Premature ventricular contraction

A premature ventricular contraction (PVC) is a relatively common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. Single beat PVC do not usually pose a danger.[1]

Premature ventricular contraction
Other namesPremature ventricular complex, ventricular premature contraction (complex or complexes) (VPC), ventricular premature beat (VPB), ventricular extrasystole (VES)
A premature ventricular contraction marked by the arrow.

The electrical events of the heart detected by the electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. However, very frequent PVCs can be symptomatic of an underlying heart condition (such as arrhythmogenic right ventricular cardiomyopathy). Furthermore, very frequent (over 20% of all heartbeats) PVCs are considered a risk factor for arrhythmia-induced cardiomyopathy, in which the heart muscle becomes less effective and symptoms of heart failure may develop.[2] Ultrasound of the heart is therefore recommended in people with PVCs.

If PVCs are frequent or troublesome, medication (beta blockers or certain calcium channel blockers) may be used. Very frequent PVCs in people with dilated cardiomyopathy may be treated with radiofrequency ablation.[2][1]

Signs and symptoms

Although there are many possible symptoms associated with PVCs, PVCs may also have no symptoms at all. PVCs may be perceived as a skipped heart beat, a strong beat, palpitations, lightheadedness. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise.[2][3] Symptoms may be more pronounced at times of stress. Women may be more aware of PVCs at the time of the menstrual period.[2]

Premature ventricular contractions may be associated with underlying heart disease, and certain characteristics are therefore elicited routinely: the presence of signs of heart disease or a known history of heart disease (e.g. previous myocardial infarction), as well as heart disease or sudden cardiac death in close relatives. PVCs and palpitation associated with syncope (transient loss of consciousness) or provoked by exertion are also concerning.[2] Physical examination is focused on identifying evidence of underlying heart disease.[2]


Premature ventricular contraction in an ECG (arrows)
Resulting "skipped beat" in the continuous blood pressure, recorded noninvasively.

Premature ventricular contractions can occur in a healthy person of any age, but are more prevalent in the elderly and in men.[4] In a very significant proportion of people they occur spontaneously with no known cause. Some possible underlying causes of PVCs include:


Normally, impulses pass through both ventricles almost at the same time and the depolarization waves of the two ventricles partially cancel each other out in the ECG. However, when a PVC occurs the impulse nearly always travels through only one bundle fiber, so there is no neutralization effect; this results in the high voltage QRS wave in the electrocardiograph.

There are three main physiological explanations for premature ventricular contractions: enhanced ectopic nodal automaticity, re-entry signalling, and toxic/reperfusion triggered.

Ectopic enhanced nodal automaticity suggests foci of sub-pulmonic valvular pacemaker cells that have 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 low blood potassium, known as hypokalemia.

Reentry occurs when an area of 1-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, one bundle tract's area of slow conduction activates the other tract's bundle fibers post block after the rest of the ventricle has recovered. This 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).

This ectopy of the ventricles when associated with a structurally normal heart most commonly occurs from the right ventricular outflow tract under the pulmonic valve. The mechanism behind this is thought to be enhanced automaticity versus triggered activity.[4]

Molecular basis

There are a number of different molecular explanations for PVCs.

  • calcium excess: One explanation is most basically due to an increased amount of cyclic AMP(cAMP) in the muscle cells of the heart's ventricles leading to increased flow of calcium ions into the cell. This may happen for the following reasons:
  • Activation of the sympathetic nervous system, due to anxiety and/or physiological stress, for example hypovolemia caused by dehydration or bleeding. This activation can cause a release of catecholamines such as epinephrine (adrenaline) which can bind to beta-1 adrenergic receptor (β1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein.[13] This type of protein stimulates the production of cAMP,[14] ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.[15]
    This has the effect of (1) increasing the strength of contraction (inotropy) and (2) depolarizing the myocyte more rapidly (chronotropy). The ventricular myocytes are therefore more irritable than usual, and may depolarize spontaneously before the SA node depolarizes. Other sympathomimetic molecules such as amphetamines and cocaine will also cause this effect.
  • Phosphodiesterase inhibitors such as caffeine directly affect the G-coupled signal transduction cascade[16] by inhibiting the enzyme that catalyzes the breakdown of cAMP,[13] again leading to the increased concentration of calcium ions in the cytosol.
  • potassium deficiency: Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells, and hypokalemia makes it more likely that cells will depolarize spontaneously. Hypercalcemia has a similar effect, although clinically it is of less concern.
  • magnesium deficiency: Magnesium ions affect the flow of calcium ions, and they affect the function of the Na+/K+ ATPase, and are necessary for maintaining potassium levels. Low blood magnesium therefore also makes spontaneous depolarization more likely.
  • myocardium damage: Existing damage to the myocardium can also provoke PVCs. The myocardial scarring that occurs in myocardial infarction and also in the surgical repair of congenital heart disease can disrupt the conduction system of the heart and may also irritate surrounding viable ventricular myocytes, make them more likely to depolarize spontaneously. Inflammation of the myocardium (as occurs in myocarditis) and systemic inflammation cause surges of cytokines, which can affect the electrical properties of myocytes and may be ultimately responsible for causing irritability of myocytes.


PVCs may be found incidentally on cardiac tests such as a 12-lead electrocardiogram (ECG/EKG) performed for another reason. In those with symptoms suggestive of premature ventricular complexes, the ECG/EKG is the first investigation that may identify PVCs as well as other cardiac rhythm issues that may cause similar symptoms. If symptoms are infrequent, other forms of continuous heart beat recording may be used, such as a 24- or 48-hour Holter monitor or even 14- to 30-day recorders if the symptoms are very occasional.[2] The advantage of these monitors is that they allow a quantification of the amount of abnormal beats ("burden") and ensure that there are no additional heart arrhythmias present that might require specific attention, such as ventricular tachycardia.[2] If symptoms are associated with exercise, a supervised cardiac stress test may be required to reproduce the abnormality. Specifically, if this shows exercise-induced ventricular tachycardia this would require specific treatment.[2] If PVCs are suppressed by exercise, this is an encouraging finding.

On electrocardiography (ECG or Holter) premature ventricular contractions have a specific appearance of the QRS complexes and T waves, which are different from normal readings. By definition, a PVC occurs earlier than the regular normally conducted beat. Subsequently, the time between the PVC and the next normal beat is longer as the result of a compensatory pause.[17] PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions, in addition to a difference in QRS appearance.[18]

In some people, PVCs occur in a predictable pattern (either for long periods or persistently). Depending whether there are one, two, or three normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. If 3 or more PVCs occur in a row it may be called ventricular tachycardia.[18] The precise shape of the QRS can give an indication as to where precisely in the heart muscle the abnormal electrical activity arises. If someone has PVCs that all have the same appearance, they are considered "monofocal", which is a more benign phenomenon. In contrast, if there are PVCs of multiple different appearances, they are labelled "multifocal"; this is a possible sign of higher a risk of complications.[2]


Isolated PVCs with benign characteristics and no underlying heart disease require no treatment, especially if there are limited symptoms.[2]

The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and certain drugs, like tobacco).[19]


As an overall medical condition PVCs are normally not very harmful to patients that experience them, but frequent PVCs may put patients at increased risk of developing arrhythmias or cardiomyopathy, which can greatly impact the functioning of the heart over the span of that patient's life. On a more serious and severe scale, frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms .[23]

Asymptomatic patients that do not have heart disease have long-term prognoses very similar to the general population, but asymptomatic patients that have ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. One drawback comes from emerging data that suggests very frequent ventricular ectopy may be associated with cardiomyopathy through a mechanism thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy. Patients that have underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.[4]

In meta-analysis of 11 studies, people with frequent PVC (≥1 time during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death 2 times higher than persons without frequent PVC. Although most studies made attempts to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.[24]

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease (i.e. in the presence of normal heart function) there were no serious cardiac events through 5.6 years on average, but there was correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. In this study absence of heart of disease was excluded by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.[25] Another study has suggested that in the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis.[20] It was study of 70 people followed by 6.5 years on average. Healthy status was confirmed by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.[26]

On the other hand, the Framingham Heart Study reported that PVCs in apparently healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death.[20] In men with coronary heart disease and in women with or without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk.[27] The at-risk people might have subclinical coronary disease.[28] These Framingham results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.[20]

In the ARIC study of 14,783 people followed for 15 to 17 years those with detected PVC during 2 minute ECG, and without hypertension or diabetes on the beginning, had risk of stroke increased by 109%.[29] Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVC.[29] It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes.[29] Those in ARIC study with any PVC had risk of heart failure increased by 63%[30] and were >2 times as likely to die due to coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.[31]

In the Niigata study of 63,386 people with 10-year follow-up period those with PVC during a 10-second recording had risk of atrial fibrillation increased nearly 3 times independently from risk factors: age, male sex, body mass index, hypertension, systolic and diastolic blood pressure, and diabetes.[32]

Reducing frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.[20][22]

Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.[22][33]


Single PVC are common in healthy persons. A study in healthy volunteers below the age of 45 years has found the prevalence to be 40.6% in a 24-Hour Holter ECG Recording.[34] Age has been seen to play a major role in the occurrence of PVCs throughout the population. The prevalence is seen to be under 1% for those under the age of 11 and ranges all the way up to 69% in subjects that are older than 75 years.[35] Older patients are more likely to experience PVCs and this may be due to its prevalence in patients with high blood pressure and heart disease, which are both commonly seen more in patients of older ages.[36] In 101 people free of heart disease during 24 hours Holter monitoring, 39 had at least 1 PVC, and 4 at least 100. Heart disease was excluded after physical examination, chest x-ray, ECG, echocardiography, maximal exercise stress test, right- and left-heart catheterization and coronary angiography.[37] In 122,043 United States Air Force flyers and cadet applicants during approximately 48 seconds of ECG 0.78% (952 males) had PVC within all age groups, but with increased incidence with increasing age.[38] Ventricular ectopy is more prevalent in men than in women of the same age 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.[4]


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Further reading

  • Levy, Matthew N.; Pappano, Achilles J. (2007). Cardiovascular physiology. Mosby physiology monograph series (9th ed.). Philadelphia: Mosby Elsevier. ISBN 978-0-323-03446-3. OCLC 63660993.
  • Nelson, David L.; Cox, Michael M. (2008). "Biosignaling". Lehninger Principles of Biochemistry (5th ed.). New York: W.H. Freeman. pp. 419–484. ISBN 978-0-7167-7108-1. OCLC 957377043 via Google Books.
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