Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Premature Ventricular Contraction Workup

  • Author: James E Keany, MD, FACEP; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Dec 07, 2015
 

Laboratory Studies

In young, healthy patients without concerning concommitant symptoms, laboratory tests are not typically necessary. The following diagnostic studies may be necessary based on the patient's history and underlying illness(es):

  • Obtain serum electrolyte levels, in particular potassium levels. Consider checking the magnesium level, especially in patients with low potassium levels.
  • In selected patients, a drug screen may be helpful.
  • For patients taking medication with known proarrhythmic effects (eg, digoxin, theophylline), drug levels may be useful.
Next

Other Tests

Electrocardiography (ECG)

ECG allows for characterization of the ventricular ectopy and determination of cause. In addition to the standard 12-lead ECG, a 2-minute rhythm strip may help in determining frequency of the ectopy and capture infrequent premature ventricular contractions (PVCs). Findings may include the following:

  • Left ventricular hypertrophy
  • Active cardiac ischemia (ST-segment depression or elevation and or T-wave inversion)
  • In patients with previous MI - Q waves or loss of R waves, bundle branch block
  • Electrolyte abnormalities (hyperacute T waves, QT prolongation)
  • Drug effects (QRS widening, QT prolongation)
  • On ECG, PVCs may be premature in relation to the next expected beat of the basic rhythm. The pause after the premature beat is usually a fully compensatory pause. The R-R interval surrounding the premature beat is equal to double the basic R-R interval, showing that the ectopic beat did not reset the sinus node.
  • PVCs may appear in a pattern of bigeminy, trigeminy, or quadrigeminy, which describe a pattern of PVCs occurring every other, every third, or every fourth beat, respectively.
  • PVCs with identical morphologies on a tracing are called monomorphic or unifocal. If the PVCs demonstrate 2 or more different morphologies, they are referred to as multiform, pleomorphic, or polymorphic.
    ECG shows frequent, unifocal PVCs with a fixed cou ECG shows frequent, unifocal PVCs with a fixed coupling interval between the ectopic beat and the previous beat. These PVCs result in a fully compensatory pause; the interval between the 2 sinus beats surrounding the PVC are exactly twice the normal R-R interval. This finding indicates that the sinus node continues to pace at its normal rhythm despite the PVC, which fails to reset the sinus node.
    On this ECG, the PVCs occur near the peak of the T On this ECG, the PVCs occur near the peak of the T wave of the preceding beat. These beats predispose the patient to ventricular tachycardia or fibrillation. This R-on-T pattern is often seen in patients with acute myocardial infarction or long Q-T intervals. In the latter case, the triggered arrhythmia would be torsade.

PVCs usually are described in terms of the Lown grading system for premature beats, as follows (the higher the grade, the more serious the ectopy):

  • Grade 0 = No premature beats
  • Grade 1 = Occasional (< 30/h)
  • Grade 2 = Frequent (>30/h)
  • Grade 3 = Multiform
  • Grade 4 = Repetitive (A = Couplets, B = Salvos of = or > 3)
  • Grade 5 = R-on-T pattern

Holter 24-hour monitoring

Holter 24-hour monitors are useful in quantifying and characterizing ventricular ectopy. Holters also have been used to determine treatment efficacy in patients with frequent or complex PVCs.

Suppression of ectopy on Holter monitoring is not always predictive of survival.

The most important role for Holter monitoring is risk stratification of patients with a recent MI or known left ventricular dysfunction.

More than 60% of healthy, middle-aged men have ventricular ectopy on Holter monitoring.

Signal-averaged ECG

Signal-averaged ECGs (SAECGs) may have a future role in identifying patients at risk for complex ventricular ectopy and nonsustained ventricular tachycardia (NSVT). SAECGs may have a role in identifying patients with complex ectopy who may benefit from electrophysiologic studies (EPS).

Echocardiography

Echocardiography is useful not only in evaluating the ejection fraction, which is important in determining the prognosis and also in identifying valvular disease or ventricular hypertrophy.

Previous
Next

Procedures

Exercise stress testing (EST) is best used complementary to Holter monitoring. In patients with complex ectopy, EST can unmask nonsustained ventricular tachycardia (NSVT) triggered by increased catecholamines or myocardial ischemia.

The role of electrophysiologic studies (EPS) in complex ventricular ectopy is an area of both intense research and debate. A joint American Heart Association (AHA)/American College of Cardiology (ACC) statement suggested the following:

  • Routine EPS are not indicated in low-risk patients after MI. Low risk refers to simple ectopy, good left ventricular function, and low congestive heart failure (CHF) class.
  • EPS are indicated in high-risk patients with complex ectopy.
  • EPS are thought to be beneficial in patients with sustained ventricular tachycardia more than 48 hours after myocardial infarction.
Previous
 
 
Contributor Information and Disclosures
Author

James E Keany, MD, FACEP Associate Medical Director, Emergency Services, Mission Hospital Regional Medical Center, Children's Hospital of Orange County at Mission

James E Keany, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, California Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Aseem D Desai, MD, FACC Cardiac Electrophysiologist, Mission Internal Medicine Group, Inc

Aseem D Desai, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Assaad J Sayah, MD, FACEP Chief, Department of Emergency Medicine; Senior Vice President, Primary and Emergency Care, Cambridge Health Alliance

Assaad J Sayah, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society, National Association of EMS Physicians

Disclosure: Nothing to disclose.

References
  1. Lee AK, Deyell MW. Premature ventricular contraction-induced cardiomyopathy. Curr Opin Cardiol. 2016 Jan. 31 (1):1-10. [Medline].

  2. Simpson RJ, Cascio WE, Schreiner PJ, et al. Prevalence of premature ventricular contractions in a population of African American and white men and women: the Atherosclerosis Risk in Communities (ARIC) study. Am Heart J. 2002 Mar. 143(3):535-40. [Medline].

  3. CAST Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989 Aug 10. 321(6):406-12. [Medline].

  4. Lee CH, Park KH, Nam JH, et al. Increased variability of the coupling interval of premature ventricular contractions as a Predictor of cardiac mortality in patients with left ventricular dysfunction. Circ J. 2015 Oct 23. 79 (11):2360-6. [Medline].

  5. Maruyama T, Fukata M. Increased coupling interval variability - mechanistic, diagnostic and prognostic Implication of premature ventricular contractions and underlying heart diseases. Circ J. 2015 Oct 23. 79 (11):2317-9. [Medline].

  6. Agarwal SK, Heiss G, Rautaharju PM, Shahar E, Massing MW, Simpson RJ Jr. Premature ventricular complexes and the risk of incident stroke: the Atherosclerosis Risk In Communities (ARIC) Study. Stroke. 2010 Apr. 41(4):588-93. [Medline].

  7. [Guideline] Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F, Calkins CH, Delacretaz E, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace. 2009 Jun. 11(6):771-817. [Medline]. [Full Text].

  8. Bala R, Marchlinski FE. Electrocardiographic recognition and ablation of outflow tract ventricular tachycardia. Heart Rhythm. 2007 Mar. 4(3):366-70. [Medline].

  9. Burkart F, Pfisterer M, Kiowski W, et al. Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS). J Am Coll Cardiol. 1990 Dec. 16(7):1711-8. [Medline].

  10. Cairns JA, Connolly SJ, Roberts R, Gent M. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Lancet. 1997 Mar 8. 349(9053):675-82. [Medline].

  11. Califf RM, McKinnis RA, Burks J, et al. Prognostic implications of ventricular arrhythmias during 24 hour ambulatory monitoring in patients undergoing cardiac catheterization for coronary artery disease. Am J Cardiol. 1982. 50:23-31. [Medline].

  12. Cha YM, Lee GK, Klarich KW, Grogan M. Premature ventricular contraction-induced cardiomyopathy: a treatable condition. Circ Arrhythm Electrophysiol. 2012 Feb 1. 5(1):229-36. [Medline].

  13. Del Gobbo LC, Song Y, Poirier P, Dewailly E, Elin RJ, Egeland GM. Low serum magnesium concentrations are associated with a high prevalence of premature ventricular complexes in obese adults with type 2 diabetes. Cardiovasc Diabetol. 2012 Mar 9. 11(1):23. [Medline].

  14. Hallstrom AP, Bigger JT Jr, Roden D, et al. Prognostic significance of ventricular premature depolarizations measured 1 year after myocardial infarction in patients with early postinfarction asymptomatic ventricular arrhythmia. J Am Coll Cardiol. 1992 Aug. 20(2):259-64. [Medline].

  15. Hammill SC, Trusty JM, Wood DL, et al. Influence of ventricular function and presence or absence of coronary artery disease on results of electrophysiologic testing for asymptomatic nonsustained ventricular tachycardia. Am J Cardiol. 1990 Mar 15. 65(11):722-8. [Medline].

  16. Hargarten K, Chapman PD, Stueven HA, et al. Prehospital prophylactic lidocaine does not favorably affect outcome in patients with chest pain. Ann Emerg Med. 1990 Nov. 19(11):1274-9. [Medline].

  17. Jouven X, Zureik M, Desnos M, et al. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med. 2000 Sep 21. 343(12):826-33. [Medline].

  18. Kennedy HL, Whitlock JA, Sprague MK, et al. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med. 1985 Jan 24. 312(4):193-7. [Medline].

  19. Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation. 1971 Jul. 44(1):130-42. [Medline].

  20. Maggioni AP, Zuanetti G, Franzosi MG, et al. Prevalence and prognostic significance of ventricular arrhythmias after acute myocardial infarction in the fibrinolytic era. GISSI-2 results. Circulation. 1993 Feb. 87(2):312-22. [Medline].

  21. Rehnqvist N, Olsson G, Erhardt L, Ekman AM. Metoprolol in acute myocardial infarction reduces ventricular arrhythmias both in the early stage and after the acute event. Int J Cardiol. 1987 Jun. 15(3):301-8. [Medline].

  22. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials. JAMA. 1993 Oct 6. 270(13):1589-95. [Medline].

  23. Yokokawa M, Kim HM, Good E, Chugh A, Pelosi F Jr, Alguire C, et al. Relation of symptoms and symptom duration to premature ventricular complex-induced cardiomyopathy. Heart Rhythm. 2012 Jan. 9(1):92-5. [Medline].

  24. Zamir M, Kimmerly DS, Shoemaker JK. Cardiac mechanoreceptor function implicated during premature ventricular contraction. Auton Neurosci. 2012 Apr 3. 167(1-2):50-5. [Medline].

  25. Zhong L, Lee YH, Huang XM, Asirvatham SJ, Shen WK, Friedman PA. Relative efficacy of catheter ablation vs antiarrhythmic drugs in treating premature ventricular contractions: A single-center retrospective study. Heart Rhythm. 2013 Oct 22. [Medline].

  26. Bradfield JS, Homsi M, Shivkumar K, Miller JM. Coupling interval variability differentiates ventricular ectopic complexes arising in the aortic sinus of valsalva and great cardiac vein from other sources: mechanistic and arrhythmic risk implications. J Am Coll Cardiol. 2014 May 27. 63 (20):2151-8. [Medline].

  27. Trevisi N, Silberbauer J, Radinovic A, et al. New diagnostic criteria for identifying left-sided ventricular ectopy using non-contact mapping and virtual unipolar electrogram analysis. Europace. 2015 Jan. 17 (1):108-16. [Medline].

 
Previous
Next
 
ECG shows frequent, unifocal PVCs with a fixed coupling interval between the ectopic beat and the previous beat. These PVCs result in a fully compensatory pause; the interval between the 2 sinus beats surrounding the PVC are exactly twice the normal R-R interval. This finding indicates that the sinus node continues to pace at its normal rhythm despite the PVC, which fails to reset the sinus node.
On this ECG, the PVCs occur near the peak of the T wave of the preceding beat. These beats predispose the patient to ventricular tachycardia or fibrillation. This R-on-T pattern is often seen in patients with acute myocardial infarction or long Q-T intervals. In the latter case, the triggered arrhythmia would be torsade.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.