Abstract
Anyone who considers the mechanism(s) of a tachyarrhythmia in humans must address both potential arrhythmia triggers as well as anatomic substrate. The anatomic substrate includes not only alterations in the myocardial architecture (for example fibrosis), but also ion channel disturbances. Arrhythmia triggers are protean and typically multiple in a given individual. For example, it is common for a patient with atrial fibrillation (AF) to relate onset of their arrhythmia on one occasion during sleep but on another occasion during activity. Further, while a patient may be susceptible to a specific trigger (for example alcohol or caffeine) it is very uncommon for the ingestion of such substances consistently to initiate their tachycardia. The diversity and complexity of arrhythmia triggers for a specific patient make it very difficult to target suppression of the triggers as the therapeutic pharmacologic goal.
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Prystowsky, E.N., Padanilam, B.J. (2003). Atrial Fibrillation: New Insights into Electrophysiologic Mechanisms. In: Gulizia, M. (eds) New Advances in Heart Failure and Atrial Fibrillation. Springer, Milano. https://doi.org/10.1007/978-88-470-2087-0_20
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DOI: https://doi.org/10.1007/978-88-470-2087-0_20
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