Chief Complaint: Chest Pain, Resolved

Chief Complaint:  Chest pain, resolved.

History of Present Illness: A 56 year-old M with h/o HTN and HLD, presents after an episode of chest pain. One hour PTA he had gradual onset of retrosternal chest pressure which was exertional, non-radiating and non-pleuritic. The pain lasted 20-30 minutes and self-resolved. The episode was associated with SOB and lightheadedness. No previous h/o similar CP. Pt has no known cardiac ischemic disease, and has never had a stress test or echo. Denies recent fever/cough, denies LE swelling, denies recent travel/immobilization. Patient is now asymptomatic.

Medical Hx: as above
Medications: simvastatin, HCTZ
Allergies: NKDA
Surgical Hx: denies
Social Hx: +tob, occasional ETOH, denies drug use

Physical Exam:
VS: BP 138/86, P 84, RR 14, O2 97% on RA, T 97.8
HEENT: NCAT, oropharynx WNL, PERRLA
Neck: supple, no JVD
CV: S1S2 RRR, no m/r/g, pulses symmetric, extremities well perfused
Lungs: CTAB, no wheezing/rales/rhonchi
Abd: obese, soft, non-tender
Extr: no edema/tenderness
Neuro: CN II-XII intact, motor 5/5 throughout, SILT throughout

Labs:
Troponin < 0.12
CBC: WBC 7, hgb 12.4, hct 36, plt 312
BMP: Na 138, K 4.2, CO2 25, Cl 111, BUN 11, Cr 0.9

An EKG is obtained in triage:

cp1

Questions:

  1. What does the EKG show, and why is it significant?
  2. What is your initial management in the ED?
  3. What is the proper disposition for this patient? Is there any test that should be avoided in this patient?

Answers:

  1. What does the EKG show, and why is it significant?

The EKG shows deep symmetric T-wave inversions in V1-V2, and a more shallow (and slightly biphasic appearing) T-wave inversion in V3. These findings are indicative of Wellens’ syndrome. Wellens’ syndrome is a pattern of inverted or biphasic T-waves in V2-V3. Deep symmetric T-wave inversions are seen in Wellens’ Type A, and biphasic T-waves (with the initial deflection positive and the terminal deflection negative) are seen in Wellens’ Type B:

cp2
cp3

(images courtesy of http://lifeinthefastlane.com/ecg-library/wellens-syndrome/)

Occasionally, T-wave changes are also seen in the other precordial leads. Classically, patients present with a history suggestive of ischemic chest pain, and are often pain-free by the time they arrive at the ED and the EKG is performed. The characteristic EKG pattern develops when the patient is not experiencing chest pain. During episodes of chest pain, the T-wave abnormalities often normalize or develop into ST elevation. Wellens syndrome is significant because it is highly specific for critical stenosis of the proximal left anterior descending artery, and these patients are at high risk for extensive anterior wall MI in the following 2-3 weeks. If left untreated, 75% will progress to MI. Troponin is usually negative or only mildly elevated.

EKG diagnostic criteria for Wellens (Mattu, 2002):

  • Symmetric and deeply inverted T-waves in leads V2 and V3 (occasionally in leads V1, V4, V5, and V6) OR biphasic T-waves in leads V2 and V3
  • Isoelectric or minimally elevated (< 1mm) ST segment
  • No precordial Q waves
  • History of angina
  • Pattern present in pain-free state
  • Normal or slightly elevated cardiac enzymes

Also important to note are other pathologies which could mimic Wellens’ pattern on EKG. These include LVH, LBBB, LV aneurysm, PE, electrolyte abnormalities, digitalis effect, and acute CNS insults. The clinician should be able to distinguish these from Wellens’ syndrome based on history, physical, and labs.

  1. What is your initial management in the ED?

For the most part, initial ED management is the same for Wellens’ as for other chest pain patients who are being admitted for ACS. As with any potentially critically ill patient, begin with the ABC’s, IV, monitor, supplemental O2 as needed. Patients should receive troponins, serial EKG’s (especially since EKG pattern will change if the patient develops chest pain while in the ED), pain control/nitroglycerin as needed, Aspirin, and consideration of Heparin.

What distinguishes ED management of patients with Wellens’ syndrome is that cardiology should be consulted, since these patients require urgent cardiac catheterization.

  1. What is the proper disposition for this patient? Is there any test that should be avoided in this patient?

The patient should receive a STAT cardiology consult from the ER, because he requires urgent revascularization. He should be admitted to a monitored setting. Patients with Wellens’ syndrome should not undergo stress testing, since increasing demand in a patient with critical LAD stenosis can precipitate an acute MI.

For a great video reviewing Wellens, please see Dr. Amal Mattu’s post on Emergency ECG Videos of the Week: http://ekgumem.tumblr.com/tagged/Wellens%20Syndrome

References

  • Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
  • Mead N, O’Keefe K. Wellens’ syndrome: an ominous EKG pattern. J Emerg Truama Shock. 2009 Sep-Dec; 2(3): 206-208.
  • Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002 Nov;20(7):638-43.
  • Wellens’ Syndome. http://lifeinthefastlane.com/ecg-library/wellens-syndrome/
Edited by Adaira Landry

4 thoughts on “Chief Complaint: Chest Pain, Resolved”

  1. This looks like a mimic to me, not the real Wellens’.

    In fact, the upper right example of “Wellens Type A” that you give here looks more like the T-waves of PE, not Wellens.

    The T-wave progression and morphology does not look right.

    You also are propagating an erroneous classification of “types”.

    Go to Wellens original papers: There is “Pattern A” which is biphasic, and “Pattern B” which is deep symmetric.

    What was the outcome? Where are subsequent ECGs? Only evolution of T-wave inversion, along with angiography (Both) can ascertain that it is truly Wellens.

    I don’t believe it is.

    Steve Smith of Dr. Smith’s ECG blog

  2. This looks like a mimic to me, not the real Wellens’.

    In fact, the upper right example of “Wellens Type A” that you give here looks more like the T-waves of PE, not Wellens.

    The T-wave progression and morphology does not look right.

    You also are propagating an erroneous classification of “types”.

    Go to Wellens original papers: There is “Pattern A” which is biphasic, and “Pattern B” which is deep symmetric.

    What was the outcome? Where are subsequent ECGs? Only evolution of T-wave inversion, along with angiography (Both) can ascertain that it is truly Wellens.

    I don’t believe it is.

    Steve Smith of Dr. Smith’s ECG blog

  3. Agree with comments by Dr. Smith. Although 2 types of Wellens ST-T wave changes are commonly described — I have been far less impressed by the presence of deep symmetric T wave inversion (sometimes with ST coving) — which is the pattern we see in your case study 12-lead. The reason I have reservations about deep symmetric T wave inversion — is that this is NOT a specific ECG indicator for a tight proximal LAD stenosis, since other entities (ie, acute pulmonary embolism, generalized ischemia that may be acute or chronic, cardiomyopathy, even severe CNS pathology …) may all produce the same pattern. In contrast — when the history is right in a patient without prior infarction, cardiomyopathy, LV aneurysm — the new finding of biphasic T waves with very steep initial downslope of the T wave in V2,V3 conveys with high accuracy likely critical proximal LAD stenosis (which is what we are interested in detecting).

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