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A premature ventricular contraction (PVC) is a 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. PVCs do not usually pose any danger.

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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. Ultrasound of the heart is therefore recommended in people with frequent PVCs.

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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. In a very significant proportion of people they occur spontaneously with no known cause. <!-- PLEASE RESPECT ALPHABETICAL ORDER WHERE POSSIBLE -->

Some possible underlying causes of PVCs include:

Non-cardiac causes

  • Adrenaline excess
  • Anemia
  • Catecholamine excess
  • Certain medicines such as tricyclic antidepressants,
  • Chemical (electrolyte) abnormalities in the blood (for example hypokalemia (low blood potassium), which can occur in those taking diuretics ("water pills") and hypomagnesaemia (magnesium deficiency)).
  • Contact with the carina (trachea/bronchi) when performing medical suctioning stimulates vagus nerve
  • Drugs/substances such as:
  • Caffeine
  • Cocaine
  • Nicotine
  • Theobromine
  • Hypercapnia (CO<sub>2</sub> poisoning)
  • Hyperthyroidism
  • Sarcoidosis
  • Smoking
  • Stress
  • Myocarditis This type of protein stimulates the production of cAMP, ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.<br /> 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 by inhibiting the enzyme that catalyzes the breakdown of cAMP,

The advantage of these monitors is that they allow a quantification of the amount of abnormal beats ("burden") and ensure that there are no heart arrhythmias present that might require attention, such as ventricular tachycardia. 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.

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 called bigeminy, trigeminy, or quadrigeminy. If 3 or more consecutive PVCs occur in a row it may be called ventricular tachycardia. If frequent, it’s possible to use:

  • Medications
  • Antiarrhythmics: moricizine increased the death rate when used with diuretics, it reduced the frequency of deaths when it was used alone.
  • Beta blockers: Reduce cardiac contractility which makes PVCs less obvious to a person; possibly reduce catecholamine induced PVCs (in catecholamine-sensitive people) due to adrenaline not reaching sinus node [citation needed]
  • Calcium channel blockers This procedure is a way to destroy the area of the heart tissue that is causing the irregular contractions characteristic of PVCs using radio frequency energy.

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.

Epidemiology

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. Rates vary by age with extremely rare for those under the age of 11 and extremely common in those older than 75 years. These differences may be due to rates of high blood pressure and atherosclerosis, which are more easy to find in older persons. 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. 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. 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.