—The kinetics of contractions and Ca²⁺ transients are slowed in myocytes from failing hearts. The mechanisms accounting for these abnormalities remain unclear. Myocardial infarction (MI) was produced by ligation of the circumflex artery in rabbits. We used confocal microscopy to record spatially resolved Ca²⁺ transients during field stimulation in left ventricular (LV) myocytes from control and infarcted hearts (3 weeks). Compared with controls, Ca²⁺ transients in myocytes adjacent to the infarct had lower peak amplitudes and prolonged time courses. Control myocytes showed relatively uniform changes in [Ca²⁺] throughout the cell after electrical stimulation. In contrast, in MI myocytes [Ca²⁺] increased inhomogeneously and localized increases in [Ca²⁺] occurred throughout the rising and falling phases of the Ca²⁺ transient. Ca²⁺ content of the sarcoplasmic reticulum did not differ between MI and control myocytes. Peak L-type Ca²⁺ current density was reduced in MI myocytes. The macroscopic gain function was not different in control and MI myocytes when calculated as the amplitude of the Ca²⁺ transient/peak I_Ca. However, when calculated as the peak rate of rise of the Ca²⁺ transient/peak I_Ca, the gain function was modestly decreased in the MI myocytes. Application of isoproterenol (100 nmol/L) improved the synchronization of Ca²⁺ release in MI myocytes at both 0.5 and 1 Hz. The poorly coordinated production of Ca²⁺ sparks in myocytes from infarcted rabbit hearts likely contributes to the diminished and slowed macroscopic Ca²⁺ transient. These abnormalities can be largely overcome when phosphorylation of Ca²⁺ cycling proteins is enhanced by β-adrenergic stimulation.