Blog post based on an Evidence Based Medicine (EBM) discussion, January 20th, 2016.
Zwaan, C de, F W Bär, and H J Wellens. 1982. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. American heart journal
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The Case:
Forty-nine year old M, no significant past medical history presents with chest pain that has since resolved. Started 3 hours ago (7pm) after refereeing a soccer game. Two episodes lasting maybe 15 minutes each. Pressure-like (places a closed fist over his chest when describing the discomfort), with questionable diaphoresis (after all, he had been running around), it does not radiate. No N/V or SOB. Prior to the game he had 3 cups of coffee and a large caffeinated ‘Monster’ energy drink, and attributes his pain to the energy drink. Is active and has never experienced this pain in the past. No cough or fever, no violent retching, no long car/plane travel or leg swelling, no trauma during the game he refereed.
Medications: none. Past Medical History: none. Past Surgical History: none. Social history: smoked cigarettes for a couple years as a teenager, but quit >25 years ago, and denies toxic habits including cocaine.
EXAM:
Vitals: T. 98.0, BP 129/98, HR 76, RR 18, O2 97% on room air
In no distress. Chatting with the nurse about all the coffee and Monster energy drink binged on. Skin warm, non diaphoretic.
No jugular venous distension
Heart rate regular, no murmurs, no POCUS performed
Lungs are clear, and he’s breathing comfortaby
No lower extremity edema, unilateral or otherwise
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10:30 pm (initial ECG)
04:24 (2nd ECG, 6 hours later), pain free. Scheduled as part of his rule out MI workup. He had been admitted, but was still in the ED.
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Echo with Anterior wall motion abnormalities
Plan: Heparin gtt, Plavix, cath lab.
Cath lab: Large caliber, critical 95% mid LAD lesion, 2 drug eluting stents placed.
**Serial Trops negative
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—-Zwann, Bar, Wellens et. al. American Hearth Journal 1982.
POPULATION: Non-randomized cohort of 145 patients in the Netherlands consecutively admitted because of impending myocadial infarction; defined as crescendo angina of recent onset, sudden worsening of recent angina, or crescendo post infarction angina developing after an initial asymptomatic period.
EXCLUSION: Patients with complete right bundle branch block, incomplete left bundle branch block, criteria for probable or definite left or right ventricular hypertrophy.
26/145 patients (18%) had unstable angina and the below ECGs.
**13/26 had these ECG findings on admission, the other 13 within 24 hours of admit.
Of those 26 patients with the above ECGs: 8 of first 9 suffered a massive anterior wall MI (prior to the realization of significance of ECG findings).
Uh oh!
In response, 10 of the next 17 were taken to the cath lab (of the 7 who were not; 2 were deemed too old to tolerate the procedure and 5 refused), plus the 1 patient from the first 9 who hadn’t had an MI. Eleven total. Take note of the column on the right, 10 patients had a critical Left Anterior Descending (LAD) stenosis, and 1 had a prolapsed mitral valve.
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This piqued interest and in a follow-up prospective study in 1989 with 1260 unstable angina patients, 180 (14%) again had this unique ECG pattern. This time, all 180 were urgently taken to the cath lab. Every single one had a greater than 50% stenosis of the proximal LAD (mean stenosis of 85%).
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T-Wave Abnormalities consistent with Wellens’ Syndrome in V2-3 (may extend to V1-6)
Type A = Biphasic, with initial positivity & terminal negativity (24% of cases)
Type B = Deeply and symmetrically inverted (76% of cases)
Plus:
- Recent history of angina (but Wellens’ ECG pattern is almost always present in pain-free state)
- Normal (or minimal elevation of) serum cardiac markers
- Isoelectric or minimally-elevated ST segment (< 1mm)
- No precordial Q waves
- Preserved precordial R wave progression
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Take home points:
It’s all the rage, and for good reason. The HEART score, however, often will not pick up unstable angina. In this case, the score was 2 or 3. One point for age, and 1 or 2 points depending on whether you deem his story moderately or highly suspicious. His initial ECG and troponin were normal.
There are many potential anchoring bias traps. Who wouldn’t rather attribute their pain to that energy drink or chunk of chocolate they ate as the root or what ails them? The left anterior descending (LAD) artery, however, is the ‘Widowmaker’ for good reason. We can’t miss this ECG. Just to make the waters more treacherous, however, is the notion that half the cohort in the original study (and the patient in this case), didn’t manifest a Wellens’ pattern until after they were admitted. A good story, and perhaps point of care ultrasound (POCUS) is all that you may have to go on in the ED; cardiac markers and ECG can, and often will be normal.
This is not a rare entity; 18% and 14% or unstable angina patients in the original and follow up study respectively, had Wellens’ syndrome.
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References:
Zwaan, C de, F W Bär, and H J Wellens. 1982. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. American heart journal, no. 4 Pt 2.
Zwaan, C de, F W Bär, J H Janssen, E C Cheriex, W R Dassen, P Brugada, O C Penn, and H J Wellens. 1989. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. American heart journal, no. 3.
FOAM Sources:
Dr. Smiths ECG Blog: Wellens’ Syndrome
Life In the Fast Lane: http://lifeinthefastlane.com/ecg-library/wellens-syndrome/
Cardiac Ultrasound: http://www.ultrasoundpodcast.com/tag/cardiac/