More recently, these clinical findings were substantiated by animal studies, which demonstrate that the negative EM Denatonium benzoate window Cabergoline markedly increases susceptibility to lifethreatening ventricular tachyarrhythmia, such as torsade de pointes. In a canine model of long QT syndrome, a negative EM window was found to be a prerequisite for VT initiation. In anesthetized guinea-pigs, administration of drugs with known high proarrhythmic potential was found to induce a negative EM window, whereas safe antiarrhythmics such as amiodarone, verapamil and diltiazem produced no effect. Increased electrical instability in the presence of the negative EM window is thought to be attributed to abnormal Ca2+ handling, wherein Ca2+ can continue to enter into the cardiac cells and trigger sarcoplasmic reticulum Ca2+ release, after completing mechanical contraction. This leads to Ca2+ overload, thus facilitating both early and delayed after-depolarizations, which are known to play a role in initiating VT. The role of the negative EM window in the mechanism of druginduced proarrhythmia was nevertheless challenged in study by Laursen et al., who showed that in perfused mini-pig and dog hearts, the EM window remained positive even in the setting wherein a blockade of the delayed rectifier current was combined with b-adrenoreceptor agonist challenge. However, no attempts have been previously made to examine whether the mismatch between the duration of electrical and mechanical systole may contribute to arrhythmic substrate in the setting of hypokalemia, the most common electrolyte abnormality seen in cardiac patients. The excitation wavelength refers to the distance travelled by the depolarization wavefront during the refractory period. As ventricular conduction time is the inverse correlate of conduction velocity, the excitation wavelength may be indirectly assessed by calculating the ratio between the effective refractory period and conduction time. In this study, hypokalemia was found to produce conduction slowing, as evidenced by increased mean LVto-RV conduction delay, an effect that is presumably accounted for by membrane hyperpolarization and the enhanced ventricular excitation threshold typically seen in hypokalemic ventricular muscle.