Inhibition of PI3Kinase-α is pro-arrhythmic and associated with enhanced late Na + current, contractility, and Ca 2+ release in murine hearts.

Pharmacological inhibition of PI3Kα is arrhythmogenic due to activation of I leading to increased sarcoplasmic reticulum Ca load and prolonged QT interval. Therefore, monitoring of cardiac electrical activity in patients receiving PI3K inhibitors may provide further insights into the arrhythmogenic potential of PI3Ka inhibition.