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Ventricular Premature Complexes

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


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, and is highly dependent on the clinical context. The prognostic significance of VPCs is variable and, again, best 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. Observational studies and inferences from typical electrophysiology studies were initially focused on ventricular ectopy triggering ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, as a mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). The Cardiac Arrhythmia Suppression Trial (CAST) and other arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.[1]



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: After depolarizations 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.


Cardiac causes of VPCs include the following:

  • Acute myocardial infarction
  • Valvular heart disease, especially mitral valve prolapse
  • Cardiomyopathy (eg, ischemic, dilated, hypertrophic, infiltrative) [2]
  • Myocardial stretch
  • Cardiac contusion
  • Bradycardia
  • Tachycardia (high-catecholamine state)

Noncardiac causes of VPCs include the following:

  • Electrolyte disturbances (hypokalemia, hypomagnesemia, or hypercalcemia)
  • Medications (eg, digoxin, tricyclic antidepressants, aminophylline, amitriptyline, pseudoephedrine, fluoxetine)
  • Other drugs (eg, cocaine, amphetamines, caffeine, alcohol)
  • Anesthetics
  • Surgery
  • Infection
  • Stress


United States data

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 infrequently noted when only a single 12-lead ECG is used for ascertainment. 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

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.[3, 4]

In a study evaluating the features of frequent idiopathic VPCs in the Korean, investigators reported a mean patient age of 54.7 ± 16.8 years and a slight female preponderance (54.8%).[5]  The most common typical VPC-related symptoms/signs were palpitation and a dropped beat (59.2%), whereas the most common ECG features were left bundle branch block, an inferior axis, and late precordial R-wave transition.

Sex- and age-related demographics

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.

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.



The prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. Overall, 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. Importantly, no survival benefit in in any population has been convincingly demonstrated as a consequence of suppressing VPCs .

In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting over 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.[6] 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 2 studies, frequent or complex ventricular ectopy (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 exercise was an independent predictor of death.[6, 7] However, in another study, frequent VPCs only during exercise did not independently predict an increased risk; instead frequent VPCs during recovery was a stronger predictor of death.[8]

Frequent VPCs, especially when they occur in a bigeminal pattern, can cause or contribute to tachycardia-induced cardiomyopathy, which reversed by elimination of the PVCs through catheter ablation.[6, 9, 10, 11]  However, the extent to which this can be generalized to larger populations remains uncertain. Caution is in order, primarily because prior attempts at pharmacologic suppression were associated with unexpected and deleterious outcomes.[12]

Contributor Information and Disclosures

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, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society

Disclosure: Speaker, consultant, DSMB for: Lundbeck; Daiichi Sankyo, Amarin, On-X, Biotronik.

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.


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.

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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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