OVERVIEW OF TREATMENT OF VENTRICULAR ARRYTHMIAS
Treatment of ventricular arrhythmias is guided by the severity and frequency of symptoms. For some, reassurance and removal of aggravating factors (e.g., caffeine) is all that is needed. For arrhythmias associated with a sudden death risk, ICD implantation is usually indicated and will provide a “safety-net” to terminate life-threatening VT or VF, preventing sudden death, but without preventing the arrhythmia. When suppression of the arrhythmia is required, antiarrhythmic drug therapy or catheter ablation are major considerations.
Use of antiarrhythmic drugs is based on consideration of the risks and potential benefit for the individual patient. Efficacy and side effects for the individual patient is not predictable and is assessed by individual therapeutic trial. Adverse effects are mostly non-cardiac and minor, but can sometimes be severe enough to limit their use. Cardiac side effects, however, include the potential for “pro-arrhythmia” whereby a drug can increase the frequency of arrhythmia or cause a new arrhythmia. Aggravation of bradyarrhythmias is also a common concern. Although anti-arrhythmic drugs are classified based on their actions on receptors or ion channels, most have multiple effects, affecting more than one channel.
Many ventricular arrhythmias are sensitive to sympathetic stimulation, and beta-adrenergic stimulation also diminishes the electrophysiologic effects of many membrane active anti-arrhythmic drugs. The safety of beta-blocking agents makes them the first choice of therapy for most ventricular arrhythmias. They are particularly useful for exercise-induced arrhythmias and idiopathic arrhythmias, but have limited efficacy for most arrhythmias associated with heart disease. Bradyarrhythmias and negative inotrophic effects are the major cardiac adverse effects.
The non-dihydropyridine calcium channel blockers diltiazem and verapamil can be effective for some idiopathic VTs. The risk of pro-arrhythmia is low, but they have negative inotropic and vasodilatory effects that can aggravate hypotension.
Sodium Channel Blocking Agents
Drugs whose major effect is mediated through sodium channel blockade include mexiletine, quinidine, disopyramide, flecainide, and propafenone, which are available for chronic oral therapy. Blockade of the fast inward sodium current has been referred to as a Class I antiarrhythmic drug effect. Antiarrhythmic actions are the result of depressing of cardiac conduction and membrane excitability. Conduction slowing can be manifest as a prolongation of QRS duration. Lidocaine, quinidine, and procainamide are available as intravenous formulations. Quinidine, disopyramide, and procainamide also have potassium channel blocking effects that prolong the QT interval (Class III antiarrhythmic drug action) that contributes to its antiarrhythmic effect. These agents have potential pro-arrhythmic effects and, with the possible exception of quinidine, also have negative inotropic effects that may contribute to increased mortality observed when some were administered chronically to patients with prior myocardial infarction. Long-term therapy is generally avoided in patients with structural heart disease, but may be used to reduce symptomatic arrhythmias in patients with ICDs.