The majority of contractile calcium in cardiac muscle is released from stores in 
the sarcoplasmic reticulum (SR), by a process of calcium-induced calcium release 
(CICR) through ryanodine receptors. Because CICR is intrinsically 
self-reinforcing, the stability of and graded regulation of cardiac EC coupling 
appear paradoxical. It is now well established that this gradation results from 
the stochastic recruitment of varying numbers of elementary local release 
events, which may themselves be regenerative, and which can be directly observed 
as calcium sparks. Ryanodine receptors (RyRs) are clustered in dense lattices, 
and most calcium sparks are now believed to involve activation of multiple RyRs. 
This implies that local CICR is regenerative, requiring a mechanism to terminate 
it. It was initially assumed that this mechanism was inactivation of the RyR, 
but during the decade since the discovery of sparks, no sufficiently strong 
inactivation mechanism has been demonstrated in vitro and all empirically 
determined gating schemes for the RyR give unstable EC coupling in Monte Carlo 
simulations. We consider here possible release termination mechanisms. 
Stochastic attrition is the spontaneous decay of active clusters due to random 
channel closure; calculations show that it is much too slow unless assisted by 
another process. Calcium-dependent RyR inactivation involving third-party 
proteins remains a viable but speculative mechanism; current candidates include 
calmodulin and sorcin. Local depletion of SR release terminal calcium could 
terminate release, however calculations and measurements leave it uncertain 
whether a sufficient diffusion resistance exists within the SR to sustain such 
depletion. Depletion could be assisted by dependence of RyR activity on SR 
lumenal [Ca(2+)]. There is substantial evidence for such lumenal activation, but 
it is not clear if it is a strong enough effect to account for the robust 
termination of sparks. The existence of direct interactions among clustered RyRs 
might account for the discrepancy between the inactivation properties of 
isolated RyRs and intact clusters. Such coupled gating remains controversial. 
Determining the mechanism of release termination is the outstanding unsolved 
problem of cardiac EC coupling, and will probably require extensive genetic 
manipulation of the EC coupling apparatus in its native environment to unravel 
the solution.