Abstract
Cardiac arrhythmias are a major cause of morbidity and mortality in heart disease, and are the likely cause of more than a quarter of a million deaths annually in the U.S. alone. While our current approach to reducing suffering and death from arrhythmias relies largely on diagnosis and therapy aimed at early recognition and treatment, the benefits of prevention could be even more substantial. As we consider how the approach to arrhythmias may evolve in the coming decades, it is useful to consider the great breadth of presentations and scenarios that are encountered. Human arrhythmias occur in two scenarios. First, and particularly early in life, they arise as a consequence of inborn (congenital) constellations of anatomy and electrophysiology that change over time. There may be no structural cardiac abnormality (e.g., long QT syndrome), a minimal structural abnormality (e.g., an accessory pathway causing WPW) or a severe structural abnormality (e.g., endocardial cushion defect with heart block). Secondly, arrhythmias emerge later in life as a consequence of acquired disease (e.g., ventricular tachycardia late after myocardial infarction) or aging (atrial fibrillation). Genetic susceptibilities influence all aspects of the pathophysiology. As approaches to prevention and therapy evolve, genetic influences will receive increasing attention.
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