Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Pflugers Arch. 2021 Mar;473(3):377-387. doi: 10.1007/s00424-020-02505-y. Epub 2021 Jan 6.
Sudden cardiac death due to malignant ventricular arrhythmias remains the major cause of mortality in the postindustrial world. Defective intracellular Ca homeostasis has been well established as a key contributing factor to the enhanced propensity for arrhythmia in acquired cardiac disease, such as heart failure or diabetic cardiomyopathy. More recent advances provide a strong basis to the emerging view that hereditary cardiac arrhythmia syndromes are accompanied by maladaptive remodeling of Ca homeostasis which substantially increases arrhythmic risk. This brief review will focus on functional changes in elements of Ca handling machinery in cardiomyocytes that occur secondary to genetic mutations associated with catecholaminergic polymorphic ventricular tachycardia, and long QT syndrome.
由于恶性室性心律失常导致的心脏性猝死仍然是工业化后世界的主要死亡原因。细胞内钙稳态的缺陷已被证实是获得性心脏病（如心力衰竭或糖尿病心肌病）中增强心律失常易感性的一个关键因素。最近的进展为一个新兴观点提供了强有力的依据，即遗传性心律失常综合征伴随着钙稳态的适应性重构，这大大增加了心律失常的风险。这篇简短的综述将重点介绍与儿茶酚胺多形性室性心动过速和长 QT 综合征相关的基因突变引起的心肌细胞中钙处理机制元件的功能变化。
