| Premature ventricular contraction | |
|---|---|
| Other names | Premature ventricular complex, ventricular premature contraction (complex or complexes) (VPC), ventricular premature beat (VPB), ventricular extrasystole (VES) |
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| Premature ventricular contraction usually originates from an area ofectopic focus. In this illustration the ectopic area is nearpapillary muscles in theleft ventricle. Most commonly in healthy hearts, PVCs occur near theright ventricular outflow tract (RVOT). | |
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| A premature ventricular contraction on anEKG, marked by the arrow | |
| Specialty | Cardiology |
Apremature ventricular contraction (PVC) is a common event where theheartbeat is initiated byPurkinje fibers in theventricles rather than by thesinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt aspalpitations in the chest. PVCs do not usually pose any danger.[1]
The electrical events of the heart detected by theelectrocardiogram (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 asarrhythmogenic right ventricular cardiomyopathy). Furthermore, very frequent (over 20% of all heartbeats) PVCs are considered a risk factor forarrhythmia-induced cardiomyopathy, in which the heart muscle becomes less effective and symptoms ofheart failure may develop.[2]Ultrasound of the heart is therefore recommended in people with frequent PVCs.
If PVCs are frequent or troublesome, medication (beta blockers or certaincalcium channel blockers) may be used. Very frequent PVCs in people withdilated cardiomyopathy may be treated withradiofrequency ablation.[2][1]
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, orlightheadedness. They may also cause chest pain, a faint feeling, fatigue, orhyperventilation after exercise.[2] Symptoms may be more pronounced at times of stress. Women may be more aware of PVCs at the time of themenstrual 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. previousmyocardial infarction), as well as heart disease orsudden cardiac death in close relatives. PVCs and palpitation associated withsyncope (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 contractions occur in healthy persons of any age, but are more prevalent in the elderly and in men.[3] In a very significant proportion of people they occur spontaneously with no known cause.[citation needed]
Some possible underlying causes of PVCs include:
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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 signaling, 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, particularlylow blood potassium, known as hypokalemia.
Reentry occurs when an area of 1-way block in thePurkinje 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 theright ventricular outflow tract (RVOT) under the pulmonic valve. The mechanism behind this is thought to be enhanced automaticity versus triggered activity.[3]
There are a number of different molecular explanations for PVCs.
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PVCs may be found incidentally on cardiac tests such as a 12-leadelectrocardiogram (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-hourHolter monitor or even 14- to 30-day recorders if the symptoms are very occasional.[2] Consumer-grade wearable devices such as the Apple Watch, KardiaMobile, and Fitbit also offer intermittent ECG recording capabilities, allowing users to capture symptomatic episodes outside of traditional clinical settings.[19]
The advantage of these monitors is that they allow a quantification of the amount of abnormal beats ("burden") and ensure that there are noheart arrhythmias present that might require attention, such asventricular tachycardia.[2] If symptoms are associated with exercise, a supervisedcardiac 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.[citation needed]
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.[20] PVCs can be distinguished frompremature atrial contractions because the compensatory pause is longer following premature ventricular contractions, in addition to a difference in QRS appearance.[21]
In some people, PVCs occur in a predictable pattern. Two PVCs in a row are called doublets and three PVCs in a rows are triplets. Depending whether there are one, two, or three normal (sinus) beats between each PVC, the rhythm is calledbigeminy, trigeminy, or quadrigeminy. If 3 or more consecutive PVCs occur in a row it may be calledventricular tachycardia.[21] 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", if PVC’s have different appearance, they are considered “multifocal”.[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 ascaffeine and certain drugs, like tobacco).[22] If frequent, it’s possible to use:
In general, PVCs are harmless. For patients with more than 1,000 PVCs per day, the risk of developing left ventricular systolic dysfunction after 5 years follow-up is low. Frequent PVCs may increase the risk of developing cardiomyopathy, which can greatly impair heart function. A PVC burden greater than 10% is the minimal threshold for development of PVC-induced cardiomyopathy. The risk is higher with a PVC burden greater than 20%. PVC burden often decreases spontaneously over time.[26]
People who do not have heart disease (with ejection fractions greater than 40%) have the same long-term prognoses as the minority of people without PVCs on the 24 hours. Emerging data also suggest that 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. For patients with underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.[3]
Inmeta-analysis of 11 studies, people with frequent PVCs (≥ once during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death twice as great as that of participants with occasional PVCs. Although most researchers attempted to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.[27]
Single PVCs are common in healthy persons. When 24-hour ambulatory monitoring is used, up to 80 percent of apparently healthy people have occasional PVCs.[28] Rates vary by age with extremely rare for those under the age of 11 and extremely common in those older than 75 years.[29] These differences may be due to rates of high blood pressure and atherosclerosis, which are more easy to find in older persons.[30] 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, maximalexercise stress test, right- and left-heartcatheterization and coronaryangiography.[31] 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.[32] Ventricular ectopy is more prevalent in men than in women of the same age; data from large, population-based studies indicate that the prevalence is less for young white women without heart disease and greater for older African American individuals with hypertension.[3]
