In this review a description and an analysis are given of the interaction of antiarrhythmic drugs with their molecular target, i.e. ion channels and receptors. Our approach is based on the concept of vulnerable parameter, i.e. the electrophysiological property which plays a crucial role in the genesis of arrhythmias. To prevent or stop the arrhythmia a drug should modify the vulnerable parameter by its action on channel or receptor targets. In the first part, general aspects of the interaction between drugs channel molecules are considered. Drug binding depends on the state of the channel: rested, activated pre-open, activated open, or inactivated state. The change in channel behaviour with state is presented in the framework of the modulated-receptor hypothesis. Not only inhibition but also stimulation can be the result of drug binding. In the second part a detailed and systematic description and an analysis are given of the interaction of drugs with specific channels (Na+, Ca2+, K+, "pacemaker") and non-channel receptors. Emphasis is given to the type of state-dependent block involved (rested, activated and inactivated state block) and the change in channel kinetics. These properties vary and determine the voltage- and frequency-dependence of the change in ionic current. Finally, the question is asked as to whether the available drugs by their action on channels and receptors modify the vulnerable parameter in the desired way to stop or prevent arrhythmias.