There are several lines of evidence indicating disruption of calcium signaling in myocytes of infarcted myocardium. To understand its basic mechanism we have studied effect of experimentally induced infarction in rats by characterizing changes in kinetics of calcium spikes. Myocardial infarction was induced by a single intraperitoneal injection of isoproterenol (150 mg/kg^-1). On day 15 after ISO application, cardiac myocytes were isolated and studied by combination of patch clamp and confocal microscopy. The efficiency of the excitation-contraction coupling was assessed by recording calcium spikes in response to membrane depolarization. We have analyzed amplitude and kinetic properties of calcium spikes, evoked by calcium current activated by step depolarizations to 0 mV. Ca spikes were recorded by Leica TCS-SP2 confocal system, using Oregon Green BAPTA-5N (1 mM) as calcium indicator and EGTA (4 mM) in the patch pipette. Temporal fluorescence profiles were fitted by a parametrical model. We have observed substantial and significant changes in the latency and synchronization of Ca spikes relative to the stimulus onset. The amplitude of Ca spikes was slightly but significantly increased. Also, the rate of rise and the duration of Ca spikes were significantly prolonged. These findings characterize changes in calcium signaling in myocytes from infarcted hearts that are consistent with delayed and less synchronous calcium release observed by others. We conclude that individual dyads may have been modified due to the remodeling of infarcted myocardium.