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Changes in intracellular Ca2+homeostasis induced by 1 μM Amiodarone solution were studied with muscle strips isolated from the right atrial auricles of patients with ischemic heart disease (IHD). The intracellular Ca2+homeostasis was evaluated through the changes in contractility in the muscle strips caused by a 60-s discontinuation of their stimulation by electrical pulses. It was found that, in 30% of the IHD patients, the atrial myocardium displayed an abnormal contractility. Myocardium samples with normal contractility displayed two types of inotropic response to the resumption of electrical stimulation. The first type was associated with a 30% decrease in the parameters of the contraction–relaxation cycle, whereas, for the second type, this decrease was stronger (by 70% or more). An incubation of the muscle samples with the Amiodarone solution suppressed the abnormal contractility, did not affect the muscles with the first type of response, and significantly (p< 0.05) increased the inotropic response in the muscles with the second type of reaction to a short interruption in their electrical stimulation. As Amiodarone itself induces no direct positive inotropic effects, it was supposed that, in some cases of IHD, the presence of Amiodarone in the atrial myocardium is associated with an increased ability of the sarcoplasmic reticulum to retain calcium ions accumulated. This phenomenon may contribute to the suppression of abnormal activity of the atrial myocardium and strengthen the direct antiarrhythmic effect of Amiodarone.