Numerous drugs from diverse classes, such as antiarrhythmics, antihistamine
s, gastrokinetics, antipsychotics and antibiotics, share the potential to i
nduce a prolongation of the QT interval on the electrocardiogram and torsad
e de pointes ventricular arrhythmias. The underlying mechanism of these sid
e-effects is the blocking of voltage-gated potassium channels, particularly
the rapid component I-Kr, of the delayed rectifier I-K. The risk of such d
rug-induced arrhythmias is far greater in women than in men. Clinical data
as well as experimental studies show that, in comparison to men, the femini
ne gender is associated with a longer baseline QT interval, a greater respo
nse to drugs that block I-Kr and a greater propensity to drug-induced torsa
de de pointes. This is most likely the result of a specific regulation of c
hannel expression by - and perhaps a direct non genomic effect of - sex ste
roids. (Eur Heart J Supplements 2001; 3 (Suppl K): K41-K47) (C) 2001 The Eu
ropean Society of Cardiology.