ABSTRACT
Sudden cardiac death due to ventricular arrhythmias is a major public health problem, claiming over 350,000 lives annually in the United States alone [1]. Arrhythmias can be either focal in nature or reentrant. Focal arrhythmias are those arising from a single cell or a population of cells and exhibiting abnormally rapid firing, which can override the natural rhythm of the heart. On the other hand, reentrant excitation, which underlies the vast majority of lethal arrhythmias, is based on a process by which abnormal electrical circuits develop in the heart, driving it at fast and highly irregular rates. This process can then lead to hemodynamic deterioration and death if normal cardiac rhythm is not restored promptly by electrical defibrillation. A fundamental requirement for the initiation and maintenance of reentry is the presence of electrical heterogeneities in the heart, which can result in variable degrees of myocardial excitability. This can cause a cardiac impulse to block selectively in certain regions, but to propagate (usually slowly) in others, thereby allowing the formation of a reentrant circuit. Unlike arrhythmia mechanisms that are dependent on focal sources, reentrant arrhythmias are by definition multicelluIar processes, involving conduction disturbances between cells. Therefore, a complete understanding
of mechanisms underlying the development and early maintenance of reentrant arrhythmias requires the measurement of electrical properties from many cells across intact heart (i.e., cardiac mapping).
