Ca 2 + sparks, the elementary units of sarcoplasmic reticulum (SR) Ca 2 + release in cardiac, smooth and skeletal muscle are localized (2-4 μm) increases in intracellular Ca 2 + concentration, [Ca 2 + ] i , that last briefly (30-100 ms). These Ca 2 + , sparks arise from the openings of a single SR Ca 2 + release channel (ryanodine receptor, RyR) or a few RyRs acting in concert. In heart muscle, Ca 2 + sparks can occur spontaneously in quiescent cells at a low rate (100 s - 1 per cell). Identical Ca 2 + sparks are also triggered by depolarization because the voltage-gated sarcolemmal L-type Ca 2 + channels (dihydropyridine receptors, DHPRs) locally increase [Ca 2 + ] i and thereby activate the RyRs by Ca 2 + -induced Ca 2 + release (CICR). The exquisite responsiveness of this process, reflected by the ability of even a single DHPR to activate a Ca 2 + spark, is perhaps due to the large local increase in [Ca 2 + ] i in the vicinity of the RyR that is a consequence of the close apposition of the DHPRs and the RyRs. In this review we examine our current understanding of cardiac excitation-contraction (EC) coupling in light of recent studies on the elementary Ca 2 + release events or Ca 2 + sparks. In addition, we further characterized Ca 2 + spark properties in rat and mouse heart cells. Specifically we have determined that: (i) Ca 2 + sparks occur at the junctions between the transverse-tubules and the SR in both species; (ii) Ca 2 + sparks are asymmetric, being 18% longer in the longitudinal direction than in the transverse direction; and (iii) Ca 2 + sparks individually do not produce measurable sarcomere shortening (< 1 %). These results are discussed with respect to local activation of the RyRs, the stability of CICR, Ca 2 + diffusion, and the theory of EC coupling.