Rhythm Nation: November 2017 Answer

Not many takers for November’s post, but a solid A+ to Dr. Birnbaum, one of our own 4th year clinical monsters. This month we have a case of Wellens’ Syndrome. Below you will find the answers to the questions in our last post as well as the hospital course of our patient. Luckily for him, the correct diagnosis was made, he was treated quickly, and he got to leave the hospital with one newly cleaned coronary.


1) What ECG finding can be identified, and what is its pathophysiologic basis?

This ECG is significant for Wellens’ Sign. What is Wellens’ Sign, you ask? Well, according to the title of the eponymous Dr. Hein J.J. Wellens’ original 1982 article, it is a “characteristic electrocardiographic pattern indicating a critical stenosis high in the left anterior descending coronary artery…”.1 Wellens’ group followed with a larger 1989 study showing that 87% of patients with Wellens’ Sign demonstrated angiographic evidence of an LAD lesion, with an average estimated stenosis of 85%.2 The original article showed that 12 of 16 patients who were not operated on developed significant anterior infarction. Subsequent research has demonstrated that significant complications occur in up to 75% of patients within one week of identifying Wellens’ Syndrome.3,4


The electrocardiographic finding itself is split into two different classifications: Type A Wellens’ is a biphasic T wave in leads V2-V4, while a Type B Wellens’ is defined by a deeply inverted symmetric T wave in the same anterior leads. It is widely reported that Type A is seen in about 25% of cases, while Type B is seen in the remaining cases. These are demonstrated in Wellens’ original paper below:


de Zwaan C, Bär 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.


The diagnostic criteria for Wellens’ Syndrome was also expanded on by Rhinehardt et al (2002). Herein, they concluded that “criteria include T-wave changes plus a history of anginal chest pain without serum marker abnormalities; patients lack Q waves and significant ST-segment elevation; such patients show normal precordial R-wave progression.”5 Together these criteria help to separate Wellens’ Syndrome from true STEMI and nonspecific ST-T wave changes without recent chest pain. Here is our patient’s ECG for comparison:


Type A Wellens’ in V2-V3, no significant Qs or ST elevations, normal R wave progression; negative troponins (Trop I: 0.12, Ref: <=0.15).


There remains some debate about the exact origin of the repolarization abnormality. The T wave changes may represent reversible ischemia resulting from a critical stenosis during exertion, or due to coronary vasospasm.6,7 An intriguing alternative theory states that the ECG finding may result from a spontaneously resolved STEMI. Wellens’ own group showed in Doevendans et al. (1995) that the ECG findings can be seen following reperfusion of a complete LAD occlusion. Upon continuous ECG monitoring, biphasic T waves can be seen immediately following successful percutaneous coronary intervention (PCI). Biphasic T waves are followed by progression to inverted T waves and eventually T wave normalization.8 The two types of Wellens’ Signs may represent the exact same mechanism but with ECG obtained at different times following reperfusion. This reperfusion may occur spontaneously or possibly due to intervention with aspirin or other medications. Many patients, including our own, report stuttering chest pain, which should not be taken lightly. One should also be on the lookout for evolution to complete occlusion, which may manifest early as “pseudo-normalization” of T waves or a return of hyperacute T waves prior to ST elevations. Wellens’ Syndrome may represent the eye of the storm between two episodes of complete occlusion and a critical moment at which we can save a patient’s life.


2) What are the next steps in the treatment of this patient?

Any patient with a suspected Wellens’ Syndrome should be treated for ACS.9 They should be placed on continuous cardiac monitoring and immediately given aspirin. Cardiology should be consulted, as the patient will require urgent catheterization. Additionally, a second antiplatelet agent such as clopidogrel or beta blockers may be considered in consultation with cardiology. Dual antiplatelet therapy is warranted in preparation for PCI, but is contraindicated for coronary artery bypass grafting (CABG). CABG is typically indicated for triple vessel disease, proximal Left Main Coronary Disease (prior to the bifurcation of LAD and LCx), or diabetics with two vessel disease involving the LAD. Although evidence is limited, patients experiencing angina pain should also receive nitroglycerin, either sublingually or intravenously as needed. Serial ECGs should be obtained to detect the early signs of re-occlusion in the absence of overt symptoms. Lastly, these patients will require urgent disposition to either the Catheterization Lab or CCU. If destined for the CCU and cath deferred, the patient should be placed on a heparin drip. At present, there are no clear guidelines for the timing of cardiac catheterization, but these patients are at high risk for MI in the following days to weeks.1, 4 In conclusion, your job as the emergency clinician is to make sure their “time bomb” coronary lesion doesn’t evolve before the cardiologist can put some metal into that patient’s artery.


3) What testing would be contraindicated given this presentation?

It may seem obvious in retrospect, but these patients should really not be stress tested. Wellens’ Syndrome would represent a very high pre-test probability for significant coronary artery disease, so a provocative test with mediocre accuracy (i.e. stress test) would not add much to patient management. Furthermore, the patient may further thrombose during the test. While it seems unlikely having read this post, it is easy to envision our patient being scored HEART 5 and finding his way to Observation with the diagnosis of ACS. Herein, the patient may be subjected to the typical management of “ACS” – troponins trended and some provocative testing, i.e. stress testing. Sounds reasonable, right? Not so much when you have a code called to the treadmill room. While no study has demonstrated negative outcomes from stress testing, significant ischemia and perfusion defect have been confirmed via single positron emission computed tomography (SPECT) in exercising patients.6 The patient with Wellens’ Syndrome ideally should proceed directly to invasive testing to confirm a significant lesion.10 Assuming a critical stenosis is identified during catheterization, the culprit lesion will more than likely be stented at that time.


4) Bonus Question: What happened to our patient?

Our patient was diagnosed with Wellens’ Syndrome early and was given aspirin, clopidogrel, nitroglycerin and heparin drips. Cardiology was consulted and the patient was admitted to the CCU for planned catheterization the following day. A transthoracic echo was done in the morning and demonstrated a normal ejection fraction. In the cath lab, the patient was found to have a 90% occlusion of the LAD and a drug eluting stent was placed with resulting TIMI 3 Flow (100% patency). The patient tolerated the procedure well and was subsequently discharged home.  



  1. de Zwaan C, Bär 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.
  2. de Zwaan C, Bär FW, Janssen JH, Cheriex EC, Dassen WR, Brugada P, 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;117(3):657–65.
  3. Meade NE, and O’Keefe KP. Wellens’ Syndrome: An ominous EKG pattern. J Emerg Trauma Shock. 2009 Sep-Dec; 2(3):206-208.
  4. S Sobnosky, R Kohli, S Bleibel. Wellens’ Syndrome. The Internet Journal of Cardiology. 2005; 3(1).
  5. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002 Nov; 20(7):638-43.
  6. Hovland A, Bjornstad H, Staub U, et al. Reversible Ischemia in Wellens’ syndrome. J Nucl Cardiol 2006(13)13-15.
  7. Sheng FQ, He MR, Zhang ML, Shen GY. Wellens’ syndrome caused by spasm of the proximal left anterior descending coronary artery. J Electrocardiol. 2015;48(3):423–5.
  8. Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bär FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol. 1995 Jun 15;75(17):1206-10.
  9. Oo S, Khalighi K, Kodali A, et al. Ominous T-wave inversions: Wellens’ syndrome revisited. J Community Hosp Intern Med Perspect. 2016; 6(4).
  10. Raheja P, Sekhar A, Lewis D, et al. Wellens’ syndrome over the past three decades. J. Cardiovasc Med. 2017 Oct (18):803-804.
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Combined EM/IM PGY-1 resident at SUNY Downstate/Kings County Medical Center. Graduate of St. George's University School of Medicine, Grenada. Alumni of Dickinson College, '08. Recent transplant from Los Angeles, but hoping to slowly develop into a true New Yorker over the next 5 years.

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