When Manual Analysis of 12-Lead ECG Holter Plays a Critical Role in Discovering Unknown Patterns of Increased Arrhythmogenic Risk: A Case Report of a Patient Treated with Tamoxifen and Subsequent Pneumonia in COVID-19

Several medicines, including cancer therapies, are known to alter the electrophysiological function of ventricular myocytes\r\nresulting in abnormal prolongation and dispersion of ventricular repolarization (quantified by multi-lead QTc measurement).\r\nThis effect could be amplified by other concomitant factors (e.g., combination with other drugs affecting the QT, and/or electrolyte\r\nabnormalities, such as especially hypokalemia, hypomagnesaemia, and hypocalcemia). Usually, this condition results\r\nin higher risk of torsade de point and other life-threatening arrhythmias, related to unrecognized unpaired cardiac ventricular\r\nrepolarization reserve (VRR). Being VRR a dynamic phenomenon, QT prolongation might often not be identified during the\r\n10-s standard 12-lead ECG recording at rest, leaving the patient at increased risk for life-threatening event. We report the case of a 49-year woman, undergoing tamoxifen therapy for breast cancer, which alteration of ventricular repolarization reserve,\r\npersisting also after correction of concomitant recurrent hypokalemia, was evidenced only after manual measurements of the\r\ncorrected QT (QTc) interval from selected intervals of the 12-lead ECG Holter monitoring. This otherwise missed finding\r\nwas fundamental to drive the discontinuation of tamoxifen, shifting to another “safer” therapeutic option, and to avoid the use of potentially arrhythmogenic antibiotics when treating a bilateral pneumonia in recent COVID-19.