## 1 Introduction  
Ischemic heart disease (IHD) is the most common cardiovascular illness, with an increasing prevalence worldwide [1]. It is estimated to affect more than 1.85% of the global population by 2030. The pathophysiological process of IHD refers to myocardial ischemia (MI), which generally occurs when blood flow through a coronary artery is physically obstructed [2]. Following this closure, the electrical impedance of myocardial tissue typically increases, resulting in a reduction in conduction velocity and changes in the action potential duration (APD) [3]. The increased electrophysiological heterogeneity between ischemic and normal myocardial regions establishes an arrhythmogenic substrate. Therefore, MI may lead to severe cardiac arrhythmias and even sudden cardiac death [4]. Cardiac repolarization alternans (CRA) triggered by MI has garnered significant clinical attention as it is considered a risk indicator and key pathophysiological mechanism underlying arrhythmias and sudden cardiac death [5]. CRA is characterized by beat-to-beat variations in the APD, AP amplitude, and intracellular calcium transient in cardiomyocytes [6]. This alternation can be observed at the cellular level and can manifest on the surface electrocardiogram (ECG) as T-wave alternans (TWA), which is a crucial biomarker of the severity of IHD [7]. Changes in multiple transmembrane ionic currents are fundamental to CRA formation [8]. Among these, the L-type calcium ion current (I\({}_{\text{CAL}}\)) is the primary inward ion flow during the repolarization phase and significantly influences the plateau phase of AP of cardiomyocytes. Pathophysiological conditions such as hyperkalemia, acidosis, and hypoxia resulting from MI can promote alternans by affecting Ca\({}^{2+}\) currents [9]. Under MI, variations in APD and the Ca transient usually occur together [10] due to the bidirectional coupling between the membrane voltage and intracellular Ca. APD directly influences the Ca transient amplitude, while the Ca transient amplitude, in turn, directly affects APD via Ca-sensitive currents such as I\({}_{\text{CAL}}\) and Na-Ca exchange (NCX), acting as a critical component to maintaining calcium homeostasis. The inhibition of NCX may help attenuate CRA [11]. The bidirectional coupling, whether voltage-driven or calcium-driven, is inherently unstable, potentially leading to complex repolarization processes and calcium cycling kinetics [6]. An understanding of CRA is essential for the early detection and prevention of life-threatening cardiac events, thus benefiting targeted treatment [6]. To date, the underlying mechanisms of CRA continue to be studied, highlighting the roles of sarcoplasmic reticulum (SR) Ca\({}^{2+}\) content, ryanodine receptor (RyR) function, and sarco-endoplasmic reticulum Ca\({}^{2+}\)-ATPase (SERCA) activity. [PERSON] et al. posited that alternans primarily stems from fluctuations in the SR Ca\({}^{2+}\) content [12]. Their findings indicated a correlation between alternans in the amplitude of systolic Ca\({}^{2+}\) transients and alternating SR Ca\({}^{2+}\) content. This alternation results from a steep dependence of Ca\({}^{2+}\) release on SR Ca\({}^{2+}\) content, facilitated by Ca\({}^{2+}\)-induced Ca\({}^{2+}\) release triggered by L-type Ca\({}^{2+}\) channels. The larger transients arise from the propagation of Ca\({}^{2+}\) waves, which are steep functions of SR Ca\({}^{2+}\) content. This steep relationship suggests that changes in SR Ca\({}^{2+}\) content are sufficient to produce alternans, where larger Ca\({}^{2+}\) transients lead to significant Ca\({}^{2+}\) efflux, lowering SR Ca\({}^{2+}\) content and resulting in a smaller subsequent Ca\({}^{2+}\) transient. The study by [PERSON] et al. challenges the notion that diastolic SR Ca\({}^{2+}\) content fluctuations are essential for alternans, suggesting that the availability and recovery of RyRs are more critical [13]. Their study showed that alternans could occur without significant diastolic SR Ca\({}^{2+}\) content fluctuations.