Wellens Syndrome 

  • Author: Benjamin B Mattingly, MD; Chief Editor: David FM Brown, MD   more...
 
Updated: May 14, 2012
 

Background

Wellens syndrome was first described in the early 1980s by de Zwaan, Wellens, and colleagues, who identified a subset of patients with unstable angina who had specific precordial T-wave changes and subsequently developed a large anterior wall myocardial infarction (MI).[1] Wellens syndrome refers to these specific electrocardiographic (ECG) abnormalities in the precordial T-wave segment, which are associated with critical stenosis of the proximal left anterior descending (LAD) coronary artery.

Wellens syndrome is also referred to as LAD coronary T-wave syndrome.[2] Syndrome criteria include the following:

  • Characteristic T-wave changes
  • History of anginal chest pain
  • Normal or minimally elevated cardiac enzyme levels
  • ECG without Q waves, without significant ST-segment elevation, and with normal precordial R-wave progression

Recognition of this ECG abnormality is of paramount importance because this syndrome represents a preinfarction stage of coronary artery disease (CAD) that often progresses to a devastating anterior wall MI.

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Pathophysiology

Wellens syndrome represents critical stenosis of the LAD artery. The LAD arises from the left coronary artery and travels in the interventricular groove along the anterior portion of the heart to the apex. This groove is situated between the right and left ventricles of the heart. The LAD gives rise to 2 main branches, the diagonals and the septal perforators.[6]

A lesion in the LAD can have severe consequences, as suggested by the common nickname given to this vessel: “widow maker.” The LAD supplies the anterior wall of the heart, including both ventricles, as well as the septum. An occlusion in this vessel can result in serious ventricular dysfunction, thus placing the patient at serious risk for congestive heart failure (CHF) and death.

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Etiology

Wellens syndrome is a preinfarction stage of CAD. Thus, the causes of Wellens syndrome are similar to the conditions that cause CAD, including the following:

  • Atherosclerotic plaque
  • Coronary artery vasospasm (cocaine is one possible cause)
  • Increased cardiac demand
  • Generalized hypoxia

Risk factors for Wellens syndrome include the following:

  • Smoking history
  • Diabetes mellitus
  • Hypertension
  • Increased age
  • Hypercholesterolemia
  • Hyperlipidemia
  • Metabolic syndrome
  • Strong family history of heart disease
  • Occupational stress
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Epidemiology and Prognosis

The characteristic ECG pattern of Wellens syndrome is relatively common in patients who have symptoms consistent with unstable angina. Of patients admitted with unstable angina, this ECG pattern is present in 14-18%.[5, 1]

Wellens syndrome represents critical LAD disease; accordingly, its natural progression leads to anterior wall MI. This progression is so likely that medical management alone is not enough to stop the natural process. Evolution to an anterior wall MI is rapid, with a mean time of 8.5 days from the onset of Wellens syndrome to infarction.[1]

If anterior wall MI occurs, there is the potential for substantial morbidity or mortality. Thus, it is of utmost importance to recognize this pattern early.

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Contributor Information and Disclosures
Author

Benjamin B Mattingly, MD  Assistant Professor, Department of Emergency Medicine, Tufts University School of Medicine, Baystate Medical Center

Benjamin B Mattingly, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin M Gentile, DO  Staff Physician, Department of Emergency Medicine, Tufts University School of Medicine, Baystate Medical Center

Kevin M Gentile, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Osteopathic Association, Emergency Medicine Residents Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Edward Bessman, MD Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

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

Disclosure: Medscape Salary Employment

References
  1. de Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. Apr 1982;103(4 Pt 2):730-6. [Medline].

  2. Nisbet BC, Zlupko G. Repeat Wellens' Syndrome: Case Report of Critical Proximal Left Anterior Descending Artery Restenosis. J Emerg Med. Apr 2 2008;[Medline].

  3. Tandy TK, Bottomy DP, Lewis JG. Wellens' syndrome. Ann Emerg Med. Mar 1999;33(3):347-51. [Medline].

  4. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med. Nov 2002;20(7):638-43. [Medline].

  5. de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J. Mar 1989;117(3):657-65. [Medline].

  6. Moore KL, Dalley AF. Thorax. In: Clinically Oriented Anatomy. 4th ed. Baltimore, Maryland: Lippincott Williams & Wilkins; 1999:135.

  7. Narasimhan S, Robinson GM. Wellens syndrome: a combined variant. J Postgrad Med. Jan-Mar 2004;50(1):73-4. [Medline].

  8. Tatli E, Aktoz M, Buyuklu M, Altun A. Wellens' syndrome: the electrocardiographic finding that is seen as unimportant. Cardiol J. 2009;16(1):73-5. [Medline].

  9. Movahed MR. Wellens' syndrome or inverted U-waves?. Clin Cardiol. Mar 2008;31(3):133-4. [Medline].

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This ECG represents a patient who came in to the emergency department with 8/10 chest pain. The patient had old right bundle-branch block (RBBB) and left ventricular hypertrophy (LVH), and this compared similarly to his previous ECGs.
Classic Wellens syndrome T-wave changes. ECG was repeated on a patient who came in to the emergency department with 8/10 chest pain after becoming pain free secondary to medications. Notice the deep T waves in V3-V5 and slight biphasic T wave in V6 in this chest pain– free ECG. The patient had negative cardiac enzyme levels and later had a stent placed in the proximal left anterior descending (LAD) artery.
A 57-year-old with 4/10 pressurelike chest pain. Improvement with treatment by EMS. The patient had this ECG on arrival. Notice perhaps the beginning of a small biphasic T wave in V2.
Pain-free ECG of a 57-year-old patient who presented with 4/10 pressurelike chest pain. Notice after the patient was treated with medications and pain subsided, the ECG shows T-wave inversion in V2 and biphasic T waves in V3-V5. This more closely resembles the less common presentation of Wellens syndrome with a biphasic T-wave pattern. This patient had a cardiac catheterization that showed a subtotal occlusion of the proximal left anterior descending (LAD) artery, which was stented, and the patient did well.
 
 
 
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