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.
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.
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.
  • 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).
  • 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.
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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