Friday, June 28, 2019

Inferior Subtle ST elevation: straight ST segment, but also no reciprocal ST depression in aVL: which is more important?

60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting.

Time zero

What do you think?

There is inferior ST elevation.  Is it normal variant?  Is it ischemic (OMI)?  [Pericarditis? (NOT!)]

There is one finding that argues against inferior OMI (There is absence of reciprocal ST depression in aVL; STD aVL is extremely sensitive for inferior OMI;   Reference: Bischof and Smith). 

However, there is also straightening of the inferior ST segments, and a straight ST segment in aVF; this is extremely rare in normal variant STE).
There is also terminal QRS distortion in II, III, aVF [absence of S-wave and J-wave (notch)].  The significance of this in inferior leads is unknown, but I suspect it is a marker for inferior OMI vs. normal variant.

Terminal QRS distortion is definitely significant for anterior OMI in V2 and V3:

An intoxicated, agitated, 20-something with chest pain


Here is an ECG from one month ago:
There is a definite change in the inferior leads, with new ST elevation.
Previously, all inferior leads had appropriate upward concavity.

The patient was given aspirin, heparin, and IV nitroglycerine.

Another ECG was recorded at 35 minutes:
It is hard to discern a difference

At this point, the first troponin I returned at 0.55 ng/mL (significantly elevated)

A D dimer was also elevated.

Another ECG was recorded at 58 minutes:
Again, no big difference.

There was concern for aortic dissection, so a CT was done and was negative.

The cath lab was activated:

Result: Thrombotic 95% stenosis at the ostium of a small LPL2 with 70% stenosis at the LPL2/LPDA bifurcation in the distal/AV groove Cx Tubular 70% stenosis in the mid-circumflex.  (In other words, inferior MI with some posterior involvement).  It was stented.

For coronary anatomy, see here:

This is the post intervention ECG:

All ST Elevation is gone (more proof that it was all a result of ischemia)

Formal Echo:

Normal estimated left ventricular ejection fraction - 55%.

Regional wall motion abnormality-mid and basal inferior .

Troponin I peaked at 12.1 ng/mL.

Learning Points:

1. Any inferior ST elevation may be acute OMI, but there are subtle differences between OMI on the one hand, and normal variant on the other.
2. 99% of inferior OMI are either obvious or have some amount of ST depression in aVL.  But 1% may be/have neither!
3. In this case, one might say it is "obvious" MI because of a straight ST segment in aVF.  A straight ST segment virtually never happens in inferior ST elevation that is NOT due to OMI (normal variant, pericarditis)
4. If a patient presents with symptoms of ACS, has an elevated troponin, and has persistent symptoms in spite of medical therapy [antiplatelet, antithrombotic, and anti-ischemic (nitro)], then cath lab activation is indicated regardless of ECG findings.
5. Compare with an old ECG.
6. Record serial ECGs.

Comment by KEN GRAUER, MD (6/28/2019):
I like this case because it provides an excellent example of how to use comparison tracings in a patient with a prior history of coronary disease.
  • For clarity — I’ve put the first 2 ECGs shown in this case together in Figure-1. To highlight KEY findings — I’ve enlarged one complex in leads II, III, aVF and aVL, that I’ve placed to the right of each of the 12-leads.
Figure-1: The first 2 ECGs shown in this case — with enlargement of leads II, III, aVF and aVL to the right of each tracing (See text).

The CASE: The patient is a 60-something who presented to the ED with new-onset chest pain. The patient had a prior history of MI stents.
  • KEY Points: This patient has known coronary disease. Therefore: iThe initial ECG may show signs of prior injury; iiECG evidence of new OMI may be subtle; it may be difficult to distinguish “new” from “old” ECG findings from the initial ECG alone (ie, from ECG #1 alone in Figure-1); andiiiFinding a prior ECG on this patient may provide invaluable assistance!

QUESTION:   regarding ECG #1: Before you looked at the prior ECG in this case (which is ECG #2 in Figure-1) — YOU should have seen abnormal findings in the chest leads of ECG #1! — Did you see these 3 abnormal findings ??? —
  • HINT: It would have been EASY to overlook these 3 findings if you were not Systematic in your interpretation ...

MTHOUGHTS on ECG #1  The rhythm is fairly regular, at a rate between 55-60/minute. The QRS is narrow. This is sinus bradycardia.
  • All intervals (PR, QRS duration, QTc) are normal.
  • The frontal plane axis is normal (about +65 degrees).
  • There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are Q waves in multiple leads, including leads I, II, III, aVL, aVF; and in leads V3-thru-V6. Most of these Q waves are small and narrow. Many are unlikely to be clinically significant. That said — although tiny, the in aVL of ECG #1 could reflect lateral MI of uncertain age given how small the QRS is in this lead (Note in the Blow-Up view that the initial deflection in lead aVL of ECG #1 is negative = a Q wave).
  • While the Q waves in leads V4V5 and V6 are narrow — they are a little deeper-than-usual for normal septal q waves. In this patient with documented coronary disease — these q waves could reflect prior lateral infarction (especially in view of the Q in lead aVL).
  • Regarding R Wave Progression —Transition is early! In fact — in lead V1, and this is not a “normal” finding! Because LV (left ventricular) forces predominate in a normal ECG — there is usually no more than a small initial r wave in lead V1, which is normally associated with a fairly deep S wave in lead V1 (this deep negative deflection in right-sided lead V1 results from the normal predominance of LV forces).
  • NOTE: Computer interpretations almost always miss detection of a Tall R Wave in Lead V1. Many (if not most) clinicians also often overlook this important finding if they are not systematic in their approach. This is precisely the reason why I add an R” to my memory aid of looking for Q-R-S-T Changes” — because it is otherwise all-too-easy to forget about routinely looking to see if R wave progression is appropriate.
  • PEARL: Recognition of a Tall Wave in Lead Vshould prompt quick recall of a list of the 6 Common Causes — one of which is posterior MI. This is highly relevant to this case! (CLICK HERE — for discussion on how to distinguish between these 6 entities).
  • For review of “My Take” on the Systematic Approach to ECG Interpretation that I favor — CLICK HERE —
Returning to this case for the last 2 parameters in my Q-R-S-T assessment of ECG #1 = ST-T Wave Abnormalities:
  • We’ve already noted small-but-present-in-all-3-inferior-lead Q waves. The Blow-Up view to the right of 12-lead for ECG #1 shows the features already highlighted above by Dr. Smith = inferior lead ST elevation straightening of the ST segment upstroke in lead aVF terminal QRS distortion (ie, lack of an S wave and J wavein each of the 3 inferior leads. More than this, the ST-T waves in each of these inferior leads just look” acute (with T waves taller-and-fatter-than-they-should-be).
  • The T wave in lead aVL of ECG #1 is not normal. Instead, the entire ST-T wave in lead aVL is flat — and it shouldn’t be.
  • In the chest leads — T waves in leads V2-thru-V5 (if not also in V6) appear taller-and-more-peaked-than-they-should-be. While I doubted hyperkalemia as the cause — I’d check serum K+ to be sure. More likely, these T waves probably reflect ischemia of uncertain age.
MIMPRESSION of ECG #1: In this patient with a history of documented coronary disease new-onset chest pain — one has to assume new inferior OMI until proven otherwise.
  • ANSWER to the above QUESION: The abnormal ECG findings in the chest leads of ECG #1 that you should have noted before you looked at ECG #2 are: iThe Tall R Wave in lead V1; iiThe Q waves that begin as early as lead V3, and which are a bit deeper-than-is-usually-seen in leads V4, V5 and V6; andiiiChest lead T waves that are taller-and-more-peaked-than-usual. In view of this patient’s history — the combination of these ECG findings suggests possible infero-postero-lateral Mof uncertain age (probably new-upon-old injury). Of note — cath findings on this patient are consistent with my impression of these 3 abnormal findings.

MTHOUGHTS on ECG #2  ECG #2 was done 1 month earlier on this patient.
  • NOTE: We are not told about what was going on clinically 1 month earlier at the time ECG #2 was recorded (ie, we don't know if the patient was admitted for their initial event during that earlier admission). That said — what we can say, is that there has been NO change in chest lead appearance between the time that ECG #1 and ECG #2 were done.
  • I would have loved to see an ECG on this patient prior to development of coronary disease. I bet that the R wave would not be comparable to S wave size in lead V1 — and, I bet chest lead T waves were not so peaked. I’d also be curious to see if there were Q waves of similar size in leads V3-thru-V6 on a prior tracing.

What is different between ECG #1 and ECG #2 — is easily seen in the magnified leads of the Blow-Up magnifications in Figure-1 to the right of each 12-lead.
  • As emphasized by Dr. Smith — 1 month earlier, there was no ST elevation in any of the inferior leads. This confirms that there is a new inferior OMI in ECG #1!
  • Note that 1 month earlier — the ST-T wave in lead aVlooks very different! Thus, in the Blow-Up of ECG #2 — lead aVL showed slight-but-real ST elevation with an upright T wave. This tells us that the flat ST-T wave in lead aVL of ECG #1 actually was reflective of acute reciprocal change (ie, in response to new inferior lead ST elevation — the ST segment and T wave in lead aVL of ECG #1 was acutely lowered compared to what it was 1 month earlier).
  • Note also that there is now no doubt from the Blow-Up of ECG #2 that an abnormal Q wave was already present in the earlier tracing ( = ECG #2) in lead aVL — most probably reflecting a prior lateral infarction.

Additional Learning Points:
  • Sometimes acute reciprocal changes in lead aVL may be masked by prior abnormalities in an earlier tracing. The flat ST-T wave in lead aVL of ECG #1 actually did represent acute reciprocal change — since a month earlier the T wave in this lead was upright, and the ST segment was slightly elevated.
  • It’s easy to miss abnormal ECG findings if you fail to routinely use a Systematic Approach. Thus, in ECG #1 — the Tall R in lead V1 the more-peaked-than-expected chest lead T waves all of those lateral lead Q waves were probably all findings reflective of this patient’s prior coronary injury and coronary anatomy (with disease in the posterior and circumflex circulation). The importance of not overlooking these findings — is that we would not be able to exclude the possibility that these were acute changes if all we had to look at was ECG #1. It was only after locating the tracing from 1 month earlier that we were able determine that none of the chest lead findings in ECG #1 were acute.

Wednesday, June 26, 2019

Serial Evolving ECGs all diagnostic of LAD OMI, but never meet STEMI criteria

A 60-something called 911 for chest pain.

Medics recorded an ECG at time zero:

What to you think?

There is no ST elevation, but V2 has a definite hyperacute T-wave.  Inferior leads have a tiny bit of ST depression (this is very significant).  aVL has a tiny amount of coved ST elevation in the presence of a tiny QRS.  These are all very very suspicious for proximal LAD OMI.

They recorded another at 20 minutes:
Evolving anterior OMI, but with barely any ST Elevation.
 Look at the huge size of the T-wave in V4 relative to the R-wave.
Increasing STE in aVL
Increasing inferior reciprocal ST depression

If you doubted LAD occlusion on the first one, there is no doubt any more.
This is diagnostic
Repeat at 25 Minutes:

Further evolution.
Absolutely diagnostic of acute LAD occlusion.

And another at 30 minutes:

The computer never noticed the myocardial infarction on any of these ECGs.

The patient arrived in the ED.

This is the first ED ECG (at t = 40 minutes):
Computer did not comment on acute MI.
The attending physician brought this to me without any of the other ECGs and asked my opinion:
With 3 seconds, I said:
Acute LAD Occlusion.
It is diagnostic of LAD occlusion all on its own, without even comparing to the others.

This is what my partner thought also, but just wanted confirmation.

The cath lab was activated.

2nd ED ECG 60 minutes
Now there is diagnostic ST Elevation, but barely.
Computer still did not comment on STEMI

A Proximal LAD occlusion was found and stented.

ECG after reperfusion
Typical Reperfusion T-waves, similar to Wellens' waves (and same pathophysiology), but different in that true Wellens' waves have preservation of R-wave.   This has a QS-wave in V2 because of extensive infarction, in spite of rapid reperfusion.

Next day
QS-waves with reperfusion T-waves again

Peak trop I 85.6 ng/mL (very large OMI)

Anterior Wall Motion Abnormality

At no point in time did the computer read a STEMI

Learning Points:

1. Acute LAD occlusion frequently does not manifest ST Elevation that meets "criteria"
2.  Look for hyperacute T-waves (relative to QRS amplitude/voltage)
3. Look for any inferior ST depression, even minimal
4. Do serial ECGs.

Comment by KEN GRAUER, MD (6/26/2019):
Our THANKS to Dr. Smith for this superb example of serial evolution of acute LAD occlusion (OMI— starting in the prehospital phase — passing through the ED — and following reperfusion of the occluded artery.
  • I limit my comments to ECG #1 = the initial ECG done by medics in the field on this 60-something patient with new-onset chest pain. For clarity — I’ve put the 2 parts of this tracing together, and have added a few aids for ST segment shaping to facilitate visualization (Figure-1).
Figure-1: The initial ECG in this case, done by medics in the field (See text).

MTHOUGHTS on ECG #1  Dr. Smith has done a great job with his tracing-to-tracing description of important findings for the 8 ECGs in this case.
  • KEY Take-Home POINT: Given the history of new-onset chest pain in this patient — you should be 100% certain of the need for prompt cath from this 1st ECG alone. Your clinical assessment of ECG #1 in Figure-1 should be acute LAD occlusion until proven otherwise!
KEY ECG Findings in Figure-1:
  • Leads V2 and V3 were the 1st to catch my eye! That the T waves in these 2 leads are hyperacute should be obvious from how disproportionate these waves are compared to the tiny r wave in V3, and lack of any r wave at all in lead V2. Note how fat-at-their-peak and wide-at-their-base these T waves are. Note also straightening of the ST segment upstroke in lead V2 (angled BLUE line in this lead) — such that the normal upward concavity of the ST segment in lead V2 has been lost.
  • There is loss of anterior wavesA tiny initial r wave seems to be present in lead V1. This is completely lost by lead V2 (which manifests a deep QS complex). The r wave returns in lead V3 — but is still considerably smaller-than-it-should-be for a lead V3.
  • Next, looking at neighboring leads” — There is at least 1 mm of ST elevation with definite coving of the ST segment in lead V1 (frowny”-shaped BLUE line in V1). This is not a normal lead V1 appearance — but rather reflects extension of the ongoing process (ie, the hyperacute T waves in leads V2 and V3). Thus, acute ST-T wave changes begin as early as lead V1.
  • Continuing with the concept of neighboring leads” — hyperacute wave changes are clearly seen in lead V4 (with a disproportionately large T wave in V4, that is more than half the height of the R wave in this lead — as well as this T wave in V4 being fat-at-its-peak and wide-at-its-base). Although the T waves in leads V5 and V6 are not particularly tall — they share the fatter-at-their-peak-than-they-should-be appearance that we have already seen in leads V2-thru-V4. Leads V5 and V6 also manifest scooped and slightly depressed ST segments — that in the context of everything else are not normal. 
  • NOTE: Confirmation that ST-T waves in all 6 chest leads were abnormal in ECG #1 is forthcoming through comparison with the last 2 tracings (obtained after reperfusion) in this case.
PEARL: When contemplating the likely location of acute LAD occlusion — I look for the following 3 Clues, which when present suggest a more proximal LAD lesion:
  • Is there ST elevation (or at least acute-looking ST segment covingin lead aVL?Yes, in Figure-1 — as suggested by the coved BLUE line in lead aVL). Note that this ST coving in lead aVL ends with terminal T wave inversion. There is also a surprisingly wide q wave in lead aVL, which may reflect the ongoing acute process.
  • Is there reciprocal ST depression in the inferior leads?Yesin the form of scooped ST segments — as highlighted by curved BLUE lines in these inferior leads). Inferior lead T waves also look prominent in Figure-1 (a bit larger, and fatter-than-they-should-be at their peak).
  • How early in the chest leads do acute/hyperacute ST-T wave changes begin? ( = slight ST elevation with ST coving begins as early as in lead V1 in ECG #1).
Bottom Line: Given the history of new-onset chest pain — You should be able within a minute (or less) of seeing this initial ECG in Figure-1 to: iBe confident in strongly suspecting acute proximal LAD occlusion until proven otherwise; andii) Know that you should immediately contact the cardiologist on call as you are activating the cath lab!
  • As per Dr. Smith — the diagnosis of acute proximal LAD OMI is solidified beyond doubt by subsequent tracings — but these subsequent tracings were not needed to justify immediate cath lab activation in this case. All that was needed given the history of new chest pain — was a quick look at ECG #1 in Figure-1.

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