Arrhythmias and contractile dysfunction both contribute to the high morbidity and mortality in patients with congestive heart failure. Contractile dysfunction is generally believed to reflect a decrease in the amplitude of intracellular Ca(2+) transients, whereas tachyarrythmias are often initiated in the setting of cellular Ca(2+) overload. In a rabbit model of left ventricular dysfunction due to myocardial infarction, we found evidence that myocyte sarcoplasmic reticulum Ca(2+) content may be normal or even increased at slow stimulation rates. This may occur because prolonged action potential duration promotes Ca(2+) influx via the Na(+)/Ca(2+) exchanger. Despite preserved SR Ca(2+) content, intracellular Ca(2+) transients and contractions may be reduced in amplitude because of impaired synchronization of Ca(2+) release events throughout the myocyte.