Ventricular tachycardia (VT) characterized by high rates of ventricular excitation may cause sudden cardiac death. Electrical remodelling of ion channels was documented to be a major contributory factor of initiating and sustaining VT. Mutations in the CACNA1C gene, coding for a calcium channel subunit, have been linked to VT.
In the present study, the researchers aimed at uncovering the mechanisms by which mutations in CACNA1C could lead to VT. The researchers developed 1D, 2D and 3D computational models of calcium dynamics changes induced by CACNA1C mutation in cardiomyocytes. The computational tools showed that increased calcium influx in the mutation provoked increased vulnerability to unidirectional conduction block in response to a premature stimulus, facilitating the initiation and maintenance of VT. The study concludes that the increased repolarization dispersion caused by the CACNA1C mutation is a primary factor contributing to cardiac arrhythmias.
Pro-arrhythmogenic effects of CACNA1C G1911R mutation in human ventricular tachycardia: insights from cardiac multi-scale models
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