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. [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:
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Patient education and reassurance
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Avoidance of aggravating factors (eg, stress, caffeine-containing products)
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Consideration of antiarrtymic agents and
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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.
Presence of underlying heart disease (eg, VPCs in patients post MI)
Management in these patients 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. [22]
Ablation therapy
The 2006 ACC/AHA/ESC guideline recommends that ablation therapy should be considered in the following [18] :
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Patients with frequent, symptomatic, and monomorphic VPCs refractory to medical therapy
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Patients who choose to avoid long-term medical therapy
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Patients with ventricular arrhythmia storm that is consistently provoked by VPBs of a similar morphology
VPCs arising from the outflow tract (OT) are the most common subtype of idiopathic VPCs; more than 70-80% of premature ventricular contractions (PVCs) originate from the right ventricular (RV) OT. The remaining VPCs originate from other sites (left and right coronary cusp, mitral annulus, and on the epicardium near the left ventricular [LV] OT). Highly symptomatic and refractory cases of VPCs especially from RVOT are appropriate for ablation therapy, with success rates over 70%.
The selection of an endocardial versus an epicardial approach to target ventricular arrythmia depends on the patient’s underlying disease substrate, as well as the location of the arrhythmogenic substrate within the myocardial wall, which can be best assessed with a cardiac MRI. [23]
Diet
Recommendations depend on the underlying cardiac disease; avoidance of caffeine, nicotine, and alcohol may reduce the frequency of VPCs.
Surgical Care
Patients deemed to be at high risk of sudden cardiac death may benefit from implantable cardioverter defibrillator (ICD) implantation.
Catheter-based renal sympathetic denervation (RSD) may have a role in reducing the arrhythmic burden of ventricular arrhythmias, including PVCs, that are refractory to pharmacotherapy. [24] In a preliminary study of 34 patients with PVCs and structurally normal hearts (20 underwent ablation RSD, 14 served as controls), investigators noted that at 3-, 6- (first month after RSD, without drugs), 7-, and 12-month (sixth month after RSD, without drugs) follow-up, those treated with RSD had significantly reduced numbers of polymorphic PVCs compared to baseline. Although neither patient group showed any changes in mean 24-hour ambulatory blood pressure monitoring (ABPM) and renal function at 12 months, the control group demonstrated a decrease in 24-hour Holter mean heart rate. The change in number of polymorphic PVCs at 6 months post RSD was significantly associated with the total number of RSD ablated sites. [24]
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, which is typically assessed by the presence of any associated cardiovascular disease, rather than the presence of VPCs per se.
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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 |
