CONTENTS

• Approach to TWI
  • 1/3: Is TWI pathological?
  • 2/3: Lead distribution?
  • 3/3: Morphology?
    • Down-up T-waves.
    • Up-down T-waves.
    • Giant T-waves.
• Wellens A & B patterns
  • PE vs. Wellens
• Biphasic up→down T-waves
  • Wellens A
  • PE
  • LV aneurysm ⚡️
  • Benign TWI ⚡️
  • LVH (pseudoWellens) ⚡️
• Other T-wave morphologies:
  • Persistent Juvenile T-wave pattern
  • Memory TWI

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approach to TWI

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1/3: Is TWI pathological?

• ⚠️ Note that TWI can result from abnormal depolarization (e.g., RBBB, LBBB, paced rhythms, LVH, RVH).  This chapter overlooks some of these issues that should be clear from the remainder of the ECG (e.g., LBBB).  This underscores the importance of always reading ECGs systematically (e.g., evaluating for LVH or RVH before looking for abnormal T-wave morphology).
• Comparison with the QRS axis is important:
  • TWI is more concerning if it occurs in a lead with an upright QRS complex.
  • If the QRS complex and T-wave are both inverted, this likely reflects an axis shift (rather than ischemia).

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2/3: What is the lead distribution of TWI? 

right precordial leads

• Persistent Juvenile T-wave pattern ⚡️
  • 🔑 Uncommon; young people (<45YO); women >> men.
  • 🔑 Occurs in ~V1-V3 territory (or even extending to V4).
  • 🔑 Shallow TWI (<~3 mm).
  • 🔑 Asymmetric (slow downstroke, rapid upstroke).
  • 🔑 Often relatively vertical QRS axis (e.g., low voltage in lead I).
• RV strain (PE or RVH) 📖
• Ischemia (Wellens) – see PE vs. Wellens: ⚡️
• Posterior MI – may reflect the mirror image of hyperacute T-waves.
• Less common:
  • ARVC. 📖
  • Athletes.
  • Pectus excavatum. 📖 (29272363)

left precordial leads

• LVH 📖
  • STD should be down-sloping and asymmetric.
  • TWI should be asymmetric with a rapid return to baseline. Overshoot of terminal positivity can occur, which may produce an inverted U-wave in the left chest leads (overshoot suggests LVH rather than ischemia). (11992349)
  • The pattern is usually maximal in V5-V6 (e.g., TWI in V6 > TWI in V4).
• Ischemia with reperfusion (Wellens). 📖
• ER with benign TWI. 📖
• Digoxin. 📖
  • Scooped ST depression (which may cause a down-up T-wave configuration).
  • Morphologic abnormalities are usually global throughout the entire ECG.
• Apical HCM (Yamaguchi syndrome). 📖

aVL

• LBBB.
• LVH (should also be associated with TWI in I).
• Inferior STEMI (TWI in aVL may precede inferior STE; look for hyperacute inferior T-waves).

inferior leads

• RV strain pattern (e.g., pulmonary embolism).
• Myocardial ischemia:
  • Reperfusion of inferior MI.
  • Mirror-image of lateral OMI with hyperacute T-wave in aVL.

diffuse or multiple territories

• MI (reperfusion of an MI involving multiple territories, such as a wraparound LAD).
• Takotsubo CM, TWI phase: 📖
• Memory T-waves after abnormal ventricular depolarization. ⚡️
• Diffuse down-up T-waves
  • Hypokalemia 📖
  • Digoxin 📖
• RV strain pattern:
  • Typically involves the right precordium + inferior leads.
  • TWI can be splayed out, mimicking Takotsubo cardiomyopathy.
• ER (early repolarization) with benign TWI 📖
• Apical HOCM (most marked in V3-V5) 📖
• Pericarditis 📖
• Myocarditis.
• Idiopathic global TWI (diagnosis of exclusion)

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#3/3: What is the morphology of TWI?

Up –>Down T-waves

• Discussed below: ⚡️

Down –>Up T-waves

• TWI with prominent U-wave
  • Hypokalemia 📖 is the most common cause (suggested by very long QT/U interval).
  • Digoxin 📖 may be another possibility.
• Reciprocal to a Wellens-A pattern.  Sometimes, the down-up T-waves can be the most prominent finding of ischemia (i.e., the “original” Wellen's A in the opposing myocardial wall may be absent or less notable).
  • V1-V3:  This is reciprocal to posterior Wellen's.
  • aVL, III:  Reciprocal to inferior Wellen's.

giant TWI (>5-10 mm): four major considerations

• [1] Acute ischemia.
  • It may be massive, sometimes resembling Takotsubo cardiomyopathy.
  • 🔑 Distribution is anatomic (e.g., anterolateral; example below).
• [2] Takotsubo cardiomyopathy: 📖
  • 🔑 Diffuse TWI involving many leads (V2-V6, I, II).
  • 🔑 T-waves are very broad, producing a markedly prolonged QT interval.
  • 🔑 T-waves are often asymmetric, with a gradual downslope followed by a rapid up-slope (Roller-coaster T-waves).
• [3] Apical HCM. 📖
  • TWI often in V3-V5.
  • It looks like LV strain but larger.
• [4] Massive pulmonary embolism (RV strain). 📖
• Other:
  • Stokes-Adams attacks (syncope due to severe bradycardia such as complete AV block).
  • Post-tachycardia syndrome.

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Wellens A & B patterns

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criteria of Wellens

• [1] Biphasic (Up –> Down) or deep and symmetric TWI in the mid-precordial leads (especially V2-V3).
  • TWI often involves V1-V4, sometimes extending out to V5 or even V6.
  • The lead with the greatest TWI is generally V3-V4 (unlike the RV strain pattern).
  • (Wellens pattern can occur in other distributions, such as the inferior leads).
• [2] No evidence of Q-wave infarction and/or aneurysm formation:
  • Preservation of the R-wave.
  • Absence of precordial Q-waves.
  • Absence of fragmentation.
• [3] There is no evidence of active OMI (e.g., STE is isoelectric or minimally elevated).
• [4] Clinical criteria (required for the diagnosis of Wellens Syndrome):
  • Chest pain previously, but currently absent.
  • Troponin levels should be normal or mildly elevated.

differential diagnosis

• If the R-wave is diminished, consider a resolving/resolved anterior OMI.
• Differential diagnosis of right-sided TWI above: ⚡️
• Wellens B-pattern: Differential of biphasic up–>down TWI above: ⚡️

clinical implications

• Wellens A pattern (25%)
  • Suggests very recent OMI with spontaneous reperfusion (at relatively high risk of re-occlusion).
  • When found in the right precordial leads, this suggests a LAD occlusion.
  • Over time, if the vessel remains open, Wellens A will evolve into Wellens B pattern.
• Wellens B pattern (75%):
  • This reflects a later stage of reperfusion.
  • Wellens B is less scary than Wellens A because it implies that the vessel has managed to stay open longer (so perhaps it is less likely to re-occlude).
• Wellens patterns are a contraindication to exercise stress testing.

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PE versus Wellens

⚠️ It may be impossible to definitively sort out PE versus Wellens based on an ECG. POCUS can be very helpful here.  

[#1/2] TWI elsewhere in the ECG

• Is there TWI in lead III?  TWI in lead III is found in ~88% of patients with PE versus ~15% of patients with MI (within a selected group of patients with right-sided TWI). (17350373)
  • Even shallow TWI in III should push towards a PE diagnosis.
  • Is there TWI in leads III & V1 & additional precordial leads? This is strongly suggestive of PE (in one study, this was found in 88% of patients with PE, compared to 1% of patients with MI). (17350373)
• TWI in leads I and aVL may support MI.

[#2/2] other findings to suggest PE?

• S-wave in lead I (especially if there is also an S-wave in V6).
• RBBB (partial or complete).
• RAA (right atrial abnormality).
• Tachycardia.
• (Other features of PE: 📖)

less helpful findings

• The deepest TWI in V1-V2 favors PE, whereas the deepest TWI in V3-V4 favors MI. However, this is often difficult to determine, varies with precise lead position, and seems unreliable.
• STE can occur in the right precordium with either PE or MI.

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biphasic up-down T-waves

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causes of up –> down T-waves

• Wellens A pattern. ⚡️
• PE (Wellens vs PE above: ⚡️).
• Benign TWI (usually within the context of Early Repolarization) 📖
• LVH causing a pseudo-Wellens pattern.
• LV aneurysm
• Pericarditis 📖

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LV aneurysm 📖

• 🔑 Typically, there are deep Q-waves in V1-V4.
  • Usually, at least one QS wave within V1-V4.
  • Sometimes, there is very poor R-wave progression, with rS in the right precordium.
  • rSr' may be seen (El-Sherif sign).
• 🔑 STE: Coved STE in V1-V4.
• 🔑 Often shallow TWI. This may have an up-down morphology that looks like Wellens A.

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benign TWI 📖

• 🔑 T-wave morphology:
  • Often shallow.
  • It may have an up –> down configuration (similar to Wellens A).
• 🔑 Distribution of TWI:
  • Benign TWI extends out more laterally (~V3-V6) than Wellens (~V2-V5).
  • Inferior leads typically have TWI.
• 🔑  Generally occurs in the context of BER. 📖 Leads with TWI have:
  • Tall R-waves, with minimal/no S-wave.
  • Usually, some STE.
  • Often J-waves.
• 🔑 QT usually short (e.g. QTc < ~425 ms).
• 🔑 TWI is relatively stable over time.

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LVH causing pseudo-Wellens pattern 📖

• Distribution tends to be V3-V6 (more lateral than Wellens, which is typically V2-V4).
• Sorting out Wellens vs LVH pseudo-Wellens:
  • (1) Distribution:
    • True Wellens is typically located in V2-V4
    • LVH pseudo-Wellens tends to be more lateral (e.g. V3-V6)
  • (2) Stability over time:  True Wellens pattern is a transitional state that will evolve into something else.

voltage criteria for LVH

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persistent juvenile T-wave pattern

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⚠️ This is NOT the same as benign TWI (often seen with Early Repolarization). 

key findings in persistent juvenile TWI pattern

• 🔑 Uncommon; young people (<45YO); women >> men.
• 🔑 Occurs in V1-V2, sometimes extending to V3 as well.
• 🔑 Shallow TWI (<~3 mm).
• 🔑 Asymmetric (slow downstroke, rapid upstroke).
• 🔑 Often relatively vertical QRS axis (e.g., low voltage in lead I).

differential diagnosis

• RV hypertrophy or pulmonary embolism (RV strain pattern). 📖
• Wellens pattern. ⚡️
• High lead placement in V1-V2 may cause TWI in these leads. 📖
• Arrhythmogenic RV dysplasia (can cause essentially the same TWI morphology pattern as persistent juvenile TWI). 📖

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memory TWI

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basics

• Occurs following abnormal ventricular conduction, e.g.:
  • Ventricular tachycardia.
  • Ventricularly paced rhythms.
  • Intermittent bundle branch block.
  • Rate-related aberrancy.
  • Ventricular pre-excitation with intermittent conduction through the accessory pathway.
• The duration of T-wave memory may relate to the duration of abnormal ventricular conduction. For example, 10 minutes of ventricular pacing may produce memory TWI for 15 minutes, whereas two years of ventricular pacing may cause memory TWI to persist for up to 18 months. (32426667)
• Memory T-waves are generally considered relatively benign. However, they have been associated with malignant arrhythmias, including torsade de pointes.

ECG features

• TWI distribution:
  • TWI occurs in leads with deep negative QRS complexes during abnormal ventricular conduction.
  • Most often:
    • TWI usually involves the precordial and inferior leads.
    • TWI usually doesn't occur in lateral leads (I or aVL).
• TWI morphology is variable. It may be deep and relatively narrow, or it can be broad and splayed. A more prolonged duration of abnormal conduction, or repeated episodes of abnormal conduction, may lead to deeper TWI. (33897151)
• Prominent positive T-waves may be seen in leads that had positive QRS complexes during abnormal ventricular conduction (the ECG “remembers” the positive QRS complex). (32426667)

differential diagnosis includes

• Takotsubo cardiomyopathy with TWI.
• Ischemia.
  • The combination of a positive T-wave in aVL, positive or isoelectric T-wave in lead I, and maximal voltage of TWI in precordial leads > lead III suggests memory TWI due to a right ventricular pacemaker rather than ischemia.  (15710753)
• (See above: causes of diffuse TWI ⚡️)

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questions & discussion

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