Since a drug-induced increased spatial APD dispersion compared to baseline may indicate an increased pro-arrhythmic risk of erythromycin [22] as identified in Langendorff-perfused rabbit hearts [20], [33] and in patients treated with antibiotics [35], the occurrence of an erythromycin-induced increased intra- and interventricular APD dispersion only in LQT1 rabbits suggests that LQT1 models may be more sensitive to detect pro-arrhythmic properties of HERG/IKr-blockers. The gene discussed is KCNH2; the disease is long QT syndrome 1.