Class I antiarrhythmic drugs are characterised by their ability to blo
ck the fast inward sodium current in cardiac muscle tissue. However, a
t the same time, they can be responsible for various effects involving
other organs and systems. Although some of these effects can be helpf
ul in specific situations, most of them, such as their pro-arrhythmic
propensity, are deleterious. Some of the adverse effects of class I an
tiarrhythmic drugs are directly linked to sodium-channel blockade (con
duction disorders, haemodynamic perturbations, and digestive and neuro
logical effects), while others are linked to other specific pharmacolo
gical properties (e.g. atropinic, or alpha- or beta-adrenergic blockad
e) or to nonspecific properties (idiosyncratic hypersensitivity, and h
aematological, dermatological or hepatic reactions). Other adverse eff
ects are associated with complex interactions between class I antiarrh
ythmics and individual predisposing factors, trigger mechanisms and ph
ysiological factors (including concomitant drug treatment). These nume
rous variations and interactions within a specific environment and und
erlying disorder might be of pharmacological or/and pharmacokinetic or
igin, making analysis of the true liability of the class I drugs very
difficult when adverse effects occur.