Amal Mattu’s ECG Case of the Week – May 17, 2021

Differential diagnoses for T wave inversions

• Coronary artery disease (Wellens’, ischemia, reperfusion)
• Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
• Neurological causes (elevated intracranial pressure, hemorrhage, etc.)
• Post-tachycardia, post-shock, post-pacing (“cardiac memory”)
• Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
• Brugada syndrome (V₁-V₂)
• Wide QRS complexes (BBB’s, PVC’s, Paced rhythms, WPW)
• High left ventricular voltage, LVH with strain pattern
• Pericarditis, myocarditis
• Vasospasm (cocaine, amphetamines, etc.)
• Hyperkalemia, hypokalemia
• Juvenile T-wave pattern, normal finding in pediatric ECGs
• Mitral valve prolapse
• Normal finding in V₁, aVR, and lead III

Wellens’ waves (T wave inversion patterns associated with ACS)

• Two distinct patterns of T wave abnormalities in the mid precordial leads (V₂-V₃, +/-V_4-6) that are highly specific for critical obstruction of the left anterior descending artery (LAD)
• Reported by Wellens’ et al in 1982, the presence of these abnormal ECG patterns during a pain-free period in patients admitted with unstable angina was associated with very high risk for impending large anterior wall MI
• Later prospective studies on patients with Wellens’ syndrome confirmed association of the findings with significant proximal LAD disease by coronary angiography

• • Pattern A describes a biphasic T wave abnormality, initially positive with terminal negativity (~25% of cases)
    • Commonly misdiagnosed as “normal” or “non-specific T wave abnormality” in patients with atypical symptoms
    • Distinct from “reverse Wellens’ waves” associated with hypokalemia (biphasic T wave abnormality, initially negative with terminal positivity)
  • Pattern B describes a deeply (> 2 mm) and symmetrically inverted T waves (~75% of cases)

• Wellens’ waves typically evolve when serial ECGs are obtained and can help diagnose LAD related ACS

• • During acute occlusion patients may have chest pain and diaphoresis with transient anterior ST elevation that may not be captured on the initial ECG
  • During reperfusion (through spontaneous lysis or with medical treatment) chest pain and clinical symptoms may resolve while ST segment elevation improves, and T waves become biphasic or deeply inverted (similar to reperfusion s/p successful PCI)
  • T waves may evolve from biphasic to deeply inverted if reperfusion is maintained, but lesions that cause these changes are considered unstable and can re-occlude at anytime
  • During re-occlusion “pseudo-normalization” may occur, and previously biphasic or inverted T waves may become prominent and upright, a sign of evolving anterior occlusion MI

• Wellens’ waves are specifically described as T wave abnormalities in the precordial leads, but similar changes can be seen in other coronary distributions during transient occlusion, reperfusion, and re-occlusion. The inciting event may be thrombus from acute plaque rupture, but has also been described in patients with vasospasm without CAD (sometimes in the setting of cocaine or amphetamine abuse)

• As an isolated ECG finding, Wellens’ waves are not specific to ACS and false positives patterns that mimic ACS will diminish diagnostic accuracy (eg. benign T wave inversions which may also evolve, vasospasm, PE, RBBB, LVH, hypokalemia, CNS injury, stress cardiomyopathy, etc.)
• Key Point: Wellens’ syndrome is a clinical diagnosis in patients with Wellens’ waves, and caution should be taken to obtain a thorough history and appreciate other potential reasons for Wellens’-like ECG patterns

Wellens’ Syndrome

• A clinical syndrome in patients with a recent history of angina or concern for unstable angina/NSTE-ACS who have Wellens’ pattern ECG abnormalities described above, PLUS the following:
  • Isoelectric or minimally elevated ST segments (no STEMI criteria)
  • No precordial Q waves, with preserved precordial R wave progression (no old anterior infarct)
  • Recent history of angina, with ECG pattern noted while chest pain free
  • Normal or slightly elevated conventional troponin
• Patients may present to the ED pain-free, comfortable, and have a normal physical exam. However, there are usually preceding symptoms concerning for ACS, or mild distress with diaphoresis
• Wellens’ syndrome is not always an acute process, and can develop sub-acutely over days to weeks
• Wellens’ syndrome exists on a spectrum of disease and biphasic T waves (pattern A) may evolve into deeply inverted T waves (pattern B) that may persist for hours or weeks, even when the patient is pain-free
• Cardiac biomarkers may be falsely reassuring, and commonly within normal limits or only slightly elevated
• While not currently a guideline indication for emergent cath or lytics (especially when pain free and without ST segment elevation), consider cardiology consultation when suspected
• Medical management alone is usually ineffective and definitive treatment is procedural with PCI. Stress testing may be hazardous in the setting of an unstable lesion and may precipitate acute MI or sudden death
• Best to diagnose in absence of high voltage, be cautious in making the diagnosis in the presence of large amplitude QRS complexes, and watch for normal variant T wave abnormalities
• When in doubt get serial ECG’s, some will evolve into STEMI!

Take home Points

• Wellens’ syndrome is the result of critical stenosis of the LAD manifesting in the characteristic ECG patterns (Wellens’ waves). It is a pre-infarction state, that tends to progress to large anterior MI with poor morbidity and mortality when not recognized early and treated appropriately
• Beware Wellens’ syndrome but also watch out for normal variants and “pseudo-Wellens’ waves” that can result in false positive cath lab activation
• This episode highlights several cases of normal variant ST elevation and T wave inversions that mimicked Wellens’ waves and STEMI. Be careful when diagnosing Wellens’ syndrome in patients with high voltage QRS complexes or features more suggestive of a normal variant:
  • Young males, especially athletes
  • Typically, African-Caribbean decent
    • Less common in Caucasians
  • Concave upward ST segment elevation, followed by a sharp drop into biphasic T waves, often with notch or “fishhook” appearance at the J-point

References:

1. Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349(22):2128–35. PMID: 14645641
2. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur. Heart J. 2010;31(2):243–59. PMID: 19933514
3. 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. PMID: 6121481