Triggered activity in the heart: cellular mechanisms of early after-depolarizations.
The arrhythmogenic effects of ischaemia and reperfusion result from the complex interplay of normal ion channels reacting to the ischaemic environment, channels made abnormal by ischaemic modification, the appearance of new currents normally not present, and possible ischaemic alteration of metabolic electrogenic processes. In this report the cellular mechanisms thought to underlie the different types of triggered activity will be discussed. The role of Ca2+ channels and Ca2+ 'window' current in the generation of early after-depolarizations (EADs) will be elucidated.
January
C T
CT
Department of Medicine (Cardiology), University of Chicago, Illinois 60637.
Chau
V
V
Makielski
J C
JC
D000200:Action Potentials; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D015220:Calcium Channels / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology
D015220:Calcium Channels; D007473:Ion Channels