Circadian rhythms are generated by cell autonomous circadian clocks that perform a ubiquitous cellular time-keeping function and cell type-specific functions important for normal physiology. Studies show inducing the deletion of the core circadian clock transcription factor in adult mouse cardiomyocytes disrupts cardiac circadian clock function, cardiac ion channel expression, slows heart rate, and prolongs the QT-interval at slow heart rates. This study determined how inducing the deletion of in adult cardiomyocytes impacted the electrophysiological phenotype of a knock-in mouse model for the arrhythmogenic long QT syndrome ( ). Electrocardiographic telemetry showed inducing the deletion of in the cardiomyocytes of mice with or without the ΔKPQ- mutation increased the QT-interval at RR-intervals that were ≥130 ms. Inducing the deletion of in the cardiomyocytes of mice with or without the ΔKPQ- mutation also increased the day/night rhythm-adjusted mean in the RR-interval, but it did not change the period, phase or amplitude. Compared to mice without the ΔKPQ- mutation, mice with the ΔKPQ- mutation had reduced heart rate variability (HRV) during the peak of the day/night rhythm in the RR-interval. Inducing the deletion of in cardiomyocytes did not affect HRV in mice without the ΔKPQ- mutation, but it did increase HRV in mice with the ΔKPQ- mutation. The data demonstrate that deleting in cardiomyocytes exacerbates QT- and RR-interval prolongation in mice with the ΔKPQ- mutation.