The KCNH2-linked short QT syndrome (SQT1) arises due to IKr mutations (such as N588K, L532P) leading to accelerated ventricular repolarization arrhythmias. In preliminary studies, the anti-arrhythmic drug quinidine produced therapeutic effects on SQT1. There is a reason to believe that it may be useful in other mutations in SQT1. In this paper, we aim to quantify the effects of quinidine on KCNH2 N588K and L532P mutations linked short QT syndrome. The channel-blocking effect of quinidine on ionic channels in healthy and SQT1 cells were incorporated into the ten Tusscher et al model of human ventricular action potential (AP) and into 1D and 2D transmural tissue. In the tissue simulations, we applied 0.5 Hz, 1.25 Hz, 2.66 Hz and 3.33 Hz of electrical stimulations. In the single-cell model, quinidine prolonged cell AP duration at repolarization (APD90) under both N588K and L532P mutations-linked short QT syndrome. In the 1D simulations, quinidine also prolonged the QT interval on the pseudo-ECGs under both SQT1 conditions. In the 2D tissue, compared with 1.25 Hz of electrical stimulation, the measured APD90 did not change noticeably at 0.5 Hz, but was reduced at 2.66 Hz. At 3.33 Hz, 1:1 response of electrical excitation wave propagation to stimuli sustained in mutation conditions, but failed in quinidine-in-action conditions. In conclusion, this study provides evidence that quinidine can extend the repolarization period and APD90 and QT interval under both mutant SQT1 conditions, and also indicates that a protective effect at high frequency of electrical stimulation may account for the termination of ventricular tachycardia and fibrillation.