RT Book, Section A1 Knollmann, Bjorn C. A1 Roden, Dan M. A1 Murray, Katherine T. A2 Brunton, Laurence L. A2 Knollmann, Björn C. SR Print(0) ID 1193233286 T1 Antiarrhythmic Drugs T2 Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 14th Edition YR 2023 FD 2023 PB McGraw-Hill Education PP New York, NY SN 9781264258079 LK hemonc.mhmedical.com/content.aspx?aid=1193233286 RD 2024/10/09 AB Cardiac cells undergo depolarization and repolarization about 60 times per minute to form and propagate cardiac action potentials. The shape and duration of each action potential are determined by the activity of ion channel protein complexes in the membranes of individual cells, and the genes encoding most of these proteins and their regulators have now been identified. Action potentials in turn provide the primary signals to release Ca2+ from intracellular stores (sarcoplasmic reticulum) and to thereby initiate contraction. Thus, each normal heartbeat results from the highly integrated electrophysiological behavior of multiple proteins on the surface and within multiple cardiac cells. Disordered cardiac rhythm can arise from influences such as inherited variation in ion channels or other genes, ischemia, sympathetic stimulation, or myocardial scarring. Available antiarrhythmic drugs suppress arrhythmias by modulating flow through specific ion channels or by altering autonomic function. An increasingly sophisticated understanding of the molecular basis of normal and abnormal cardiac rhythm may lead to identification of new targets for antiarrhythmic drugs and perhaps improved therapies (Al-Khatib et al., 2018).