DESCRIPTION

• Premature ventricular contractions (PVCs) involve depolarization of the ventricle with inscription of QRS earlier than expected.
• The depolarization is initiated in the ventricles, causing the QRS morphology to be bizarre and not typical of depolarization via the normal conducting system.
• Synonym(s): Premature ventricular beats; Premature ventricular depolarizations; Ventricular premature contractions; Ventricular premature beats; Ventricular premature depolarizations

Pregnancy Considerations

• Contraindications related to underlying heart disease
• No contraindication if structurally normal heart; symptoms may increase during pregnancy

EPIDEMIOLOGY

• Frequent after MI, and ubiquitous as age increases and in setting of cardiomyopathy
• May occur at any age, but prevalence increases with age, and PVCs are ubiquitous in the elderly.
• Can occur in otherwise healthy individuals [idiopathic ventricular tachycardia (VT)]; usually associated with good prognosis. In these patients, PVCs are monomorphic and have a typical right bundle–branch block (RBBB)/inferior axis or left bundle–branch block (LBBB) pattern

RISK FACTORS

• Increasing age
• Structural heart disease

ETIOLOGY

• Reentry, automaticity, and triggered mechanisms
• Most frequently seen in structural heart disease, especially during and after MI and cardiomyopathy
• Drug toxicity (digitalis, QT-prolonging agents)
• Sympathetic stimulation (eg, -agonists used to treat bronchospasm, caffeine)
• Slow heart rates during which ventricular beats may represent escape rhythms

COMMONLY ASSOCIATED CONDITIONS

Because the frequency of ischemic heart disease and cardiomyopathy increases with age, PVCs are seen in association with these diseases.

Outline

• Description
  • Pregnancy Considerations
• Epidemiology
• Risk Factors
• Etiology
• Commonly Associated Conditions

History

• Symptoms may be absent.
• Palpitations
• Dyspnea

Physical Exam

• On physical exam, PVCs are associated with early beats, followed by a pause that may be either compensatory (depolarization does not change timing of intrinsic rhythm) or not.
• Giant A waves may be seen in the neck veins because, with PVC, there is atrial contraction against a closed tricuspid valve.
• There may be an absent peripheral pulse with the early beat because the heart has not had time to fill in diastole, and the contraction pattern of the ventricles is abnormal.

DIAGNOSTIC TESTS & INTERPRETATION

• EKG
• Ambulatory (Holter) monitor
• Event recorder
• Evaluate for underlying heart disease:
  • Ischemia (exercise test)
  • Myocardium [echo, MRI]
• Pathology: Depends on substrate, but usually scar/fibrosis; sometimes in a structurally normal heart, PVCs arise from triggered activity or automatic focus in normal tissue

Imaging

• Depends on age and suspicion for heart disease
• ECG
• Perfusion imaging to evaluate ischemia (eg, thallium) and ejection fraction
• MRI (also called nuclear magnetic resonance, or NMR)

DIFFERENTIAL DIAGNOSIS

Atrial premature contractions (APCs) with aberrancy

Outline

• History
• Physical Exam
• Diagnostic Tests & Interpretation
  • Imaging
• Differential Diagnosis

• -Blocker if ischemic heart disease:
  • Even though -blockers may not suppress PVCs, they have been shown to increase survival.
  • In symptomatic patients, -blockers may decrease symptoms by decreasing vigor of post-PVC beat that is usually responsible for the palpitation (increased contraction after pause via Starling principle).
• Acute setting: Lidocaine or IV amiodarone are usually used in acute settings such as MI:
  • Lidocaine should not be used prophylactically because meta-analyses suggest an increase in mortality due to bradycardic deaths when the drug is used in this manner.
  • If the patient has had ventricular tachycardia or ventricular fibrillation, IV amiodarone is the usual 1st antiarrhythmic drug chosen.
• Chronic therapy: If symptomatic despite -blocker therapy antiarrhythmic drugs are used chronically
• Class I drugs such as flecainide or propafenone are often useful in patients without structural heart disease
• Amiodarone or sotalol used in patients with structural heart disease
• Anxiolytic can be helpful if patient worried about palpitations
• Contraindications:
  • In patients with structural heart disease, class IC drugs are contraindicated, and all class I drugs are probably inadvisable
  • Proarrhythmia:
    • May manifest as increased mortality from class I drugs in ischemic heart disease
    • Torsade de pointes ventricular tachycardia with class IA and class III drugs
    • Avoid class I and III drugs if corrected QT interval prolonged at baseline.

ADDITIONAL TREATMENT

General Measures

• Treat underlying heart disease.
• -Blockers if ischemic heart disease
• There is no evidence that treatment of PVCs extends life; in patients with prior MI treatment with certain antiarrhythmic drugs has been shown to increase mortality (Cardiac Arrhythmia Suppression Trial), 1st therapy choice should be reassurance avoidance of PVC triggers if possible (caffeine, alcohol, etc.).
• The Canadian Amiodarone MI Arrhythmia Trial and the European MI Amiodarone Trial showed that prophylactic amiodarone following MI does not improve overall survival.
• see topic on Ventricular Tachycardia for management of nonsustained ventricular tachycardia (PVCs occur in runs of 3):
  • For patients with ischemic heart disease and low LV ejection fractions, electrophysiologic study can be justified, and if sustained ventricular tachycardia is induced, an implantable defibrillator can be offered (refer to Buxton et al. and Mess et al. in References).
• The best prevention of PVCs is the prevention of heart disease.

SURGERY

Not applicable; however, in patients with idiopathic PVCs may be "cured" by ablation of arrhythmia focus in RV outflow tract and in fascicles of His-Purkinje system.

IN-PATIENT CONSIDERATIONS

Admission Criteria

All attempts should be made to avoid treating PVCs per se. -Blockers and (rarely) anxiolytics can be started on an outpatient basis. For patients with structural heart disease, admission is indicated for loading of drugs with pro-arrhythmic potential. Amiodarone is often started as an outpatient with close clinical follow-up.

Outline

• Additional Treatment
  • General Measures
• Surgery
• In-Patient Considerations
  • Admission Criteria

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• Monitor online with telemetry and record EKG at least daily in acute setting.
• Outpatients may have repeat Holter monitors or event recorders to correlate symptoms with the rhythm if empiric therapy does not decrease symptoms.

PATIENT EDUCATION

• Teach patients that PVCs per se are not a cause for mortality alone, and that antiarrhythmic drug treatment may worsen prognosis.
• In setting of structurally normal heart, prognosis is normal. There is no indication for treatment in the absence of symptoms.
• No specific diet is indicated, although in some individuals caffeine/alcohol may increase frequency of PVCs.
• Teach that antiarrhythmic drugs may be proarrhythmic.

PROGNOSIS

• Normal if structurally normal heart
• Decreased survival if ischemic heart disease
• Controversial if cardiomyopathy

Outline

• Follow-Up Recommendations
  • Patient Monitoring
• Patient Education
• Prognosis

CODES

ICD9

427.69 Other premature beats

SNOMED

17338001 ventricular premature beats (disorder)

ADDITIONAL READING

• Buxton AE, Lec KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Engl J Med. 1999;341:1882–1890.
• Cairns JA, Connolly SJ, Roberts R, et al., for the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Lancet. 1997;349:675–682.
• The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227–233.
• Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo: The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324:781–788.
• Epstein AE, Bigger JT, Wyse DG, et al. Events in the Cardiac Arrhythmia Suppression Trial (CAST): Mortality in the entire population enrolled. J Am Coll Cardiol. 1991;18:14–19.
• Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet. 1997;349:667–674.
• Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med. 1996;335:1933–1940.

Peter Ott

Andrew E. Epstein