Current Treatments

Current antiarrhythmic therapy is either with drugs or uses electrical devices to detect and treat arrhythmias by electroshock or pacing. Electrical techniques can either be applied externally to the chest, or can be implanted within the body together with batteries to power all its components. Electrical devices continue to improve in terms of utility, reduced cost, ease of implantation, and effectiveness. As a result we are in a period where such devices are increasingly used, due in no small part to their advantages over drug therapy in many situations. Drugs generally have inadequate efficacy, are too toxic, or have too many side effects, and this is unfortunate since it will never be practical to treat every arrhythmia electrically.

The clinical utility and prescribing trends for current antiarrhythmic drugs show small regional differences, but in essence they are reasonably consistent throughout the world. For instance, in Japan there is a tendency to treat premature ventricular contractions (PVCs) that would not be treated in the USA or Europe. Changes in antiarrhythmic drug use worldwide reflect a falling drug use, and the increasing use of electrical devices.

As indicated above, the major cause of death from arrhythmias is ventricular tachycardias, particularly ventricular fibrillation, and this remains a problem despite the increasing use of electrical devices. There is a lower morbidity and mortality associated with atrial fibrillation, but this arrhythmia also still remains a problem. In the past, treatment of arrhythmias often reflected the treatment of an ECG pattern, rather than the patient, but it is increasingly recognized that it is pointless to treat the ECG when the drugs used for this purpose cause more morbidity and mortality than when the arrhythmia is left untreated.17 The reason for this conundrum is that all antiarrhythmic drugs, in addition to their own peculiar toxicity, are also arrhythmogenic when given in the wrong situation, and/or at the wrong dose. Thus, the overexpression of their main pharmacological actions (channel block) causes arrhythmias (i.e., many antiarrhythmic drugs are proarrhythmic). In addition, such drugs also have their own toxicity unrelated to their antiarrhythmic mechanism.18

The success of electrical devices has raised the question of whether antiarrhythmic drugs are still needed, or have drugs been superseded? The answer to this question has to be in the negative since, for ventricular fibrillation and atrial arrhythmias, there is a specific need for better drugs, as well as a need for drugs that are more efficacious and less toxic than those currently available.

The question becomes, can we create new and better antiarrhythmics? The unlimited potential of science means the answer has to be yes, although the routes to achieving this are not immediately clear. There has been a failure to answer clear questions, such as, do antiarrhythmic drugs have to be arrhythmia-specific? If the answer is yes, how are such drugs developed? Some of the answers to such questions occupy the remainder of this chapter.

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