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Wellens Syndrome Workup

  • Author: Benjamin B Mattingly, MD; Chief Editor: Erik D Schraga, MD  more...
 
Updated: Jan 02, 2015
 

Laboratory Studies

The following laboratory studies may be indicated as adjunctive tests in patients with suspected coronary artery disease (CAD), acute coronary syndrome (ACS), and Wellens syndrome:

  • Complete blood count (CBC) - To ensure that anemia is not precipitating the angina, red blood cell (RBC) transfusions may be necessary
  • Basic metabolic profile - This includes electrolyte, blood urea nitrogen (BUN), creatinine, and glucose levels
  • Typing and screening - These are indicated if immediate cardiac catheterization is planned
  • D-dimer, international normalized ratio (INR), partial thromboplastin time (PTT) - These are ordered only as medically necessary
  • Cardiac biomarkers - In Wellens syndrome, cardiac biomarkers can be falsely reassuring, in that they are typically normal or only minimally elevated; only 12% of patients with this syndrome have elevated cardiac biomarker levels, and these are always less than twice the upper limit of normal, in the absence of myocardial infarction (MI) [5]
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Plain Radiography and CT of Chest

Chest radiography should be performed to look for side effects of ischemia, such as pulmonary edema. In addition, this test should be performed to help exclude other possible causes of chest pain, such as thoracic aneurysm or dissection, pneumonia, and rib fracture.

Computed tomography (CT) of the chest is performed only as indicated to help rule out other causes of chest pain, such as aortic dissection or pulmonary embolus. The value of CT angiography of the chest in the evaluation of chest pain, CAD, and ACS is currently being investigated.

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Electrocardiography

ECG should be performed on any patient with a complaint of chest pain if noncardiac causes cannot be diagnosed by other means, including physical examination. It may be helpful to perform ECG both while the pain is present and after the pain has resolved. The ECG changes seen in Wellens syndrome typically are manifested when the patient is pain-free but usually occur in the context of recent anginal chest pain.

In Wellens syndrome, the ECG pattern shows significant involvement of the T wave, with minimal ST-segment alteration. The ST segments themselves are usually isoelectric, but if they are abnormal, there will be less than 1 mm of elevation, with a high takeoff of the ST segment from the QRS complex. The characteristic ECG changes of this syndrome occur in the T-wave and occur in 2 forms.

The more common of the 2 forms, which occurs 76% of the time, is deep inversion of the T-wave segment in the precordial leads (see the images below).[6] The ST segment will be straight or concave and will pass into a deep negative T wave at an angle of 60°-90°. The T wave is symmetric. In Wellens syndrome, these changes generally occur in leads V1 -V4 but occasionally may also involve V5 and V6. V1 is involved in approximately 66% of patients, and V4 is involved nearly 75% of the time.[7]

This ECG represents a patient who came in to the e 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 r 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.

The less common of the 2 forms of Wellens syndrome, which occurs in 24% of patients, consists of biphasic T waves (see the images below), most commonly in leads V2 and V3 but also, on occasion, in leads V1 through V5 or even V6.[5]

A 57-year-old with 4/10 pressurelike chest pain. I 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 present 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.

The characteristic pattern classically presents only during chest pain–free periods. Noticing this pattern is crucial because it is a sign of LAD disease. This association underscores the importance of serial ECGs and a pain-free ECG on patients with unstable angina. Because the LAD supplies the anterior myocardium, failure to recognize this pattern can result in anterior wall myocardial infarction (MI), significant left ventricular dysfunction, or death.

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Other Tests

Angiography has demonstrated that 100% of patients with Wellens syndrome will have 50% or greater stenosis of the proximal LAD.[5] More specifically, 83% will have the lesion proximal to the second septal perforator.[7]

Stress testing is generally not indicated in patients with this ECG presentation, because it places them at risk for acute anterior wall MI. Ideally, therefore, these patients would bypass stress testing and undergo urgent angiography to determine the extent of disease and potentially provide information about the need for percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), or medical management.[6, 8] If provocative testing is determined to be necessary, it should be done cautiously and only in close conjunction with a cardiologist.[6, 9]

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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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Kevin M Gentile, DO Attending Physician, Department of Emergency Medicine, MEP at Bristol Hospital

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, Massachusetts Medical Society, Emergency Medicine Residents' Association

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.

Acknowledgements

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. 1982 Apr. 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. 2008 Apr 2. [Medline].

  3. Patel K, Alattar F, Koneru J, Shamoon F. ST-Elevation Myocardial Infarction after Pharmacologic Persantine Stress Test in a Patient with Wellens' Syndrome. Case Rep Emerg Med. 2014. 2014:530451. [Medline]. [Full Text].

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

  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. 1989 Mar. 117(3):657-65. [Medline].

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

  7. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med. 2002 Nov. 20(7):638-43. [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. Narasimhan S, Robinson GM. Wellens syndrome: a combined variant. J Postgrad Med. 2004 Jan-Mar. 50(1):73-4. [Medline].

  10. Sowers N. Harbinger of infarction: Wellens syndrome electrocardiographic abnormalities in the emergency department. Can Fam Physician. 2013 Apr. 59(4):365-6. [Medline]. [Full Text].

  11. Balasubramanian K, Balasubramanian R, Subramanian A. A dangerous twist of the 'T' wave: A case of Wellens' Syndrome. Australas Med J. 2013. 6(3):122-5. [Medline]. [Full Text].

  12. Singh B, Singh Y, Singla V, Nanjappa MC. Wellens' syndrome: a classical electrocardiographic sign of impending myocardial infarction. BMJ Case Rep. 2013 Feb 18. 2013:[Medline].

  13. Movahed MR. Wellens' syndrome or inverted U-waves?. Clin Cardiol. 2008 Mar. 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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