Loss-of-function and gain-of-function mutations in the KCNH2 gene cause long and short-QT syndromes (LQTS or SQTS), respectively, predisposing to life-threatening cardiac arrhythmias. KCNH2 encodes the voltage-gated K+ channel hERG that generates the delayed rectifier K+ current IKr controlling the action potential (AP) duration. Prolonged or shortened ventricular AP durations are visualized as abnormal QT interval duration on the electrocardiogram. The occurrence and severity of KCNH2-related arrhythmias are determined by the variant functional impact. Sequencing KCNH2 has provided a plethora of variants associated or not with pathological cardiac phenotypes and indexed in the ClinVar NCBI database. Discriminating pathogenic variants from benign ones would clarify the genetic background of patients and relatives, and stratify the risk of adverse events. In the face of a wide spectrum of hERG functional defects, we looked for a way to summarize the net loss or gain of function in a unique index. We defined the repolarization power as the time integral of the K+ current (IhERG) developed during an AP clamp.