How are ventricular premature complexes (VPCs) treated?

Updated: Nov 26, 2016
  • Author: Jatin Dave, MD, MPH; Chief Editor: Jose M Dizon, MD  more...
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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. [19]

In the absence of significant structural heart disease (eg, normal ventricular function, no coronary or valvular heart disease) and the presence of asymptomatic VPCs, no therapy is required.

For symptomatic VPCs, recommended treatment usually involves the following:

  • Patient education and reassurance
  • Avoidance of aggravating factors (eg, stress, caffeine-containing products)
  • Consideration of antiarrtymic agents and
  • Anxiolytic drugs if education, targeted pharmacologic treatment and avoidance of aggravating factors are ineffective. 

Step 1: 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. [20, 21]

Step 2: The use of antiarrhythmic therapy is not typically recommended and best targeted to address limiting symptoms. The risk of the drug (including the risk of arrhythmic death from proarrhythmia) must be weighed against the benefits of VPC suppression. The risk of adverse events is higher in patients with structural heart disease.

In patients without structural heart disease who have refractory symptoms and are using beta-blockers and/or calcium channel blockers, cautious use of antiarrhythmic drugs is the appropriate next step. Class Ic drugs (flecainide and propafenone) are effective in such patients without structural heart disease or coronary heart disease.

Step 3: The next step in patients who cannot take flecainide or propafenone is to consider amiodarone or sotalol.

Because interest in VPC supression decreased when it was shown to be typically deleterious in patients with coronary artery disease, this literature is not current, and specifically the role of newer class III antiarrhythmic like dofetilide and azimilide for VPCs is unclear at present.

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