Cardiac excitation-Ca²⁺ release coupling is, in essence, a tale of two molecules, sarcolemmal voltage-gated L-type Ca²⁺ channels (LCCs) and intracellular ryanodine receptors (RyRs), communicating via the Ca²⁺-induced Ca²⁺ release mechanism. Recent advances have provided a microscopic view of the intermolecular Ca²⁺ signaling between LCCs and RyRs. In a dyadic junction or a "couplon", LCCs open and close stochastically upon depolarization, delivering a train of high local Ca²⁺ pulses ("Ca²⁺ sparklets") to the RyRs in the abutting SR terminal cisternae. Stochastic activation of RyRs discharges "Ca²⁺ sparks" from different couplons, which summate into global Ca²⁺ transients. Hence, ignition of Ca²⁺ sparks by Ca²⁺ sparklets constitute elementary events of EC coupling. While the sparklet-spark coupling is of low fidelity (at 0 mV, about one out of 50 sparklets triggers a spark under physiological conditions), the high-gain amplification of CICR (approximately 15 at 0 mV) is achieved because of the greater single-channel flux and open time of RyRs and multi-RyR origin of Ca²⁺ spark. The global stability of CICR is safeguarded by many factors acting in synergy, including physical separation of RyR clusters, sheer Ca²⁺ gradients around the channel pores, low intrinsic Ca²⁺ sensitivity of RyRs in vivo, and high cooperativity for the Ca²⁺-dependent spark activation. The local stability of CICR is insured because of strong, use-dependent inactivation of RyRs, that terminates Ca²⁺ sparks and confers persistent local SR refractoriness.