The ECG in the figure below was obtained from an alert 50-year-old man with chest pain. Unfortunately, no other clinical information is available. How should one interpret this 12-lead ECG? What clinical entities should one consider in the differential diagnosis?
The rhythm is sinus at a rate of about 60/min. The PR, QRS, and QT intervals are normal. The axis is normal at +20 degrees. Voltage for left ventricular hypertrophy (LVH) is clearly present, with increased amplitude and overlap between QRS complexes in leads V4, V5, and V6.
Regarding QRST changes, there are no Q waves. R wave progression shows normal transition between V2-V3. The most remarkable finding is the extremely deep and symmetric T wave inversion that nearly attains 10 mm in depth in leads V5 and V6. A proportionally comparable degree of T wave inversion (considering relative QRS amplitude) also occurs in four of the limb leads. ST segments are coved (albeit without significant ST elevation) in many of the leads with T wave inversion. There is also 1-2 mm of J-point ST depression in lateral chest leads prior to the deep T wave inversion. Finally, there is 1-2 mm of upward sloping (“smiley” shape) ST elevation in leads V1 and V2.
Clinical correlation is essential for optimal interpretation of this tracing. That said, the size of the inverted T waves in many leads is striking. These are “Giant T Waves,” which are said to exist when the depth of T wave inversion clearly exceeds 5 mm in at least several leads. This classification is helpful because it focuses attention to a short list of clinical entities most commonly associated with this syndrome. These clinical entities include:
- apical hypertrophic cardiomyopathy
- a catastrophic central nervous system (CNS) event such as stroke, intracerebral bleed, brain tumor, coma, or trauma
- Stokes-Adams attacks (especially when associated with severe bradycardia and AV block)
- anterior ischemia or an acute coronary syndrome.
- post-tachycardia syndrome (following an episode of sustained supraventricular or ventricular tachycardia).
- massive pulmonary embolism with acute right heart strain.
While additional clinical information is clearly needed, close scrutiny of this ECG narrows diagnostic considerations. Alert status and normal QT interval are against Stokes-Adams attacks or a catastrophic CNS event. Chest pain (rather than shortness of breath) and ST elevation (rather than T wave inversion) in leads V1 and V2 make massive pulmonary embolism unlikely. There is no history of a previous sustained tachycardia. Tall R wave amplitude in the lateral chest leads suggests that LVH and possible cardiomyopathy are at least partially responsible for the T wave appearance. Given the history of “chest pain,” comparison with prior tracings and further evaluation (including an echocardiogram) will be needed to determine if an acutely evolving coronary event is now superimposed on longstanding hypertension, LVH, and/or a preexisting cardiomyopathy. Given the amplitude of chest lead R waves, the size and diffuseness of ST-T wave changes, and the benign (upward concavity) appearance of ST elevation in leads V1 and V2, it is possible these changes are not acute. That said, clinical correlation is essential to confirm this.
Please see: https://youtu.be/gtdLfS4Q3Gw for more on Giant T Waves.
Chest pain (rather than shortness of breath) and ST elevation (rather than T wave inversion) in leads V1 and V2 make massive pulmonary embolism unlikely.
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