Cellular electrophysiological properties in myocardial infarction.
Important ventricular arrhythmias consequent upon myocardial infarction have several pathophysiological features. Because the arrhythmogenic substrate following myocardial infarction gradually changes different electrophysiological and biochemical determinants can be related to ventricular arrhythmias at distinct periods. In acute ischaemia and infarction, multiple ionic and metabolic changes result in marked electrophysiological inhomogeneity at the cellular level, in which post-repolarization refractoriness and cellular uncoupling are involved in conduction disturbances. Twenty-four to 72 h after coronary occlusion (subacute phase), action potential abnormalities, in addition to abnormal impulse generation in surviving cell layers within and in the border zone of the infarcted area, contribute mainly to arrhythmias. In healed infarcted myocardium, changes in intercellular impulse propagation as well as non-uniform anisotropic cardiac tissue play a major role in the maintenance of arrhythmias, whereas the initiating mechanisms are less well defined.
Wiecha
J
J
Department of Cardiology, University of Ulm, Germany.
Hombach
V
V
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D015220:Calcium Channels / Q000378:metabolism; D004594:Electrophysiology; D006329:Heart Conduction System / Q000166:cytology / Q000503:physiopathology*; D006801:Humans; D016623:Ion Pumps; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D015221:Potassium Channels / Q000378:metabolism; D011690:Purkinje Fibers / Q000503:physiopathology; D013997:Time Factors
D015220:Calcium Channels; D016623:Ion Pumps; D015221:Potassium Channels