It is well established that most of the Ca2+ that activates contraction in mammalian heart is released from the sarcoplasmic reticulum (SR) through ryanodine receptors (RyR) and that the RyR are themselves activated by Ca2+ in the mechanism known as “Ca2+ induced Ca2+ release”(CICR). 1 Confocal imaging has made possible the visualization of localized Ca2+ release through RyR, in the form of Ca2+ sparks. 2 It appears that Ca2+ sparks are triggered by a local [Ca2+] i,, which is different from the spatial average [Ca2+] i, and which is established first in the region of the RyR by the opening of a single L-type Ca2+ channel. 3, 4 These phenomena are the basis of the theory of excitationcontraction (EC) coupling known as “local control,” which was predicted so presciently by Michael D. Stern in 1992. 5 Nevertheless, the molecular mechanisms of Ca2+ sparks and the nature of the triggering by Ca2+ entry are still obscure. To complicate matters further, other possible sources of Ca2+ that activate, or “trigger,” this release have been proposed recently, and it has even been suggested that a voltage-sensitive release mechanism, which does not require Ca2+, may exist in cardiac muscle, similar to that in skeletal muscle. 6 It is our intention here to review the evidence for local control of EC coupling in normal heart muscle and to evaluate critically the evidence for additional sources of trigger Ca2+ or mechanisms of SR Ca2+ release. We emphasize, however, that concepts about cardiac Ca2+ sparks, and their possible role in cardiac EC coupling, do not necessarily extend to Ca2+ sparks that occur in smooth muscle and skeletal muscle. Local Ca2+ release in smooth muscle cells has also been called Ca2+ sparks, 7 but is thought to modulate relaxation, 8 rather than contraction. Local release events similar to Ca2+ sparks are not observed in adult mammalian skeletal muscle at all during EC coupling. 9