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Cardiac excitation is determined by interactions between the source of electric activation (membrane depolarization) and the load that cardiac tissue presents. This relationship is altered in pathology by remodeling processes that often create a substrate favoring the development of cardiac arrhythmias. Most studies of arrhythmia mechanisms and arrhythmogenic substrates have been conducted in animal models, which may differ in important ways from the human pathologies they are designed to represent. Electrocardiographic imaging is a noninvasive method for mapping the electric activity of the heart in humans in real-world conditions. This review summarizes results from electrocardiographic imaging studies of arrhythmogenic substrates associated with human clinical arrhythmias. Examples include heart failure, myocardial infarction scar, atrial fibrillation, and abnormal ventricular repolarization.
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