodine receptor (RyR), in response to Ca²⁺ entering the cell on the L-type Ca²⁺ current. This phenomenon is termed Ca²⁺-induced Ca²⁺ release (CICR). However, under certain circumstances, the SR can become overloaded with Ca²⁺ and once a threshold SR Ca²⁺ content is reached Ca²⁺ is released spontaneously. Such spontaneous Ca²⁺ release from the SR propagates as a Ca²⁺ wave by CICR. Some of the Ca²⁺ released during a wave is removed from the cell on the electrogenic Na - Ca exchanger resulting in depolarization. This is the cellular mechanism producing delayed afterdepolarizations and is common to those arrhythmias produced by digitalis toxicity and right ventricular outflow tract tachycardia. More recently it has been suggested that arrhythmogenic Ca²⁺ waves can also occur if the properties of the RyR are altered, resulting in increase of RyR open probability, for example by phosphorylation. However, in this review experimental evidence will be presented to support the view that such arrhythmias still require a threshold SR Ca²⁺ content to be exceeded and that this threshold is decreased by increasing RyR open probability. (Circ J 2009; 73: 1561-1567)