AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. Assessment and treatment of VPCs is challenging and complex. The significance of VPCs is interpreted in the context of the underlying cardiac condition.

The approach to the evaluation and management of VPCs has undergone dramatic changes in the last decade. Ventricular ectopy leading to ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, is one of the common mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). Recent arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.

Pathophysiology

Very few studies have evaluated the pathophysiology of VPCs in human subjects. Most of the information is derived from animal studies. Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity, as follows:

• Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. In animal models, focal mechanisms without evidence of macro-reentry play a major role in the origin of ventricular arrhythmia associated with ischemic cardiomyopathy. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.
• Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI.
• Triggered activity: Afterdepolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a VPC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated VPCs, but they also can be present with ischemia and electrolyte abnormalities.

Frequency

United States

The reported prevalence of VPCs varies between studies, depending on the population studied, duration of observation, and method of detection. In asymptomatic patients, VPCs are infrequent when only a single 12-lead ECG is used for screening. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more VPCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. VPCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.

International

Data from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 VPCs per hour when 24-h Holter monitoring was used.

Mortality/Morbidity

Prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. VPCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between VPC frequency and mortality, even in this group, is not robust and no benefit results in suppressing VPCs to improve survival in any population.

• In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting >10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death. Less frequent VPCs did not increase the risk.
• In general, multimorphic VPCs connote a poorer prognosis than uniform morphologic VPCs. In patients post-MI, frequent VPCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.
• In a recent study, a frequent VPC (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during recovery from exercise was an independent predictor of death. However, frequent VPCs only during exercise did not independently predict an increased risk.
• Frequent VPCs, especially when they occur in a bigeminal pattern, can precipitate tachycardia-induced cardiomyopathy that can be reversed by elimination of the PVCs through catheter ablation.

Sex

The Framingham heart study demonstrated increased prevalence of VPCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.

Age

VPCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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History

Various symptoms are associated with VPCs, but the exact prevalence of symptoms is not known. Typical symptoms include palpitations, light-headedness, syncope, atypical chest pain, or fatigue. Palpitations are due to an augmented post-VPC beat and may be sensed as a pause rather than an extra beat.

Physical

VPCs frequently are associated with variable or decreased intensity of heart sounds. The augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon A wave) from a loss of atrioventricular (AV) synchrony may be present. The follow-up beat after a VPC is stronger due to the postextrasystolic compensatory pause, allowing greater left ventricular (LV) filling, which usually causes greater intensity of that beat. This is known as extrasystolic potentiation.

Causes

• Cardiac causes include the following:
• • Acute myocardial infarction
  • Valvular heart disease, especially mitral valve prolapse
  • Cardiomyopathy (eg, ischemic, dilated, hypertrophic, infiltrative)
  • Myocardial stretch
  • Cardiac contusion
  • Bradycardia
  • Tachycardia (high-catecholamine state)
• Noncardiac causes include the following:
• • Electrolyte disturbances
  • Hypokalemia
  • Hypomagnesemia
  • Hypercalcemia
  • Medications (eg, digoxin, tricyclic antidepressants, aminophylline, amitriptyline, pseudoephedrine, fluoxetine)
  • Other drugs (eg, cocaine, amphetamines, caffeine, alcohol)
  • Anesthetics
  • Surgery
  • Infection
  • Stress

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Differentiating VPCs from other arrhythmias can be challenging because the following arrhythmias may mimic VPCs:

Aberrant premature atrial contractions: The presence of ectopic P waves, usually absence of full compensatory pause (R-R interval containing the premature contraction is <2 times the R-R interval of basic rhythm), and a relatively narrow QRS complex morphology help differentiate atrial premature complexes from VPCs. In general, the sinus node is not always reset by VPCs because the ectopic impulse meets the sinus impulse more distal to the sinus node (either at the AV node or in the ventricles). Thus, VPCs frequently cause a fully compensatory pause (R-R interval containing the premature contraction is equal to 2 times the R-R interval of basic rhythm). On rare occasions, the ectopic impulse conducts retrogradely to the sinus node; resets the sinus node; and a shorter, noncompensatory pause occurs. If the sinus impulse is able to conduct despite the VPC, then the VPC is termed interpolated and no compensatory pause occurs.

Fusion beat: Simultaneous activation of the ventricle by 2 sources can lead to a beat with characteristics between the conducted sinus beat and the ectopic beat.

Premature junctional contractions: The origin of this arrhythmia is automaticity or reentry in AV junctional tissues. The P waves usually are inverted because of retrograde atrial depolarization. If the ectopic beat originates in high nodal tissue, the QRS complex can be narrow.

Idioventricular escape rhythms: A very slow pacemaker in the ventricle takes over when sinoatrial node and AV junctional pacemakers fail to function. The rate usually is less than 45 beats per minute, which helps to differentiate it from other arrhythmias.

Ventricular tachycardia: When 3 or more consecutive ventricular contractions occur, they are called VT. VT that persists for 30 seconds or causes hemodynamic collapse is called sustained VT.

Parasystole: Parasystole occurs when a protected focus discharges independently of the dominant pacemaker. The characteristics of parasystole include wide QRS complexes with a varying coupling interval between the ectopic (parasystolic) and the dominant (usually sinus) complex, fusion beats, and variable coupling interval.

Fixed versus variable coupling interval: Fixed coupling refers to a fixed interval between the sinus QRS complex and the VPC; this indicates reentry or a triggered focus as the possible cause. Variable coupling could be due to parasystole or multifocal ectopy.

Interpolated VPC: When the sinus rate is slow, a short-coupled VPC can occur between sinus beats. If concealed retrograde conduction occurs, the subsequent PR interval can be prolonged.

VPCs as a proarrhythmic effect: VPCs can be exacerbated by catheters in the heart or pacemaker leads. They can occur in response to an antiarrhythmic drug. If they are worsened with an antiarrhythmic drug and the QT is prolonged from the drug, a risk of torsades de pointes exists.

WORKUP

Section 5 of 11  

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• Follow-up
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Lab Studies

• Look for correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI.
• Obtain serum electrolyte and magnesium levels.

Imaging Studies

• Look for underlying structural heart abnormalities that can predispose to VPCs.
• • Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging.
  • Echocardiography may be preferable because it also provides structural information about the heart.

Other Tests

• In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
• • The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
  • Suppressing the VPCs themselves is not the focus of treatment unless patients are extremely symptomatic; rather, treatment may be implemented if the patient is felt to be at high risk of sudden cardiac death.
  • Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
• ECG should be performed to look for structural cardiac abnormalities. Diagnostic criteria include the following:
• • Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
  • No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
  • The T wave usually is in the opposite direction from the R wave.
  • Full compensatory pause is common.
  • VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
  • VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
  • Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle rightward axis morphology.
• Electrophysiologic study
• • Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
  • According to current American College of Cardiology/American Heart Association guidelines, class I indications for EPS are patients with CAD, low EF (<0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
• Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.

Procedures

• In patients suspected of having coronary artery disease, a noninvasive evaluation to rule out this possibility or even a cardiac catheterization may be helpful diagnostically. This is based on not just the presence of VPCs, but on all risk factors and symptoms— onset in an elderly patient should be a red flag to consider the possibility of progressive structural heart disease.

Staging

VPCs can be classified in different ways. The Lown classification was introduced to gauge effects of antiarrhythmic drugs.

Table 1. Lown Classification

• Clinical classification is as follows:
• • Benign
  • Potentially malignant
  • Malignant
• Classification according to frequency is as follows:
• • Frequent - 10 or more VPCs per hour (by Holter monitoring) or 6 or more per minute
  • Occasional - Fewer than 10 VPCs per hour or fewer than 6 per minute
• Classification according to relationship to normal beats is as follows:
• • Bigeminy - Paired complexes, VPC alternating with a normal beat
  • Trigeminy - VPC occurring every third beat (2 sinus beats followed by VPC)
  • Quadrigeminy - VPC occurring every fourth beat (VPC following 3 normal beats)
  • Couplet - 2 consecutive VPCs
  • Nonsustained VT - 3 or more consecutive VPCs (<30 s)
• Classification according to origin is as follows:
• • Number of foci
  • • Unifocal/unimorphic - Beats originate from 1 focus, ie, all VPCs have the same morphology
    • Multifocal/multimorphic - VPCs have more than 1 morphology and may originate from more than 1 site
  • Site of origin
  • • Left ventricular
    • Right ventricular
  • Associated heart disease
  • • None (idiopathic)
    • Structural heart disease present

TREATMENT

Section 6 of 11  

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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.

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. 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

Section 7 of 11  

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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, even if their EF is reduced.

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, even though they do not reduce the risk of death.

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. 

Drug Category: Antiarrhythmic agents

Alter the electrophysiologic mechanisms responsible for arrhythmia.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• Further care depends on the underlying condition and the treatment selected.

Deterrence/Prevention

• For symptomatic VPCs, patients should avoid aggravating factors (eg, stress, caffeine-containing products).

Patient Education

• For symptomatic VPCs, patient education and reassurance are necessary.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• 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.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  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.
	View Full Size Image
Media type:  Rhythm Strip

REFERENCES

Section 11 of 11

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Article Last Updated: May 31, 2006