Premature Ventricular Contraction

Updated: Jan 13, 2017
  • Author: James E Keany, MD, FACEP; Chief Editor: Erik D Schraga, MD  more...
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A premature ventricular contraction (PVC) is caused by an ectopic cardiac pacemaker located in the ventricle. PVCs are characterized by premature and bizarrely shaped QRS complexes that are unusually long (typically >120 msec) and appear wide on the electrocardiogram (ECG). These complexes are not preceded by a P wave, and the T wave is usually large and oriented in a direction opposite the major deflection of the QRS.

The clinical significance of PVCs depends on their frequency, complexity, and hemodynamic response.



PVCs reflect activation of the ventricles from a site below the atrioventricular node (AVN). Suggested mechanisms for PVCs are reentry, triggered activity, and enhanced automaticity.

Reentry occurs when an area of one-way block in the Purkinje fibers and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, the area of slow conduction activates the blocked part of the system after the rest of the ventricle has recovered, resulting in an extra beat. Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia.

Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).

Enhanced automaticity suggests an ectopic focus of pacemaker cells in the ventricle that has a subthreshold potential for firing. The basic rhythm of the heart raises these cells to threshold, which precipitates an ectopic beat. This process is the underlying mechanism for arrhythmias due to excess catecholamines and some electrolyte deficiencies, particularly hyperkalemia.

Ventricular ectopy associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract beneath the pulmonic valve. The mechanism is thought to be enhanced automaticity versus triggered activity. These arrhythmias are often induced by exercise, isoproterenol (in the electrophysiology laboratory), the recovery phase of exercise, or hormonal changes in female patients (pregnancy, menses, menopause).

The characteristic ECG pattern for these arrhythmias is a large, tall R wave in the inferior leads with a left bundle-branch block pattern in V1 . If the source is the left ventricular outflow tract, there is a right bundle-branch block pattern in V1 . Beta-blocker therapy is first-line treatment for symptomatic patients.

Factors that increase the risk of PVCs include male sex, advanced age, African American race, hypertension and underlying ischemic heart disease, a bundle-branch block on 12-lead ECG, hypomagnesemia, [1] and hypokalemia.



Cardiac causes of premature ventricular contractions include the following:

Other causes of PVCs include the following:

  • Hypoxia and/or hypercapnia
  • Medications (eg, digoxin, sympathomimetics, tricyclic antidepressants, aminophylline, caffeine)
  • Illicit substances (eg, cocaine, amphetamines, alcohol, tobacco)


United States statistics

PVCs are one of the most common arrhythmias and can occur in patients with or without heart disease. Their prevalence varies greatly, with estimates ranging from less than 3% to more than 60% in asymptomatic individuals. Data from large, population-based studies indicate that the prevalence ranges from less than 3% for young white women without heart disease to almost 20% for older African American individuals with hypertension.

Race-, sex-, and age-related demographics

Black race is associated with an increased frequency of PVCs on routine monitoring. [5] In a large population-based study of PVC prevalence, black race alone increased the risk of PVCs by 30% in comparison with the risk in white individuals.

Ventricular ectopy is more prevalent in men than in women of the same age. Male sex alone increases the risk of identifying PVCs on routine screening, with an odds ratio for male sex of 1.39 as compared with female sex.

PVC frequency increases with age, reflecting the increased prevalence of hypertension and cardiac disease in aging populations.



In asymptomatic patients without underlying heart disease, the long-term prognosis is similar to that of the general population. Asymptomatic patients with ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. Therefore, in patients with no evidence of heart disease on noninvasive workup, reassurance is appropriate.

One caveat to this is that emerging data suggest that very frequent ventricular ectopy (>4000/24 hr) may be associated with the development of cardiomyopathy related to abnormal electrical activation of the heart. This mechanism is thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy.

In the setting of acute coronary ischemia/infarction, patients with simple PVCs rarely progress to malignant arrhythmias. However, persistent complex ectopy after MI is associated with increased risk of sudden death and may be an indication for electrophysiologic studies (EPS).

In patients with underlying chronic structural heart disease (eg, cardiomyopathy, infarction, valvular disease) and complex ectopy (eg, >10 PVCs/hr), mortality is significantly increased. The following points should be kept in mind.

First, understanding of the role of antiarrhythmic therapy in the months after MI is poor. The Cardiac Arrhythmia Suppression Trial (CAST) studied patients with ventricular ectopy after MI to see if antiarrhythmic therapy improved survival rates. [6]  Despite suppression of ectopy on Holter monitoring, patients treated with encainide, flecainide, or moricizine had increased rates of sudden death and death from all causes. Findings have suggested a role for amiodarone in this patient population and have had significant reductions in rates of post-MI ventricular arrhythmias and death. Moricizine was discontinued in July 2007 because of diminished market demand.

Second, left ventricular dysfunction has a stronger association with increased mortality rate than do PVCs. Many now believe that PVCs reflect the severity of heart disease rather than contribute to arrhythmogenesis. Some studies in recent years suggest that increased variability of the PVC coupling interval in patients with underlying heart diseases, including left ventricular dysfunction, is a predictor of cardiac death; however, this remains a matter of debate. [7, 8]

Third, EPS has a primary role in risk stratification of patients with frequent or complex PVCs. Patients with PVCs that are noninducible (ie, unable to trigger ventricular tachycardia during stimulation) have a low risk of sudden death.

Frequent PVCs may be associated with increased risk of stroke in patients who do not have hypertension and diabetes. [9]


The clinical significance of PVCs depends on the clinical context in which they occur, as follows:

  • PVCs in young, healthy patients without underlying structural heart disease are usually not associated with any increased mortality
  • PVCs in older patients, in particular those with underlying heart disease, are associated with an increased risk of adverse cardiac events, particularly sustained ventricular dysrhythmias and sudden death
  • In patients who have had a MI, the risk of malignant ventricular arrhythmias and sudden death is related to the complexity and frequency of the PVCs; patients with PVCs in Lown classes 3-5 are at greatest risk (see Lown grading criteria in Workup)