Key result
Ion channel changes, genetic mutations, and reperfusion mediators drive ventricular arrhythmias and offer antiarrhythmic targets.
Why the study?
To understand the various factors governing ventricular arrhythmias, including ion channel-related action potential changes, ECG manifestations, reperfusion mediators, and pharmacological approaches to their attenuation.
This review provides a comprehensive overview of the electrophysiological mechanisms underlying ventricular arrhythmias and the pharmacological basis for antiarrhythmic therapy.
May guide antiarrhythmic target selection; leaves open prospective validation before practice change.
This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na+, K+, and Ca2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.
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Árpád Tósaki (2020) conducted a review in Cardiac arrhythmias. Ion channel-related changes, genetic mutations, and arrhythmogenic mediators of reperfusion play crucial roles in the occurrence of ventricular arrhythmias and serve as targets for antiarrhythmic pharmacotherapy.
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