Drug-induced repolarization abnormalities put vulnerable patients at risk of torsades de pointes and sudden cardiac death. Drugs that inhibit the rapidly activating component of the delayed rectifier potassium current in the myocardium manifest in the ECG by prolonging the QT interval, which has been associated with drug-induced TdP and SCD. The risk of TdP increases exponentially at a rate of 5% with every 10 ms prolongation of QTc beyond 440 ms. However, the relation between the prolongation of QTc and proarrhythmic risk is not straightforward. QTc is a mediocre parameter for assessing risk of drug-induced TdP and there are a number of QTc prolonging drugs with very limited or no proarrhythmic history. We have inverstigate if the T-wave morphology parameter MCS can be used to identify the +TdP patients and –TdP patients at baseline and after sotalol challenge, with QTc as reference measure.