Saturday, April 23, 2016

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

Thursday's case, read by 60,000 people, provoked a bit of anguish among readers because they weren't all sure they would recognize this finding of LAD occlusion.  Others thought it was obvious.  Others thought they would detect it with troponins or serial EKGs (serial EKG was done and did not change; I don't know about serial trops, but one was "negative.")  Some persistently denied that the T-wave in V2 was a specific sign of ischemia.

These are 10 cases of LAD occlusion with subtle Hyperacute T-waves in lead V2 (or V3) only.

Steps to verify LAD occlusion, or exclude it:

1. Use of the LAD occlusion/early repolarization formula.  But beware the few false negatives, especially when there are hyperacute T-waves but no ST elevation (see Case 2 below):

Formula to differentiate Normal Variant ST Elevation (Early Repolarization) from Anterior STEMI.  

2. Use contrast echocardiography (This is the most reliable, short of angiography).  Bedside echo without contrast or speckle tracking can be misleading.  You must be an expert at this to rule out a wall motion abnormality.

3. A positive troponin is useful.  A negative one does not rule out MI.  2 or 3 do not rule out unstable angina, even in the era of high sensitivity troponin: this study by Thelin et al. showed 100% sensitivity for MI, but only 95% sensitivity for ACS using hs-TnT. 

4. Angiography.

Ten (10) Cases of Acute LAD occlusion manifesting as subtle hyperacute T-waves

Case 1

Case 2

Case 3 (April 20 case that provoked this post)

Case 4

Case 5

Case 6

Case 7 (this one links to many other cases of hyperacute T-waves.

Case 8

Case 9

Case 10
This one is not posted, but was an LAD occlusion that went unrecognized.  The patient lived but lost the entire anterior wall.


  1. THANKS so much to Dr. Stephen Smith for assembling these 10 cases from prior Blog posts of his to definitively illustrate the phenomenon of anterior hyperacute T waves. My SUGGESTION — For anyone involved in acute care who is not yet familiar with (and regularly following) Dr. Smith’s ECG Blog — SHOW THEM these 10 ECGs and tell them ONLY that these are ECGs from 10 patients who presented to the ED with atypical chest discomfort (I suggest using “atypical” chest discomfort as the ED presentation — so as not to make things too obvious). Then ASK THEM to indicate which (if any) of these tracings should be suspicious for possible acute anterior STEMI? Do NOT tell them that they ALL are … Ask them to brief say WHY or WHY NOT each tracing is (or should not be) suspicious for acute anterior stemi.

    Dr. Smith has given links to the detailed answers in his prior Blog posts. I’ll offer the following “quick” answers to the above questions. Anyone not scoring 100% should ideally review each of the links provided under the figures.

    ECG-1 — Disproportionately tall anterior T waves (ie, hyperacute-looking anterior T waves in V2,3,4). The leads of most concern to me are V3,V4 — in which the T wave is fatter-than-it-should be with a wider-than-it-should-be base. Leads III and aVF confirm the abnormality by the presence of reciprocal ST-T depression.

    ECG-2 — Disproportionately tall anterior T waves. Leads V2,V3 are of most concern (the T clearly much taller-than-it-should-be in those leads) — with inf. reciprocal changes and an overly tall T in tiny aVL (compared to the tiny size of the QRS in this lead) confirming the abnormality.

    ECG-3 — the case that prompted this post (See link under the figure for details).

    ECG-4 — Lead V2 is of most concern (the T taller-than-it-should-be) — with reciprocal changes in leads III,aVF. Additional subtle changes confirming the abnormality are ST straightening (that should not be) in lead II — and a clearly more-peaked-than-it-should-be T wave in lead V1. (The T in V1 might not by itself be abnormal — but it IS abnormally peaked in context with what we see in V2,3,4 given the history of ED presentation for chest discomfort.)

    ECG-5 — Clearly wider (and fatter at the peak) T waves in V2,3,4 — with definitely abnormal initial ST segment straightening (that confirms the abnormality) in lead V2. Similar fat/wide T in aVL — with clear reciprocal ST-T changes in III,aVF (note tell-tale biphasic T waves in these two inferior leads).

    ECG-6 — Disproportionately tall T wave in V2. Other leads are more subtle — but ST segment flattening before the T wave in V3 is definitely not normal — and leads III,aVF suggest reciprocal changes …

    ECG-7 — Disproportionately tall T waves in V2,3,4. Note initial q waves that shouldn’t be there in V2,V3 — with subtle-but-real inf. reciprocal change (and subtle q + ST elevation in aVL) to confirm the abnormality.

    RAN OUT OF ROOM — ECGs 8,9,10 coming next

  2. STEVE — This is the continuation:

    ECG-8 — Perhaps the most subtle example … but in a patient who presents to the ED for chest discomfort (even if the discomfort is atypical) — there ARE ECG signs of concern. Leads V3,V4 to me are the most abnormal (the T just looks broader and fatter-than-it-should-be in these leads) — and the ST segment (before the T wave) in leads I,II,aVL; and V4,V5,V6 is straight (instead of showing the usual normal gradual upsloping) — with suggestion of some reciprocal change in lead III. Stat Echo and serial tracings might be needed for confirmation here …

    ECG-9 — Disproportionately tall anterior T waves + subtle ST elevation in aVL with subtle inferior abnormalities (flat ST in II; shallow T inversion in III; slight J-point ST dep in aVF). This one is also subtle — but the onus is on the provider to rule out acute change for those tall-looking T waves in V2,3,4 given predominant negativity of the QRS in these leads …

    ECG-10 — Lead V2 is the key lead here, as the T wave is taller with a wider base than one usually sees with early repol (compare the ST-T in V2 to V3, as the T wave in V3 almost looks normal). Support that the changes in lead V2 are likely to be real is found in leads III,aVF (straight ST segment that esp. in lead aVF is not normal) and V1 appearance. While slight ST coving/elevation in V1 is not necessarily abnormal if the rest of the tracing is unremarkable — in the context of the clearly abnormal-looking ST-T wave in lead V2 — V1 is suspicious …

    THANKS again to Dr. Smith. Detailed discussions can be found in the links below each figure.

  3. Thats some difficult cases! Noticed that in all but one case (nr 8) there is more or less of inferior st depression (nr 10 also very subtle, if any). Nr 8 has lateral depression. Also, the r wave progression is often affected. Thanks for postinf these cases!

  4. This synopsis is very helpful. Thanks for compiling.

  5. Great examples Dr Smith, thank you for sharing your wisdom.

    Interestingly, in half of those 10 tracings there is tall TW in lead V1 whether it means anything or not is up for a debate.

    The changes on ECG often are so subtle, that one would have to have their paranoid ACS radar constantly on, and then one will have dickens of a time arguing and trying to prove the point with cardiology that these patients need to be taken seriously.

    The other night, at 4am I was trying to convince cardiology resident that an old woman was having cardiac event with STE in posterior leads of 0.5mm and almost arguable STE in V6. Once hsTnI came back at 20,000 no more words were needed.

    Great cases, a lot to learn.

  6. Thanks Dr. Smith for your excellent illustration : )
    People tends to believe that a "smiling" ST elevation in right precordial lead is due to Benign Early Repolarisation or Pericarditis ECG changes, I have seen few patients with acute total occlusion of LAD with so call "benign smiling" ST elevation ECG.
    I would feel that it is definitely not BENIGN, at least not in all patients : )


Recommended Resources