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Ventricular Premature Complexes Workup

  • Author: Jatin Dave, MD, MPH; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 30, 2015
 

Approach Considerations

Obtain laboratory studies to evaluate or correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI. Obtain serum electrolyte and magnesium levels.

Imaging studies may help to identify any 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 the preferred imaging modalitybecause it also provides structural information about the heart.

Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.

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.

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Electrocardiography

The diagnosis of VPCs is typically established by electrocardiography. The presence of a VPC on a 12-lead ECG provides essential information about the origin of that extrasystole, as well as providing important information about the ventricular site-of-origin of the VPC. Accordingly, an ECG should be performed to look for pathophysiologic cardiac abnormalities as well as documenting the presence of VPCs and potentially providing information about their specific mechanism and frequency.

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 inferior axis morphology. See the image below.
    Ventricular premature complexes (VPCs). Ventricula 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.

Noninvasive mapping of cardiac arrhythmias is also possible with a 252-lead ECG and computed-tomography scan–based three-dimensional electroimaging.[13]

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Holter Monitoring

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.

Suppression of VPCs by beta-blocker or calcium blocker, together with a typical VPC morphology (inferior axis, LBBB morphology) can be helpful in establishing typical right ventricular outflow tract ectopy.

Suppressing the VPCs themselves is not the focus of treatment unless patients are significantly symptomatic.

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.[14]

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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 the American College of Cardiology/American Heart Association guidelines,[15, 16] 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.

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Classification of Ventricular Premature Contractions

VPCs can be classified in different ways. The Lown classification was introduced to gauge effects of antiarrhythmic drugs and widely assumed to encapsulate prognostic significance—it is not clear that it fulfills either of these goals, but this classification is still employed.

Table 1. Lown Classification (Open Table in a new window)

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

 

The Lown classification does not necessarily imply a continuum of increasing risk.

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) or multifocal/multimorphic (VPCs have more than one morphology and may originate from more than one site)
  • Site of origin: Left or right ventricular
  • Associated heart disease: None (idiopathic) or structural heart disease is present
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Contributor Information and Disclosures
Author

Jatin Dave, MD, MPH Part-Time Clinical Instructor, Department of Medicine, Harvard Medical School; Attending Physician, Division of Aging, Department of Medicine, Brigham and Women's Hospital; Medical Director of Geriatrics, Tufts Health Plan

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Tufts Health Plan, a not for profit organization.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors John Michael Gaziano, MD, MPH; Revat Lakhia, MD; and Shivkumar H Jha, MD, to the development and writing of this article.

References
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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.
Table 1. Lown Classification
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
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