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A cardiac arrhythmia is an abnormal electrical signal in the heart, which in some cases cause the heart to lose its functionality as a pump. A large problem in the pharmaceutical industry is unforeseen pro-arrhythmic drug effects. In fact, many drugs that are designed to prevent cardiac arrhythmias can in some circumstances induce arrhythmias. The pro-arrhythmic side effects of drugs usually result from their binding to and altering the kinetics of ion channel proteins. Hence, a better understanding of how drug effects on ion channel kinetics influence electrical signaling at the cell and tissue levels would be greatly beneficial to the drug development and drug screening processes. While several experimental and modeling studies have examined how drug-ion channel interactions of specific drugs translate to effects on cardiac electrical signaling, no unifying principles have been identified. We have begun to develop a framework that connects common drug-ion channel binding motifs to effects on the propensity of arrhythmias at the cellular and tissue levels.

A reception follows at 4:00 (after the talk).