Friday, January 11, 2013

ECG Interpretation Review #59 (T Wave Inversion – Giant T Waves – Ischemia – Long QT – CNS – Yamaguchi Cardiomyopathy – LAD Ischemia)


No history is available for the ECG shown in Figure 1. That said:
  • How would you interpret this ECG?
  • What clinical conditions should be considered?
Figure 1:  No history is available. What clinical conditions should be considered? (Reproduced from ECG-2014-ePub)NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
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INTERPRETATION: The rhythm is sinus bradycardia and arrhythmia, with an overall heart rate just under 60/minute. All intervals (PR/QRS/QT) are normal. The axis is normal at +50 degrees. Voltage for LVH is present (deepest S in V1,V2 + tallest R in V5,V6 ≥35mm). The most remarkable changes are seen with respect to Q-R-S-T Changes:
  • There are no Q waves.
  • Transition occurs slightly early (between leads V2-to-V3) – with relatively tall R waves in leads V1,V2.
  • There is diffuse, deep symmetric T wave inversion. T wave inversion is almost 15mm deep in leads V2,V3.
  • Other subtle-but-real ST-T wave findings include 1-2mm of J-point ST depression in multiple leads – suggestion of ST segment coving in leads I, aVL, V2,V3,V4 – and a hint of ST elevation in leads III, aVR and V1.
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Giant T Wave Syndrome
The overall impression is consistent with Giant T Wave Syndrome. Although some T wave inversion is common in many conditions — the term “giant T waves” is reserved for a select number of clinical entities that produce truly deep (>5-10 mm amplitude) T wave inversion. When this clinical picture is seen (as it is in Figure 1) — one should think of the following diagnostic entities.
  • Apical (Yamaguchi) Cardiomyopathy.
  • Takotsubo Cardiomyopathy.
  • Severe CNS disorders (increased intracranial pressure).
  • Stokes-Adams attacks (especially when due to severe bradycardia, complete AV block).
  • Acute ischemia/coronary artery disease.
  • Post-Tachycardia Syndrome.
  • Massive Pulmonary Embolism (acute right heart strain).
Without any history — it is impossible to know which of the above entities is most likely:
  • We doubt massive PE (pulmonary embolism) — because none of the other stigmata of acute right heart strain are present (no right or indeterminate axis, no right atrial enlargement, no T inversion in lead III, no tall R wave in lead V1). T wave inversion with acute PE is most often limited to right-sided leads (V1,V2,V3 and II,III,aVF) — and is usually not nearly as deep as seen here.
  • Any of the other entities on the above list are possible.
  • Increased voltage is consistent with apical cardiomyopathy (that may produce identical ST-T wave changes as seen here). 
  • Takotsubo Cardiomyopathy may produce a somewhat localized or generalized Giant T wave pattern, often with a prolonged QTc (dependent on what areas of the heart are affected).
  • Anterior ischemia/infarction from high-grade LAD (Left Anterior Descending) coronary artery narrowing/occlusion should be high on the list because of the J-point ST depression, ST segment coving, and subtle ST elevation in leads III, aVR and V1.
  • Acute CNS disorders (stroke, subarachnoid or intracranial hemorrhage, seizure, coma, brain tumors, trauma) may produce some of the most bizarre ST-T wave abnormalities. That said — the QT interval will usually be prolonged with CNS disorders and there will often be manifest T wave broadening (neither of which is seen here).
  • Finally – a less commonly appreciated cause of diffuse T wave inversion is post-tachycardia syndrome. Diffuse T wave inversion not due to ischemia/infarction may sometimes transiently be seen following conversion of sustained SVT/VT rhythms.
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NOTE: Although many authorities suggest a minimum of ≥10mm for T wave depth sufficient to qualify as "Giant T waves" — for practical purposes (ie, in our experience) — the entities suggested by the above bullets should be considered in cases in which very deep (ie, ≥5mm) but not necessarily "giant" T waves are seen in a number of leads.
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2 comments:

  1. Hello Professor.
    1)Can you tell us more about differentiating between
    Apical CM and HCM?
    2)If this patient presented with chest pain without prior ECGs for comparison and in view of ST elevations in Lead 3 and ST depressions and Twave inversions in aVL, will activating cath lab justified??

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  2. @ MG — My impressions are: i) that the ECG may be highly variable for HCM — ranging from LBBB, LVH, RBBB, pseudo-MI patterns, prominent septal forces (tall anterior R waves and/or deep lateral or inferior Q waves) — to being NORMAL; and ii) that Apical CM is not any more “predictive” from ECG than is HCM — therefore distinction between the 2 is not something that can readily be done by ECG. As to your 2nd question — the ST elevation is isolated to lead III, and the overall pattern seen on this ECG is dominated by diffuse and very deep T wave inversion — so to me, the ST elevation does not weigh into my decision for justifying calling the cath lab. As per the theme of this Blog #59 — there is a big differential diagnosis — so history and exam and close follow-up are the factors that would determine if the cath lab should or should not be activated.

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