RT Book, Section
A1 Sampson, Kevin J.
A1 Kass, Robert S.
A2 Brunton, Laurence L.
A2 Chabner, Bruce A.
A2 Knollmann, Björn C.
SR Print(0)
ID 1127867929
T1 Anti-Arrhythmic Drugs
T2 Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e
YR 2015
FD 2015
PB McGraw-Hill Education
PP New York, NY
SN 9780071624428
LK accessmedicine.mhmedical.com/content.aspx?aid=1127867929
RD 2023/09/22
AB Cardiac  cells  undergo  depolarization  and  repolarization  to  form  cardiac  action  potentials  ∼60  times/  minute.  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  now  have  been  identified.  Thus,  each  heartbeat  results  from  the  highly  integrated  electrophysiologic  behavior  of  multiple  proteins  on  multiple  cardiac  cells.  Ion  channel  function  can  be  perturbed  by  inherited  mutation/polymorphism,  acute  ischemia,  sympathetic  stimulation,  or  myocardial  scarring  to  create  abnormalities  of  cardiac  rhythm,  or  arrhythmias.  Available  anti-arrhythmic  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  anti-arrhythmic  drugs  and  perhaps  improved  therapies.