Heart failure (HF) is a progressive syndrome that appears as the final phase of most cardiac diseases and is manifested as a decreased contractile function. Contraction in cardiomyocytes arises by the Ca²⁺ induced Ca²⁺ release mechanism, where Ca²⁺ entry (I_Ca) through Ca²⁺ channels (DHPRs) activates Ca²⁺ release channels (RyRs) in the junctional sarcoplasmic reticulum (SR). This is the base of cardiac excitation-contraction (EC) coupling. To elucidate the mechanisms underlying depressed function of the failing heart, analysis of EC coupling main elements have been undertaken. I_Ca density is usually maintained in HF. However, failing myocytes show a reduced SR Ca²⁺ release. Then, if the trigger of SR Ca²⁺ release is maintained, why is SR Ca²⁺ release depressed in HF? Analyses of the DHPR-RyR coupling efficiency have revealed a decrease in the I_Ca efficacy to trigger Ca²⁺ release in failing myocytes. In terminal heart failure without hypertrophy, a decrease in SR Ca²⁺ load can account for the decreased SR Ca²⁺ release. Fewer Ca²⁺ sparks (elementary units of SR Ca²⁺ release) are triggered by an equivalent I_Ca in hypertrophied failing myocytes, suggesting a functional or spatial reorganization of the space T-tubule junctionnal SR. This theory is supported by new data showing that the T-tubule density is reduced in failing cells.