Calcium handling and ventricular tachyarrhythmias.
Pharmacologic modification of cellular calcium handling recently moved into focus as an alternative for prevention and treatment of ventricular tachyarrhythmias. Calcium overload and spontaneous calcium release from the sarcoplasmatic reticulum are regarded as possible initiations of early and delayed afterdepolarization thereby triggering ventricular arrhythmias. In chronic heart failure, calcium overload is more likely to occur compared with healthy hearts, which is one explantation for the increased vulnerability in this condition. L-type calcium channel, sodium-calcium-exchanger (NCX), and ryanodine receptor are crucial for calcium homeostasis and therefore represent potential targets for antiarrhythmic drug therapy. Experimental studies have proven beneficial effects for all these three mechanisms in prevention and suppression of tachyarrhythmias. However, clinical data is mainly available for the L-type calcium channel inhibitor verapamil. Therefore, it is still a long way to clinical employment of drugs modifying cellular calcium handling for antiarrhythmic therapy.
Division of Clinical and Experimental Electrophysiology, Department of Cardiology and Angiology, University of Münster, Albert-Schweitzer Campus 1, 48149 Münster, Germany. gerrit.frommeyer@ukmuenster.de
Gerrit
G
Frommeyer
Lars
L
Eckardt
Peter
P
Milberg
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000502:physiology; D004562:Electrocardiography; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D019837:Ryanodine Receptor Calcium Release Channel / Q000187:drug effects / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000502:physiology; D019831:Sodium-Calcium Exchanger / Q000187:drug effects / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology*; D014700:Verapamil / Q000627:therapeutic use
D000889:Anti-Arrhythmia Agents; D020746:Calcium Channels, L-Type; D019837:Ryanodine Receptor Calcium Release Channel; D019831:Sodium-Calcium Exchanger; D014700:Verapamil; D002118:Calcium