RT Book, Section A1 Knollmann, Bjorn C. A1 Roden, Dan M. A2 Brunton, Laurence L. A2 Hilal-Dandan, Randa A2 Knollmann, Björn C. SR Print(0) ID 1162538774 T1 Antiarrhythmic Drugs T2 Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 13e YR 2017 FD 2017 PB McGraw-Hill Education PP New York, NY SN 9781259584732 LK accessbiomedicalscience.mhmedical.com/content.aspx?aid=1162538774 RD 2024/03/28 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 now have been identified. Action potentials in turn provide the primary signals to release Ca2+ from intracellular stores 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 channel or other genes, ischemia, sympathetic stimulation, or myocardial scarring. Available antiarrhythmic drugs suppress arrhythmias by blocking 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 (Dobrev et al., 2012; Van Wagoner et al., 2015).