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Recent years have witnessed important advances in our understanding of the molecular and electrophysiologic mechanisms underlying the development of a variety of cardiac arrhythmias (Table 79–1) and conduction disturbances. Progress in our understanding of these phenomena has been fueled by innovative advances in our understanding of the genetic basis and predisposition for electrical dysfunction of the heart. These advances notwithstanding, our appreciation of the basis for many rhythm disturbances is incomplete. This chapter examines our present understanding of cellular, ionic, and molecular mechanisms responsible for cardiac arrhythmias, placing them in historical perspective whenever possible.
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Cardiac activation and repolarization are controlled by movement of ions across channels in the cell membrane of cardiomyocytes, which in turn are strongly influenced by the activity of the autonomic nervous system. Abnormal activity of these ionic movements is important in cardiac arrhythmogenesis.1,2,3 Arrhythmic activity can be categorized as passive (eg, atrioventricular [AV] block) or active. The mechanisms responsible for active cardiac arrhythmias are generally divided into two major categories: (1) enhanced or abnormal impulse formation, and (2) reentry (Fig. 79–1). Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to reexcite the heart after expiration of the refractory period. Evidence implicating reentry as a mechanism of cardiac arrhythmias stems back to the turn of century.4,5,6 Multichannel mapping studies subsequently documented that reentrant wavefronts may underlie the mechanisms of atrial and ventricular tachyarrhythmias.7,8,9 Phase 2 reentry,10 spiral waves of excitation,...