Thursday, July 9, 2020

Chest pain and Inferior T-wave Inversion. Does this patient need emergent cath lab activation?

This ECG was texted to me, initially with no information:

What do you think?

There are QS-waves in III and aVF.  There is a qR in lead II.  There is minimal STE, upsloping, with T-wave inversion in lead II.  Leads III and aVF only have deep, fairly symmetric T-wave inversion.

My interpretation and reply (paraphrase): There is subacute inferior MI and there has probably been prolonged pain.  The initial troponin will be high.  With T-wave inversion, it is possible that the artery has opened, but with subacute MI, the T-wave may be inverted even with persistent occlusion.  If there is persistent pain, then it is persistent OMI and the patient should go to the cath lab.

Notice also:  the T-wave in aVL is large and upright.  Is this a hyperacute T-wave?  No!  It is reciprocal to the negative T-waves in inferior leads.  See explanation at bottom of case.

Here is the history:

A 50-something woman chest pain for the last week that acutely got worse in the last day and was associated with nausea, diaphoresis, vomiting.  This pain is been ongoing for many hours.

The first troponin I was very elevated at 9.13 ng/mL.

The interventionalist was not entirely on board with this and said "It is not a STEMI."  My very astute partner said, "No.  It is an OMI."

Angiogram showed a 100% subacutely occluded RCA. It was opened and stented.

The estimated left ventricular ejection fraction is 59 %.
Regional wall motion abnormality-inferior and lateral, akinetic.

The final diagnosis was "NonSTEMI."

Learning Points:
1. Q-waves may be old or new.  When associated with deep T-wave inversion, especially with any ST Elevation, and especially when upsloping, they are likely new (subacute MI).  --old MI also has T-wave inversions, but they are more shallow.  Old MI may also have some ST elevation ("Old MI with persistent STE, otherwise known as LV aneurysm morphology) shallow T-wave inversions may be present with old MI, and may also be associated

2. Inverted reperfusion T-waves may result in Pseudo hyperacute T-waves in opposite leads.  In this case, the large upright T-wave in aVL is reciprocal to the deeply inverted T-wave in III.  See case below.

3.  STEMI, NonSTEMI, OMI.  The ECG in the clinical scenario is diagnostic of OMI.  As you can see, the diagnosis of NonSTEMI is meaningless on an anatomic level.  It is correct that 1 mm of STE was never measured.  It is possible that, had an ECG been done earlier in the course of this MI that there would have been STE diagnostic of STEMI.  Or maybe not.  In any case, it is the presence of an occluded artery (OMI) that is important, not the presence of, extent of, or magnitude of any ST Elevation.

4. Reciprocal Pseudo Hyperacute T-waves can mimic real hyperacute T-waves.  See this ECG from this post:

How do you explain these inferior hyperacute T-waves?

This was a case of Wellens' syndrome of proximal LAD (I, aVL, V2, V3).  See the very large inferior T-waves, reciprocal to the large inverted reperfusion T-waves in I and aVL.

MY Comment by KEN GRAUER, MD (7/9/2020):
Today’s case is “an ECG read”. By this I mean — No clinical information was available to Dr. Smith at the time he was initially texted the ECG shown in Figure-1. The KEY clinical question is whether the patient with this ECG is in need of acute reperfusion?
  • Sometimes it is obvious from the initial ECG (even before you know the history) — that acute coronary occlusion is ongoing. At other times — the initial ECG will clearly show no acute changes. Today’s case is challenging — because ECG #1 is equivocal. I would interpret this tracing as showing inferior MI of uncertain age.

Figure-1: The ECG that was texted to Dr. Smith in this case (See text).

I’d add the following thoughts to the above discussion by Dr. Smith:
  • The rhythm in ECG#1 is sinus bradycardia at 50-55/minute.
  • The PR interval is slightly prolonged at ~0.23 second ( = 1st-degree AV block).
  • The QRS complex is narrow. The QTc is not prolonged. The frontal plane axis is slightly leftward — but not leftward enough to qualify as LAHB (ie, the QRS is not predominantly negative in lead II). There is no chamber enlargement.
  • Q waves are present in each of the inferior leads. This includes QS complexes with a notch on the S wave upstroke in leads III and aVF. This patient has at some point had an inferior MI.
  • Transition is normal (ie, the R wave becomes taller than the S wave is deep between leads V2-to-V3).

The most concerning findings in ECG #1 relate to ST-T wave changes:
  • As per Dr. Smith — there is ST segment coving in lead II (curved RED line) — with slight ST elevation followed by shallow T wave inversion in this lead. The ST segment is not elevated in the other 2 inferior leads — but the shape of these ST segments in leads III and aVF also hints at coving, and evolves into deep, symmetric T wave inversion.
  • Lead aVL is remarkable for showing a precise mirror-image reflection of both the QRS complex and T wave that is seen in lead III. This T wave in lead aVL is disproportionately tall given the modest R wave amplitude in this lead — as well as being wider-than-it-should-be at its base. To a lesser extent — lead I shows a similar picture. These high lateral lead ST-T wave changes raise concern for being an acute reciprocal change.
  • Finally — there has also been posterior involvement. Normally, leads V2 and V3 show a gently upsloping ST segment (often with 1-2 mm of ST elevation). As per the RED line over the ST segment in lead V2 — this ST segment is uncharacteristically straight without the slightest amount of elevation.

IMPRESSION: This patient has had infero-postero MI of uncertain age that could be recent or ongoing.
  • The inferior Q waves and QS complexes are large, suggesting the MI did not just happen. That said, as has been previously shown on Dr. Smith’s ECG Blog — it is possible for Q waves to develop surprisingly soon after acute coronary occlusion (ie, as soon as within the 1st hour after acute occlusion!) — so inferior lead Q wave size on ECG #1 does not rule out the possibility of a single recent event.
  • With the exception of the slight ST elevation in lead II — lack of ST elevation elsewhere is against recent acute coronary occlusion. And, although definitely abnormal — the flat (straight) ST segments in leads V2 and V3 suggest posterior infarction is not new.
  • On the Other Hand — Sinus bradycardia with 1st-degree AV block are consistent with enhanced parasympathetic tone often seen during the early hours of acute inferior MI. In addition — there is some ST elevation in lead II, together with inferior lead ST coving + very deep inferior lead T wave inversion with a mirror-image hyperacute-looking T wave appearance in the high lateral leads. These findings suggest that the MI could be recent, or even ongoing. Clinical correlation (and ideally finding a prior tracing for comparison) is needed to make sense of these findings.

Follow-Up: The history for the patient in today’s case — is that this 50-something woman had a 1-week history of chest pain that became much worse on the day of admission. Her chest pain was ongoing for many hours at the time ECG #1 was obtained.
  • The clinical course of acute infarction is not always explained by a single cardiac event. Acute coronary occlusion may occur either at the onset of symptoms, or some time thereafter. There may be spontaneous reopening of the occluded vessel — followed by reocclusion — and then, sometimes repeating this process a number of times over ensuing hour or days.
  • BOTTOM LINE: In view of this history — my guess would be that this patient had her initial event a number of days earlier (perhaps at the time her symptoms began). That said — there are enough potentially acute findings in ECG #1 in this patient with ongoing severe chest pain that prompt cardiac cath is indicated for clarification of the clinical picture. As per Dr. Smith — the inferior T wave inversion might reflect spontaneous reperfusion — but, the overall findings in ECG #1 might also reflect either persistent coronary occlusion or new reocclusion. Persistence of this patient’s chest pain facilitated decision-making — and cardiac cath confirmed 100% RCA occlusion.


  1. dear dr: thanks . i have more notes about your interpretation of this ecg
    1st:the reciprocal leads in the frontal plane are lead (AVL vs lead3 not(AVL vs lead2 which they are 90 degree(30+60)) while 180 degree in the 1st group
    2nd : the ST elevation in V2 0R V3 doesnt meet the definition criteria of STEMI in precordial leads which is more than 2mm thus the posterior MI diagnosis is completly rouled out
    3d:no body had noted the notched j points in left leads( 1 AVL V5 V6) and the signifcant STE in V5 V6

    1. Correct — the “magical” reciprocal relationships in the limb leads is between leads III and aVL (which as you say, are nearly opposite each other). This relationship is extremely useful in confirming that even subtle ST elevation in the inferior leads in a patient with new symptoms is likely to indicate acute OMI. In contrast — ST elevation in the inferior leads from a repolarization variant or acute pericarditis will not show true reciprocal (mirror-image) ST-T wave depression in lead aVL.

      That said — if you think about the LV as a “cylinder” — you can actually see “reciprocal changes” anywhere (ie, in lateral, inferior, anterior leads — depending on where the acute injury current is occurring.

      The reason I said there is posterior MI in Figure-1 — is the SHAPE of the ST-T wave in lead V2, in association with what we KNOW has been an inferior MI that most likely was recent. As per the RED line I drew — this shape in lead V2 is clearly abnormal. There should be gradual upsloping with slight-but-real ST elevation — but instead the ST segment in V2 is flattened, because it has been depressed by posterior MI. This is a subtle-but-real finding. I cannot “date” the posterior MI from this single ECG — but it most likely is related to the inferior event(s). And as you say — this is not a “STEMI” because it lacks the millimeter definition for that. But what “counts” is not whether there has been a STEMI, but rather whether there has been OMI ( = Occlusion-based MI) with persistence of coronary occlusion because of the persistent pain this patient has — which is why cath was indicated in this case.

      Finally — GOOD point you raise about the notches. I saw these — and actually there is notching in MANY leads in ECG #1 (ie, leads I, III, aVL, aVF, V1, and V5, V6). I wasn’t sure what to make of these, so I decided not to comment on them. The shape and trivial amount of ST elevation in V5,V6 did not appear significant to me (I thought it might reflection repolarization changes). Of interest — we have reported cases of Osborn waves being associated with acute ischemia/infarction (See My Comment in the November 22, 2019 post — ) — but the ST-T wave changes in today’s case did not look so acute, so I did not think them to represent ischemia-related Osborn waves.

      THANKS for your comments! — :)


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