Premature ventricular contraction

From WikiProjectMed
Jump to navigation Jump to search
Premature ventricular contraction
Other names: Premature ventricular complex; ventricular premature contraction (complex or complexes) (VPC); ventricular premature beat (VPB); ventricular extrasystole (VES); ventricular premature depolarisation
A premature ventricular contraction marked by the arrow.
SymptomsNone, feeling of skipped beat[1]
ComplicationsHeart problems[2]
CausesNormal, heart disease[2]
Risk factorsAlcohol, stimulants including caffeine, electrolyte abnormalities, low oxygen, high CO2[2]
Diagnostic methodElectrocardiogram (ECG), holter monitor, heart ultrasound[2]
Differential diagnosisAberrant premature atrial contractions, bigeminy, premature junctional contractions[2]
TreatmentReassurance, beta blockers, calcium channel blockers[3]

A premature ventricular contraction (PVC) is an early extra beat that arise from the ventricle of the heart.[2] They often result in no symptoms but may be felt as a "skipped beat" in the chest.[1] Others report tiredness and lightheadedness.[2] Occasional PVCs do not pose a danger; while, frequent PVCs can represent or result in heart problems.[2][4] If a prolonged QT is present, Torsades de Pointes may occur.[5]

Generally they are a normal phenomenon.[1] Triggers may include anxiety, alcohol, stimulants including caffeine, electrolyte abnormalities, low oxygen, and high CO2.[2][5] Underlying heart disease, including a heart attack, mitral valve prolapse, and myocarditis, is also a risk factor.[2] Diagnosis is by electrocardiogram (ECG), which generally shows a QRS complex greater than 120 ms.[2] Generally they occur early and are followed by a pause.[4] If more than 10% of heartbeats are PVCs an ultrasound of the heart is recommended.[3]

Often no treatment is needed.[1][3] In those who are bothered beta blockers or certain calcium channel blockers may be used.[3] If this is not effective an antiarrhythmic medication or radiofrequency ablation may be considered.[3] They are common.[2] They are present on an ECG in about 0.5% of those under 20 and 2.2% of those over 50 years old.[2]

Signs and symptoms

PVCs may be perceived as a skipped heart beat, a strong beat, palpitations, or lightheadedness; though many have no symptoms. They may also cause chest pain, tiredness, or fast breathing after exercise.[3][6] Symptoms may be more pronounced at times of stress. Women may be more aware of PVCs at the time of the menstrual period.[3]

Premature ventricular contractions may be associated with underlying heart disease including a previous myocardial infarction. PVCs and palpitation associated with syncope (transient loss of consciousness) or provoked by exertion are also concerning.[3] Physical examination is focused on identifying evidence of underlying heart disease.[3]


If more than 6 PVCs occur a minute, further investigation may be warranted.[4] More than 10 to 15% PVCs is associated with cardiomyopathy and heart failure; though, this generally takes months or years to occur.[7][8] Other features of concern include PVCs that are not followed by the usual pause and PVCs that occur at various durations from the proceeding normal beat.[7][8] In those with long QT or Brugada syndrome, PVCs may also be concerning.[7]


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

PVCs can occur in a healthy person of any age, but are more common in the elderly and in men.[9] In a most people they occur spontaneously with no known cause. Some possible underlying causes 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.[9]

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 receptor1 receptors) on cardiac myocytes, activating a type of guanosine nucleotide-binding protein called Gs protein.[18] This type of protein stimulates the production of cAMP,[19] ultimately increasing the flow of calcium ions from the extracellular space and from the sarcoplasmic reticulum into the cytosol.[20]
    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[21] by inhibiting the enzyme that catalyzes the breakdown of cAMP,[18] 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.[3] 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.[3] 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.[3] 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.[22] 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.[23]

PVCs may 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.[23] 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 a greater risk of complications.[3]

Generally the distance between the prior beat and the PVCs is constant; however, if this is variable it is associated with greater risks.[7]


Isolated PVCs with benign characteristics and no underlying heart disease require no treatment, especially if there are limited symptoms.[3]

The most effective treatment is the elimination of triggers (particularly stopping the use of substances such as caffeine and tobacco).[24]


In general, PVCs are harmless, but frequent PVCs may increase the risk of developing arrhythmias or cardiomyopathy, which can greatly and permanently impair heart function. On a more serious and severe scale, frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms .[28]

Asymptomatic patients who do not have heart disease have long-term prognoses very similar to the general population, but asymptomatic patients with ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. 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. And for patients with underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.[9]

In meta-analysis of 11 studies, people with frequent PVC (≥ 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 without frequent PVC. 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.[29]

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 established by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.[30]

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.[25] It was study of 70 people followed by 6.5 years on average. Healthy status was verified by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.[31]

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.[25] 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.[32] The at-risk people might have subclinical coronary disease.[33] These Framingham results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.[25]

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%.[34] Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVC.[34] 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.[34] Those in ARIC study with any PVC had risk of heart failure increased by 63%[35] and were > twice as likely to die from coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.[36]

In the Niigata study of 63,386 people with a 10-year follow-up period, subjects with PVC during a 10-second recording had triple the risk of atrial fibrillation of those without PVC, independently of these risk factors: age;male sex; high simple body mass index (a possible signifier of obesity); hypertension (systolic and diastolic blood pressure within certain abnormal limits); and diabetes.[37]

Reducing frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.[25][27]

Recent studies have shown that those subjects with extremely frequent 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.[27][38]


Single PVCs are common in healthy persons. 41% of healthy volunteers below the age of 45 years have been found to have PVCs on 24-hour Holter ECG recording.[39] Rates vary by age with under 1% for those under the age of 11 and 69% in those older than 75 years.[40] These differences may be due to rates of high blood pressure and heart disease, which are more common in older persons.[41] 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.[42] 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.[43] 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.[9]


  1. 1.0 1.1 1.2 1.3 "Types of Arrhythmia". July 1, 2011. Archived from the original on 7 June 2015. Retrieved 19 March 2015.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 Sattar, Y; Hashmi, MF (January 2020). "Ventricular Premature Complexes". StatPearls. PMID 31613493.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 Akdemir, B.; Yarmohammadi, H.; Alraies, M. C.; Adkisson, W. O. (1 July 2016). "Premature ventricular contractions: Reassure or refer?". Cleveland Clinic Journal of Medicine. 83 (7): 524–530. doi:10.3949/ccjm.83a.15090. PMID 27399865.
  4. 4.0 4.1 4.2 Dubin, Dale (2000). Rapid Interpretation of EKG's: An Interactive Course. Cover Publishing Company. p. 137. ISBN 978-0-912912-06-6. Archived from the original on 2024-04-24. Retrieved 22 April 2024.
  5. 5.0 5.1 Burns, Ed; Buttner, Robert (1 August 2020). "Premature Ventricular Complex (PVC)". Life in the Fast Lane • LITFL. Archived from the original on 24 December 2023. Retrieved 22 April 2024.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6,[dead link] Up-to-date
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Manolis, Antonis (March 2024). "Premature ventricular complexes: Clinical presentation and diagnostic evaluation". UpToDate. Archived from the original on 26 October 2023. Retrieved 22 April 2024.
  8. 8.0 8.1 Manolis, Antonis (March 2024). "Premature ventricular complexes: Treatment and prognosis". UpToDate. Archived from the original on 24 April 2024. Retrieved 22 April 2024.
  9. 9.00 9.01 9.02 9.03 9.04 9.05 9.06 9.07 9.08 9.09 9.10 9.11 9.12 9.13 Keany, James E.; Desai, Aseem D. (13 January 2017). Schraga, Erik D. (ed.). "Premature Ventricular Contraction". eMedicine. Archived from the original on 30 March 2017. Retrieved 5 April 2017.
  10. MedlinePlus Encyclopedia: Ectopic heartbeat
  11. 11.0 11.1 Kulick, David Lee (23 March 2016). Shiel, William C., Jr. (ed.). "Premature Ventricular Contractions (PVCs, PVC): What causes premature ventricular contractions?". MedicineNet. Archived from the original on 2017-03-01. Retrieved 2017-02-21.
  12. Emilsson, Kent (3 June 2008), "Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report", Journal of Medical Case Reports, 2: 192, doi:10.1186/1752-1947-2-192, PMC 2427047, PMID 18522736 open access
  13. Mayo Clinic Staff (26 April 2014). "Premature ventricular contractions (PVCs) Causes". Mayo Clinic. Mayo Foundation for Medical Education and Research. Archived from the original on 24 March 2014. Retrieved 24 March 2014.
  14. Lebowitz, Michael. "Methylxanthine Toxcity Syndrome". Body Restoration: An Owner's Manual. Archived from the original on 1 February 2016. Retrieved 25 January 2016.
  15. "Premature ventricular contractions (PVCs) Risk factors - Mayo Clinic". Mayo Clinic. Archived from the original on 2017-03-22. Retrieved 2017-03-01.
  16. 16.0 16.1 Guyton, Arthur C.; Hall, John E. (2006). Textbook of medical physiology (11th ed.). Philadelphia: Elsevier Saunders. p. 151. ISBN 0-7216-0240-1.
  17. Birnie, David H.; Sauer, William H.; Bogun, Frank; Cooper, Joshua M.; Culver, Daniel A.; Duvernoy, Claire S.; Judson, Marc A.; Kron, Jordana; Mehta, Davendra; Nielsen, Jens Cosedis; Patel, Amit R.; Ohe, Tohru; Raatikainen, Pekka; Soejima, Kyoko (July 2014), "HRS Expert Consensus Statement on the Diagnosis and Management of Arrhythmias Associated With Cardiac Sarcoidosis", Heart Rhythm, 11 (7): 1304–23, doi:10.1016/j.hrthm.2014.03.043, PMID 24819193
  18. 18.0 18.1 Nelson & Cox 2008, p. 424
  19. Levy & Pappano 2007, p. 62
  20. Levy & Pappano 2007, p. 24
  21. Nelson & Cox 2008, p. 430
  22. Levy & Pappano 2007, pp. 49–50
  23. 23.0 23.1 Haist, Steven A.; Gomella, Leonard G. (2004), "19 Basic ECG Reading: Ventricular Arrhythmias", Clinician's pocket reference, Lange Clinical Science Series (10th ed.), New York: McGraw-Hill, p. 390, ISBN 0-07-140255-1, OCLC 53929979
  24. "Premature ventricular contractions (PVCs) Treatments and drugs - Mayo Clinic". Mayo Clinic. Archived from the original on 2017-04-15. Retrieved 2017-04-20.
  25. 25.0 25.1 25.2 25.3 25.4 25.5 G André Ng (2006). "Treating patients with ventricular ectopic beats". Heart. 92 (11): 1707–12. doi:10.1136/hrt.2005.067843. PMC 1861260. PMID 17041126.
  26. Anderson, JL; Platia, EV; Hallstrom, A; Henthorn, RW; Buckingham, TA; Carlson, MD; Carson, PE (December 1994). "Interaction of baseline characteristics with the hazard of encainide, flecainide, and moricizine therapy in patients with myocardial infarction. A possible explanation for increased mortality in the Cardiac Arrhythmia Suppression Trial (CAST)". Circulation. 90 (6): 2843–52. doi:10.1161/01.cir.90.6.2843. PMID 7994829.
  27. 27.0 27.1 27.2 Belhassen B (2005). "Radiofrequency ablation of "benign" right ventricular outflow tract extrasystoles: a therapy that has found its disease?". J. Am. Coll. Cardiol. 45 (8): 1266–8. doi:10.1016/j.jacc.2005.01.028. PMID 15837260.
  28. "Premature ventricular contractions (PVCs) Complications - Mayo Clinic". Mayo Clinic. Archived from the original on 2017-04-20. Retrieved 2017-04-19.
  29. Ataklte, F; Erqou, S; Laukkanen, J; Kaptoge, S (15 October 2013). "Meta-analysis of ventricular premature complexes and their relation to cardiac mortality in general populations". The American Journal of Cardiology. 112 (8): 1263–70. doi:10.1016/j.amjcard.2013.05.065. PMID 23927786.
  30. Niwano, S; Wakisaka, Y; Niwano, H; Fukaya, H; Kurokawa, S; Kiryu, M; Hatakeyama, Y; Izumi, T (August 2009). "Prognostic significance of frequent premature ventricular contractions originating from the ventricular outflow tract in patients with normal left ventricular function". Heart. 95 (15): 1230–7. doi:10.1136/hrt.2008.159558. PMID 19429571.
  31. Kennedy, HL; Whitlock, JA; Sprague, MK; Kennedy, LJ; Buckingham, TA; Goldberg, RJ (24 January 1985). "Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy". The New England Journal of Medicine. 312 (4): 193–7. doi:10.1056/nejm198501243120401. PMID 2578212.
  32. Bikkina, M; Larson, MG; Levy, D (15 December 1992). "Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study". Annals of Internal Medicine. 117 (12): 990–6. doi:10.7326/0003-4819-117-12-990. PMID 1280018.
  33. Moss, AJ (15 December 1992). "Asymptomatic ventricular arrhythmias in healthy persons: smoke or smoke screen?". Annals of Internal Medicine. 117 (12): 1053–4. doi:10.7326/0003-4819-117-12-1053. PMID 1443975.
  34. 34.0 34.1 34.2 Worthington, JM; Gattellari, M; Leung, DY (April 2010). "'Where there's smoke ...': are premature ventricular complexes a new risk factor for stroke?". Stroke: A Journal of Cerebral Circulation. 41 (4): 572–3. doi:10.1161/strokeaha.109.574426. PMID 20167909.
  35. Agarwal, SK; Simpson RJ, Jr; Rautaharju, P; Alonso, A; Shahar, E; Massing, M; Saba, S; Heiss, G (1 January 2012). "Relation of ventricular premature complexes to heart failure (from the Atherosclerosis Risk In Communities [ARIC] Study)". The American Journal of Cardiology. 109 (1): 105–9. doi:10.1016/j.amjcard.2011.08.009. PMC 3242884. PMID 21945138.
  36. Massing, MW; Simpson RJ, Jr; Rautaharju, PM; Schreiner, PJ; Crow, R; Heiss, G (15 December 2006). "Usefulness of ventricular premature complexes to predict coronary heart disease events and mortality (from the Atherosclerosis Risk In Communities cohort)". The American Journal of Cardiology. 98 (12): 1609–12. doi:10.1016/j.amjcard.2006.06.061. PMID 17145219.
  37. Watanabe, H; Tanabe, N; Makiyama, Y; Chopra, SS; Okura, Y; Suzuki, H; Matsui, K; Watanabe, T; Kurashina, Y; Aizawa, Y (October 2006). "ST-segment abnormalities and premature complexes are predictors of new-onset atrial fibrillation: the Niigata preventive medicine study". American Heart Journal. 152 (4): 731–5. doi:10.1016/j.ahj.2006.05.032. PMID 16996849.
  38. Shiraishi H, Ishibashi K, Urao N, Tsukamoto M, Hyogo M, Keira N, Hirasaki S, Shirayama T, Nakagawa M (2002). "A case of cardiomyopathy induced by premature ventricular complexes". Circ. J. 66 (11): 1065–7. doi:10.1253/circj.66.1065. PMID 12419942.
  39. Pooja Hingorani et. al: Arrhythmias Seen in Baseline 24‐Hour Holter ECG Recordings in Healthy Normal Volunteers During Phase 1 Clinical Trials (2015); 56 (7), p. 885–893; doi:10.1002/jcph.679
  40. Cha, Yong-Mei; Lee, Glenn K.; Klarich, Kyle W.; Grogan, Martha (February 2012). "Premature Ventricular Contraction-Induced Cardiomyopathy". Circulation: Arrhythmia and Electrophysiology. 5 (1): 229–236. doi:10.1161/CIRCEP.111.963348. ISSN 1941-3149. PMID 22334430.
  41. Kulick, David Lee (23 March 2016). Shiel, William C., Jr. (ed.). "Premature Ventricular Contractions (PVCs, PVC): What happens during a premature ventricular contraction?". MedicineNet. Archived from the original on 2017-03-14. Retrieved 2017-02-21.
  42. Kostis, J.B.; McCrone, K.; Moreyra, A.E.; Gotzoyannis, S.; Aglitz, N.M.; Natarajan, N.; Kuo, P.T. (June 1981). "Premature ventricular complexes in the absence of identifiable heart disease". Circulation. 63 (6): 1351–1356. doi:10.1161/01.CIR.63.6.1351. PMID 7226480.
  43. Hiss, Roland G.; Lamb, Lawrence E. (June 1962). "Electrocardiographic Findings in 122,043 Individuals". Circulation. 25 (6): 947–961. doi:10.1161/01.CIR.25.6.947. PMID 13907778.

Further reading

External links

External resources