See article by Liu et al. \[4\] (pages 28–36) in this issue. As highlighted by a recent ‘Spotlight’ issue of Cardiovascular Research [1], the existence of major differences between men and women in the function and pathophysiology of the cardiovascular system implicates the need for gender-specific optimisation of patient treatment. One key gender difference resides in the electrocardiogram: it has long been known that women have higher resting heart rates than men, but that the rate-corrected QT interval (QTc) is longer in women (by 2–6%) [2,3]. As will be discussed below, this difference is an important factor in sex-linked differences in pro-arrhythmic risk, and its basis is the subject of an article in this edition of the journal by Liu et al. [4]. Women are at significantly greater risk than men of developing the potentially lethal ventricular tachyarrhythmia torsades de pointes in response to certain drugs that prolong ventricular repolarisation [3,5–7]. Excessive prolongation of ventricular repolarisation, known as the long QT syndrome owing to the increase in duration of the QTc interval, is thought to favour the generation of early after depolarisations (EADs), cellular proarrythmic events that, with the appropriate dispersion of repolarisation, in turn may initiate torsades de pointes [8–10]. Long QT syndrome can be either inherited through mutations in ion channels or, as alluded to above, acquired through administration of drugs that block cardiac K+ channels (in particular channels responsible for the rapid delayed rectifier current, I Kr) [8,9,11,12]. Female gender is also an independent risk factor for the incidence of syncope and sudden death in the inherited long QT syndrome [3]. The basis for the gender difference in risk of torsades de pointes is unclear, but is likely to reflect the influence of sex hormones on ventricular repolarisation. In … * Corresponding author. Tel.: +44-117-928-9187; fax: +44-117-928-8923.