eMedicine Specialties > Cardiology > Arrhythmias
Ventricular Premature Complexes: Treatment & Medication
Updated: Aug 24, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Deciding when to treat VPCs is difficult because not all patients with VPCs are at risk of sudden death and treatment is associated with risk. The approach to VPCs depends on the frequency of VPCs, attributable symptoms, the presence or absence of underlying structural heart disease, and the estimated risk of sudden cardiac death.
- Absence of significant structural heart disease (eg, normal ventricular function, no coronary or valvular heart disease)
- Asymptomatic VPCs require no therapy.
- For symptomatic VPCs, recommended treatment usually involves patient education and reassurance, avoidance of aggravating factors (eg, stress, caffeine-containing products), and anxiolytic drugs if education and avoidance of aggravating factors are ineffective. Beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) can be used to treat symptomatic patients. Beta-blockers with intrinsic sympathomimetic activity may be particularly helpful. The use of antiarrhythmic therapy is not generally recommended and is only used to prevent symptoms. The risk of the drug (including the risk of arrhythmic death from proarrhythmia) must be weighed against the benefits of VPC suppression. In patients who are symptomatic on beta-blockers and/or calcium channel blockers, consider cautious use of Amiodarone. The role of newer class III antiarrythmic like dofetilide and azimilide for VPCs is unclear at present.
- Presence of underlying heart disease (eg, VPCs in patients post-MI)
- Various strategies, both invasive and noninvasive, predict prognosis in patients with VPCs post-MI.
- The most powerful combination of noninvasive prognostic variables that identify patients in whom invasive strategies are suitable includes the presence of 2 or more of the following variables, (1) LV EF less than 0.40, (2) ventricular late potentials (on signal-averaged ECG), and (3) repetitive VPCs.
- Supportive management
- Treatment should include limiting transient ischemia.
- Optimal treatment for congestive heart failure (CHF), CAD, or both should be instituted.
- Maintain electrolyte balance.
- Blood pressure control should be obtained because LV hypertrophy is associated with increased VPCs.
- The 2006 ACC/AHA/ESC guideline recommends that ablation therapy should be considered in the following:2
- Patients with frequent, symptomatic, and monomorphic VPCs refractory to medical therapy
- Patients who choose to avoid long-term medical therapy
- Patients with ventricular arrhythmia storm that is consistently provoked by VPBs of a similar morphology
Surgical Care
Patients deemed to be at high risk of sudden cardiac death may benefit from implantable cardioverter defibrillator (ICD) implantation.
Consultations
Consultation with a cardiac electrophysiologist may be beneficial. As described above, select patients with symptomatic idiopathic VPCs may benefit from catheter ablation. EPS may help define risk for sudden death in some patients with structural heart disease. ICD implantation is beneficial in patients at high risk of sudden cardiac death.
Diet
Recommendations depend on the underlying cardiac disease; avoidance of caffeine, nicotine, and alcohol may reduce the frequency of VPCs.
Medication
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.
Class IV drugs (calcium channel blockers), in general, have no role in the treatment of VPCs. However, occasionally these drugs may suppress triggered automaticity or idiopathic 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.
Antiarrhythmic agents
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.
Adult
Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk, and decrease to 600-800 mg/d in 1-2 doses for 1 mo
Maintenance dose: 400 mg/d PO
Alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h and then, 540 mg over next 18 h
Pediatric
10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia is attained
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by macrolide antibiotics, ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers, may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels; protease inhibitors (eg, indinavir, ritonavir, amprenavir, nelfinavir) inhibit amiodarone metabolism resulting in increased serum levels and may prolong QT interval; coadministration may increase myopathy/rhabdomyolysis risk; associated with HMG-CoA reductase inhibitors (eg, simvastatin); other drugs which prolong the QT interval (eg, fluoroquinolones, erythromycin, dofetilide, tricyclic antidepressants, thioridazine) may increase life-threatening arrhythmia risk
Documented hypersensitivity, complete AV block, and intraventricular conduction defects
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Known to cause serious (and at time fatal) toxicities including pulmonary and liver toxicities; may cause prolonged proarrhythmic effects; may cause optic neuritis/neuropathy or hypo- or hyperthyroidism; CNS and GI toxicity may occur and typically dissipates with dose reduction
Metoprolol (Lopressor, Toprol XL)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions.
Adult
5 mg IV q2min for 3 doses in acute situation, particularly MI
25-100 mg or more PO bid
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity, uncompensated CHF, bradycardia, asthma, cardiogenic shock, AV conduction abnormalities
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor closely and withdraw drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
More on Ventricular Premature Complexes |
| Overview: Ventricular Premature Complexes |
| Differential Diagnoses & Workup: Ventricular Premature Complexes |
 Treatment & Medication: Ventricular Premature Complexes |
| Follow-up: Ventricular Premature Complexes |
| Multimedia: Ventricular Premature Complexes |
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Further Reading
Keywords
ventricular premature complexes, ventricular extrasystole, ventricular ectopic beats, benign ventricular arrhythmia, missed beats, VPC, PVC, premature ventricular complex, VPD, ventricular premature depolarization, VPB, ventricular premature beat, ventricular arrhythmia, beta-blockers, myocardial infarction, MI, postmyocardial infarction, post-MI, congestive heart failure, CHF, coronary artery disease, CAD, ventricular ectopy, ventricular tachycardia, VT
