Medication Summary
Acute management
Treatment steps for VPC include looking for and correcting the reversible causes (eg, hypoxia, hypokalemia, hypomagnesemia).
Long-term treatment
The long-term treatment of VPCs is highly controversial. Class I drugs affect fast sodium channels; they are classified into A, B, and C groups according to effects on phase 0 of the action potential, repolarization, and conduction.
Class IA drugs (eg, procainamide, quinidine, disopyramide) are moderately effective but have proarrhythmic effects. Procainamide is associated with a high incidence of allergic reactions, and quinidine is poorly tolerated due to adverse effects.
Class IB drugs (eg, mexiletine) may have less proarrhythmic effect (although one post-MI trial showed higher mortality for mexiletine than placebo) than class I antiarrhythmic drugs. They have a high incidence of adverse noncardiac effects. These drugs may show reasonable efficacy in some patients.
Class IC drugs (eg, flecainide, propafenone) are effective for reducing ventricular ectopy and are relatively well tolerated in patients with normal or minimally reduced LV function and no ischemic heart disease. They are not recommended in patients with ischemic heart disease because of the adverse outcome observed in the Cardiac Arrhythmia Suppression Trial (CAST). In CAST II, moricizine (Ethmozine) demonstrated neither benefits nor adverse effects long term, but, in the early use of the drug, increased mortality on moricizine occurred. Moricizine was discontinued in July 2007 because of diminished market demand.
Class II drugs (beta-blockers) are the drugs of choice in patients who are symptomatic but do not have structural heart disease. Also, class II drugs are considered the first choice of therapy for patients with underlying heart disease, especially if their EF is reduced. Beta-blockers or calcium blockers often suppress VPCs of right ventricular outflow tract origin.
Drug of choice in patients with VPC postmyocardial infarction
Class III drugs (eg, amiodarone, sotalol) are approved for use only in life-threatening arrhythmia. Recent data suggest that amiodarone is safe post-MI for patients with VPCs, but does not reduce mortality. Amiodarone is the drug of choice in patients who can not tolerate beta-blockers. A meta-analysis comparing efficacy and safety of amiodarone and metoprolol in the treatment of VPC concluded that the response rate of amiodarone did not seem to be superior to metoprolol; amiodarone was associated with higher incidence of adverse reactions. [25, 26]
Class IV drugs (calcium channel blockers), in general, have a limited role in the treatment of VPCs. However, occasionally, these drugs may suppress triggered automaticity or idiopathic VPCs. Verapamil is recommended for treatment of idopathic LVOT VPCs.
Currently, no evidence supports treatment of asymptomatic VPCs after MI with medication other than beta-blockers. Treatment considerations include symptoms caused by VPC, other prognostic variables (ie, presence or absence and type of structural heart disease, CAD, and LV dysfunction), and adverse effects (specifically proarrhythmic effects of medications).
Clinical trials have suggested that type I antiarrhythmic agents and racemic sotalol increase mortality in patients post-MI. Amiodarone may have no adverse effect on mortality in this setting. [27]
Antiarrhythmic agents
Class Summary
Alter the electrophysiologic mechanisms responsible for arrhythmia.
Amiodarone (Cordarone, Pacerone)
Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit A-V conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.
Has low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.
Metoprolol (Lopressor, Toprol XL)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.
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Ventricular premature complexes (VPCs). Ventricular trigeminy is present. Note that the VPCs are unimorphic and that a compensatory pause follows each VPC. This patient has asymptomatic idiopathic VPCs originating from the right ventricular outflow tract.
Tables
Class |
Arrhythmia |
0 |
None |
1 |
Unifocal; < 30/h |
2 |
Unifocal; ≥ 30/h |
3 |
Multiform |
4A |
2 consecutive |
4B |
≥ 3 consecutive |
5 |
R-on-T phenomenon |
