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- W2912167741 abstract "Calsequestrin 2 (CASQ2) is high capacity and low-affinity Ca2+-binding protein expressed in the sarcoplasmic reticulum (SR) of cardiac myocyte. Mutation that occurs in CASQ2 expressing gene have been linked to arrhythmia and possibly sudden cardiac death (SCD) with acute emotional stress or exercise. This inherited genetic disorder is known as catecholamine polymorphic ventricular tachycardia (CPVT). Understanding the subcellular mechanisms of CPVT is experimentally challenging because the arrhythmias are rare and the development of SCD are even rarer. The underlying causes of CPVT have been described as delayed afterdepolarizations (DADs), early afterdepolarizations (EADs) or Ca2+ signaling alternans. To gain insight into the nature of this rare disease, we have developed a local control stochastic model of the cardiac myocyte to investigate how the mutant CASQ2s may be responsible for the development of an arrhythmogenic episode under the condition of beta-adrenergic stimulation or in the pauses afterward. We choose a long action potential model to contrast with our previous studies with the short action potential rat model. Experimental observation indicate that the mutation is accompanied by increased ryanodine receptor open probability and increased junctional sarcoplasmic reticulum volume. The model simulates EADs at low pacing frequency. At high pacing frequency, alternans occurs not due to spark restitution as seen in the rat model, but by the accumulated inactivation of the sodium channel. These alternans do not require changes in jSR volume which were important in the spark restitution-based mechanism. The model offers novel insights into how mechanisms can vary between a long- and short- action potential models of arrhythmia." @default.
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- W2912167741 date "2019-02-01" @default.
- W2912167741 modified "2023-09-26" @default.
- W2912167741 title "Early Afterdepolarizations and Alternans are the Underlying Mechanism to Cause Arrhythmogenic Disorder in the Mutant Calsequestrin 2 (CASQ2)" @default.
- W2912167741 doi "https://doi.org/10.1016/j.bpj.2018.11.2077" @default.
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