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The Devil Is in the T Wave: Wellens Syndrome

The Devil Is in the T Wave: Wellens Syndrome

Wellens' syndrome Figure 1. Note deeply inverted, symmetric T wave in leads V3 to V5, co...
Figure 2. Biphasic T wave abnormalities are seen in leads V2 and V3, c...
Figure 3. T wave abnormalities seen in Wellens’ syndrome. A. Deeply in...
Figure 4. Coronary angiography prior to PCI, demonstrating proximal le...

A 42-year-old man with a history of hypertension was driven to the emergency department (ED) by his wife on a Sunday morning for evaluation of chest pain. The pain, which had spontaneously resolved before presentation, was described as a central to left aching sensation, occurring with exertion; on the morning of presentation, the pain had occurred at rest. The pain was associated with nausea and diaphoresis. On ED arrival, the patient was normal-appearing without significant distress; his examination was largely unrevealing. A 12-lead ECG (Figure 1) was performed.

Based on the ECG findings noted in Figure 1, which of the following strategies best describes the appropriate management plan?  

A. Aspirin administration, biomarker testing (troponin) one time, exercise stress test with nuclear imaging if troponin is negative.

B. Aspirin administration, serial ECGs and biomarkers, discharge if the patient remains pain-free and evaluation is negative.

C. Aspirin administration, immediate exercise stress test with nuclear imaging.

D. Aspirin administration, serial ECGs and biomarkers, cardiology consultation for admission and probable coronary angiography. 

E. Aspirin administration, serial ECGs and biomarkers, stress echocardiography with cardiology consultation, disposition based on results of evaluation.

Answer: D. Aspirin administration, serial ECGs and biomarkers, cardiology consultation for admission and probable coronary angiography. 


Discussion

The 12-lead ECG is frequently the initial diagnostic tool used by clinicians when evaluating patients with suspected acute coronary syndrome (ACS); information obtained in the ECG can provide the diagnosis, indicate certain therapies, and assist with disposition and risk prognostication considerations. Certain ACS ECG patterns are suggestive of significant arterial occlusion and related high-risk presentations. 

One such high-risk ECG pattern is termed “Wellens syndrome.”1-4 This high-risk ACS presentation is noted in patients with active or recent chest discomfort, precordial T-wave abnormalities (Figures 1, 2, and 3), and without ECG or biochemical evidence of acute myocardial infarction (MI). The high-risk nature is based on a very frequent association with proximal left anterior descending artery occlusion (LAD) (Figure 4); this coronary lesion can progress over a very short period (hours to days) to anterior wall ST-segment elevation myocardial infarction (STEMI).1-4    

The T-wave abnormalities include two basic configurations. The more common ECG presentation is the deeply inverted, symmetric T wave (Figures 1 and 3A); it is seen in 75% of such patients. In the remaining patients, a biphasic T wave is seen; these T waves include both upright (positively oriented) and inverted (negatively oriented) components within a single T wave (Figures 2 and 3B). These abnormal T waves are usually seen in the anterior distribution, including leads V1, V2, V3, and/or V4; the T-wave abnormalities can also extend into the lateral region, with leads V5 and V6 involvement.1-4        

Wellens syndrome is defined as follows: (1) precordial T-wave abnormalities as described above; (2) active or recent chest pain; (3) negative serial biomarkes; and (4) no ECG evidence of MI (ie, significant ST-segment elevation, significant Q waves, and loss of R waves).1-4

Patients presenting with Wellens syndrome should be managed for an unstable ACS. Antiplatelet and anticoagulant therapies should be considered while serial ECGs and cardiac biomarkers are obtained. Cardiology consultation is suggested, with admission and performance of cardiac catheterization. Stress imaging of any type is strongly discouraged; markedly positive results in the form of STEMI and cardiac arrest have been reported.4 It must be noted that patients may experience active pain or may be pain-free on presentation—either presentation is considered high risk; the ECG findings will persist into the pain-free state without change and will only resolve with correction of the coronary obstructing lesion.4

Case Conclusion

Take-home points

1. Wellens’ syndrome is associated with significant LAD occlusion with anterior wall STEMI as natural history.

2. The T wave abnormalities can be encountered in patients with or without active pain; in both instances, the presentation should be considered high risk.

3. It is strongly recommended to avoid stress cardiac imaging in these patients. Timely cardiology consultation with cardiac catheterization is recommended.

The initial ED ECG (Figure 1) demonstrated prominent T-wave inversion in the precordial leads, a concerning finding. Despite the patient’s stable clinical presentation and pain-free state on ED arrival, the ECG was correctly recognized as high risk. Serial troponin values were normal; repeated ECGs did not demonstrate change. The patient remained sensation-free. Wellens syndrome was felt to be a likely issue. The patient was admitted to the cardiology service with coronary angiography performed later that day. A proximal LAD occlusion was noted (Figure 4) and successfully managed via intracoronary stent placement. The patient did well and was discharged from the hospital on day 2.

 

References

  1. de Zwann 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;103(4, pt 2):730-736.
  2. de Zwann C, Bär 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;117:657-665.
  3. Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. Ann Emerg Med.  1999;33:3:347-351.
  4. Reinhardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002;20:638-643.
 
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