In cardiac myocytes, calcium cycling links the dynamics of the membrane potential to the activation of the contractile filaments. Perturbations of the calcium signalling toolkit have been demonstrated to disrupt this connection and lead to numerous pathologies including cardiac alternans. This rhythm disturbance is characterised by alternations in the membrane potential and the intracellular calcium concentration, which in turn can lead to sudden cardiac death. In the present computational study, we make further inroads into understanding this severe condition by investigating the impact of calcium buffers and L-type calcium channels on the formation of subcellular calcium alternans when calcium diffusion in the cytosol is weak and the main route of ${\mathrm{Ca}}^{2+}$ transport in the myocyte is via the sarcoplasmic reticulum. Through numerical simulations of a two dimensional network of calcium release units, we show that increasing calcium entry is proarrhythmogenic and that this is modulated by the calcium-dependent inactivation of the L-type calcium channel. We also find that while calcium buffers can exert a stabilising force and abolish subcellular ${\mathrm{Ca}}^{2+}$ alternans, they can significantly shape the spatial patterning of subcellular calcium alternans. Taken together, our results demonstrate that subcellular calcium alternans can emerge via various routes and that calcium diffusion in the sarcoplasmic reticulum critically determines their spatial patterns.

在心肌细胞中，钙循环将膜电位的动力学与收缩细丝的激活联系起来。钙信号传导工具包的扰动已被证明破坏了这种联系，并导致了许​​多疾病，包括心脏交替素。这种节律紊乱的特征在于膜电位和细胞内钙浓度的交替变化，这又可能导致心脏猝死。在目前的计算研究中，我们通过研究钙缓冲液和L型钙通道对钙在细胞质中的扩散较弱时钙缓冲液和L型钙通道对亚细胞钙交替素形成的影响以及进一步研究的主要途径，进一步深入了解这种严重状况。${\mathrm{钙}}^{2+}$肌细胞中的转运是通过肌浆网。通过钙释放单元的二维网络的数值模拟，我们表明增加的钙进入是致心律失常的发生，并且这是由L型钙通道的钙依赖性失活调节的。我们还发现，尽管钙缓冲液可以发挥稳定作用并消除亚细胞${\mathrm{钙}}^{2+}$它们可以显着影响亚细胞钙交替蛋白的空间分布。两者合计，我们的结果表明，亚细胞钙交替蛋白可以通过各种途径出现，并且钙在肌质网中的扩散决定了它们的空间分布。