Key result
In a simulated human ventricular cell model of myocardial infarction, the combined use of telmisartan and nifedipine restored action potential amplitude, resting potential, and action potential duration to normal values, and maximum depolarization rate to 85% of normal.
Why the study?
Current simulation research mainly focuses on myocardial fibrosis effects on wave propagation, with few studies examining antiarrhythmic drugs for treating myocardial infarction.
Does the combination of telmisartan and nifedipine improve electrophysiological parameters in a simulated human ventricular cell model of myocardial infarction?
Does the combination of telmisartan and nifedipine improve electrophysiological parameters in a simulated human ventricular cell model of myocardial infarction?
A computational simulation demonstrates that combining telmisartan and nifedipine can theoretically restore normal electrophysiological function in myocardial infarction.
Should not change post-MI therapy; hypothesis-generating for telmisartan-nifedipine effects in simulated ventricular models.
Cardiovascular diseases can lead to sudden cardiac death, most of which were caused by arrhythmias induced by myocardial infarction (MI). However, current simulation researches mainly focus on the effect of myocardial fibrosis on wave propagation in tissues, and few studies gave attention to antiarrhythmic drugs for the treatment of MI. Therefore, the aim of this study is to simulate the therapeutic effect of antiarrhythmic drugs. Firstly, this paper constructed the human ventricular cell model in MI based on the TP06 model according to the experimental data. Then, the single-cell model was remodeled by adding the change of ion currents after drug action. We simulated the therapeutic effects of the two drugs (telmisartan and nifedipine) at different concentrations, and compared the changes of parameters before and after the drug action. At the same time, the coaction of the two drugs were simulated on the cell model in MI. The simulation results showed INa agonist telmisartan could increase the maximum depolarization rate of cells in MI, but the drug had no effect on APD. On the contrary, ICaL blocker nifedipine mainly affected the APD and had no effect on the depolarization stage. Under the combined action of the two drugs, APA, RP and APD basically returned to normal values, and dV/dtmax returned to 85% of the normal value.
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Liang et al. (2022) studied Myocardial Infarction. Telmisartan and nifedipine vs. Untreated simulated myocardial infarction cells was evaluated on Electrophysiological function recovery (APA, RP, APD, dV/dtmax). In a simulated human ventricular cell model of myocardial infarction, the combined use of telmisartan and nifedipine restored action potential amplitude, resting potential, and action potential duration to normal values, and maximum depolarization rate to 85% of normal.
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