Abstract
Abnormalities in cardiac rhythm, or arrhythmia, affect more than 2% of individuals and can cause sudden cardiac death. Amiodarone, the most frequently prescribed antiarrhythmic drug, is effective yet exhibits significant toxicity. Amiodarone is extensively metabolized and displays a prolonged elimination half-life, lipophilic partitioning, and blockade of multiple ionic currents that form the cardiac action potential, complicating characterization of its therapeutic mechanisms. Further constraining this effort is the limited availability of clinical samples of healthy human cardiac cells and tissues.
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