Protective effects of propafenone, propranolol, and amiodarone against isoproterenol-induced lethal arrhythmias in IGF1R deficiency mice.

The study investigates the role of the insulin-like growth factor 1 receptor (IGF1R) in cardiac function and its impact on stress-induced arrhythmias. IGF1R is a key receptor involved in cardiomyocyte growth and metabolism, with significant implications for cardiac development and stress response. However, its role in arrhythmias remains underexplored. The research utilized echocardiography to assess cardiac function in wild-type (WT) and IGF1R+/- mice, revealing no significant differences in cardiac contraction or relaxation indices under basal conditions. This suggests that IGF1R may not be essential for routine cardiac function maintenance under normal physiological conditions. However, under stress conditions induced by isoproterenol (ISO), IGF1R+/- mice exhibited a high incidence of lethal arrhythmias, with a mortality rate of 46.15 %. This highlights the crucial role of IGF1R in maintaining cardiac electrophysiological stability under stress. The study further explored the effects of antiarrhythmic drugs, finding that propranolol and amiodarone effectively mitigated these arrhythmias, reducing mortality rates to 0 %, while propafenone had a less pronounced effect, with a mortality rate of 33.3 %. These findings underscore the potential therapeutic value of targeting IGF1R signaling pathways in the management of stress-induced arrhythmias and highlight the need for further research into the precise molecular mechanisms underlying IGF1R's protective effects and the development of novel antiarrhythmic therapies.