The pharmacological therapy of cardiac arrhythmias is still challenging. As is well known, antiarrhythmic drugs have a narrow therapeutic-toxic window and can induce lethal proarrhythmia (antiarrhythmic drug-induced arrhythmia). The harmful
effect
of
antiarrhythmic drug was proven by CAST and so many clinical trials. Thus we need strict indications for prescription and objective parameters for monitoring of the drug action and side effects.
The cardiac arrhythmias are classified as ectopic beats, bradyarrhythmia, and tachyarrhythmia. The main target of antiarrhythmic drugs is tachyarrhythmia. The clinical role of antiarrhythmic drugs is the acute conversion of arrhythmia to sinus
rhythm
and the chronic suppression/prevention of tachycardia. The cardiac arrhythmia (arrhythmogenesis) occurs in harmony of 3 components, namely, substrate, precipitating (modulating) factors, and trigger. The acute modification of arrhythmogenic
environment
by drug may be efficient, but the chronic suppression of arrhythmia only by the drug may not be complete. Recently, the clinical role of chronic drug therapy is replaced by RFCA (in patients with SVT except atrial fibrillation) and ICD (VT/SCD).
The antiarrhythmic drugs are usually classified into Class Ⅰ (sodium channel blocker), Class Ⅱ (beta-blocker), Class Ⅲ (potassium channel blocker), Class Ⅳ (calcium channel blocker), and others (digoxin and adenosine), according to
Vaughn-Williams
suggestion. Nowadays, the clinical electrophysiologist reclassified the agents into calcium channel-dependent drug (Class Ⅱ, Ⅳ, digoxin, and adenosine) and sodium/potassium channel-dependent drug (Class Ⅰ and Ⅲ).
The drug is effective only when the concentration in blood or tissue is sufficient to modify the arrhythmogenic substrate. We need to know the pharmacokinetic and pharmacodynamic properties of antiarrhythmic drugs exactly. We can expect the blood
concentration of a drug if we know the elimination half-life and the dosing schedule of the drug because most drugs (including antiarrhythmic agents) have the first-order (elimination) kinetic. For a new steady-state of drug concentration, we
should
wait for 3 to 4 times of the half-life after changing the dosage (prescription).
Finally, the consideration and management of the underlying heart disease and precipitating/modulating factors are needed for the effective antiarrhythmic drug therapy.
|