A 40-something man with very elevated blood pressure and acute severe chest pain

This 40-something male whose only medical history was hypertension presented with acute chest pain.

A 12-lead ECG was immediately recorded within minutes of arrival at triage: 

What do you think?  

Is the STE in V2-V4 due to normal variant ST Elevation (so called "Early repolarization") or is the STE due to LAD Occlusion (OMI)?

The very astute triage physician immediately recognized LAD Occlusion (LAD Occlusion MI or OMI).  Why?

There is some ST elevation, but it does not meet "STEMI criteria".  But there are hyperacute T-waves (wide and "bulky" in proportion to the QRS). There are also down-up T-waves in III and aVF, which is a quite specific sign of LAD OMI.

Moreover, there is a touch of ST depression in lead V6; normal variant STE never has any ST depression except for lead aVR.

In a male over age 40, the Universal Definition of MI accepts as normal up to 2.0 mm STE in V2 and V3 and up to 1 mm in all other leads (for women it is 1.5 mm, and for men under age 40 it is 2.5 mm).  There are not 2 consecutive leads meeting these criteria.  But as we always point out, ＜50% of acute Occlusion MI meet these criteria.  

David Marti et al. found that 18% of LAD Occlusion have no lead with more than 1 mm STE.  Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction.  And there are many other similar publications.

If we apply the formula for differentiating LAD Occlusion from Normal Variant STE, and we use QTc of 436 ms (computer measured), R-wave amplitude in V4 = 14 mm,  QRS in V2 = 7 mm,  and STE at 60 ms after the J-point = 2.5 mm, we get 20.5, which is very high and confirms LAD Occlusion.

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2 days ago I posted an ECG with normal ST Elevation that could mimic OMI.  

Here is today's ECG placed below that normal ECG: 

Normal on top; LAD OMI on the bottom

In both cases, without measuring anything, an experienced interpreter knew instantly that the top ECG is normal and the bottom one is LAD Occlusion.  

Learn to recognize ECGs in the same way that you recognize faces.

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The cath lab was activated emergently.

In the meantime, the patient's pain dropped from "11/10" to "5/10" and another ECG was recorded at 14 minutes after the first, using exactly the same lead stickers:

What do you think?

This ECG had normalized (due to partial reperfusion)  Such normalization further proves that the first one is diagnostic!

This shows resolution of hyperacute T-waves and of much of the STE.  Notice that, in this ECG, the T-wave in V2 is larger than it was in the first one!!  However, it is SMALLER in proportion to the size of the QRS, and PROPORTION IS ALL THAT MATTERS.  In V3 and V4, the T-wave is now smaller in absolute terms and MUCH smaller in proportion to the QRS.  So this implies spontaneous reperfusion. 

There is also resolution of the small amount of STE in aVL and I.

Notice that the QRS voltage has increased.  Occlusion and reperfusion affect not only the ST-T, but the QRS.

Case continued

Several minutes later while waiting for the cath team, the patient was again having excruciating pain and another ECG was recorded at 32 minutes after the first.

Obvious Anterolateral STEMI [STEMI (+) OMI]

LAD Occlusion Proximal to First Diagonal - we know the location due to the STE in I, aVL and inferior reciprocal ST Depression.

Notice the S-wave in V3 has nearly disappeared.

The patient's blood pressure was very high (170/115) and so he was given several sublingual NTG and also started on a Nitroglycerine drip and titrated up to 150 mcg/min until blood pressure was 150/90.  We should have given him metoprolol, as this is indicated in anterior STEMI of symptom duration less than 6 hours, going to cath lab, with Systolic BP ＞120 mmHg (mortality decreased in randomized trials).  See the discussion of beta blockade for Anterior STEMI at this post.  (We only thought of that after cath lab was ready.)

The patient was taken to the cath lab and found to have a thrombotic 99% Proximal LAD Occlusion with TIMI-1 flow (greatly decreased flow).  

We do not know whether or not there would have been any flow (TIMI-0 vs. TIMI-1) at the time of the ECG.  [We do know that only 64% of True STEMI have TIMI-0 flow; 36% have TIMI 1, 2, or 3 flow. This is because coronary thrombi are dynamic, and change between the time of the ECG and the time of the angiogram.]

The LAD was opened and stented.

Next Day:

Reperfusion T-waves, identical to Wellens' waves

The initial high sensitivity troponin I was 236 ng/L.  No further trops were measured.

Echo showed no wall motion abnormality.  Rapid recognition and cath lab activation saves myocardium!!

The patient was discharged from the hospital 48 hours after admission.

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MY Comment, by KEN GRAUER, MD (2/21/2022):

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Today's case is an excellent one for honing our skills in recognizing acute OMI in the absence of satisfying millimeter criteria for an acute STEMI. As per Dr. Smith — In a patient with new-onset chest pain — the initial ECG in today's case (that I reproduce below in Figure-2) — is diagnostic of acute LAD occlusion.

• By way of review — I wanted to summarize those ECG findings, that when seen in association with new cardiac symptoms — should immediately suggest acute OMI regardless of whether or not millimeter-based criteria for a STEMI are met (Figure-1).

Figure-1: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

WHY is ECG #1 Diagnostic of Acute OMI?

I focus my comments on a number of findings in the initial ECG (Figure-2). These highlight the 1st and 3rd bullets in the Table shown above in Figure-1.

• As per Dr. Smith — there are hyperacute T waves. Realizing that this term is subject to individual interpretation — I define "hyperacute" T waves as being disproportionately tall and/or fatter-at-their-peak or wider-at-their-base than should be expected given R wave and S wave amplitude in the lead being looked at. Simply stated — Hyperacute T waves are overly "voluminous", in that they take up more than the expected amount of space under the T wave.
• 
  
• Although there is some ST elevation in leads V2, V3 and V4 — there does not have to be ST elevation for T waves to be "hyperacute".
• 
  
• As emphasized in the Table in Figure-1 — the more leads with suspicious findings — the greater the concern for an acute ongoing event. I start with those 1 or 2 leads that are definitely "hyper-voluminous" — which in the case of Figure-2, are leads V2 and V3. Not only does the T wave in lead V2 tower over the small R wave in this lead — but the peak of this T wave is "fat" — and the base of this T wave takes up the major part of the QT interval. 
• Similarly — the T wave in lead V3 is much taller, with a much wider base than expected given the size of the QRS complex in this lead. 
• By the concept of "neighboring leads" — the T wave in lead V4 is also (by my definition) hyperacute. One might not think so if you only looked at the T wave in lead V4 by itself — but given that the T waves in leads V2 and V3 are definitely abnormal — I thought the T wave in lead V4 was clearly more "voluminous" than I would have expected.

But there are other leads in Figure-2 that I assessed as definitely abnormal!

• The ST segments in lateral chest leads V5 and V6 are flattened (straightened RED lines in these leads) — and — these ST segments in V5, V6 are accompanied by relatively low amplitude T waves (ie, Normally, the T waves in these lateral chest leads are not this much smaller in size than T waves in the anterior leads).
• The ST-T wave for the 2 beats in lead V1 look different. IF the "correct" ST segment is that for the 2nd beat in lead V1 — then this subtle ST elevation with ST segment coving is not a normal lead V1 finding.
• In the Limb Leads — there are subtle-but-real abnormalities in 5 of the 6 leads. In addition to the "down-up" T waves highlighted by Dr. Smith that shouldn't be there (BLUE arrow in lead aVF) — the ST segments in leads II and aVF are abnormally straightened (RED lines in these leads). In the context of clearly hyperacute T waves in the chest leads — I took the subtle-but-real ST elevation with wide-based T waves in leads I and aVL as suggestive of hyperacute change. In that context — the small q waves in these high lateral leads might or might not be significant.
• Finally — I thought the inverted T wave in lead III was probably a reciprocal change. To Emphasize: The T wave in lead III may normally be negative, especially when the QRS complex is predominantly negative in this lead. But, given clear abnormalities in the other 2 inferior leads (leads II and aVF) — I interpreted this T wave inversion in lead III as a mirror-image opposite reciprocal change to the subtle ST-T wave abnormalities seen in lead aVL

BOTTOM LINE:

• In this 40-something man with new-onset chest pain — definite hyperacute T waves (with some ST elevation) are seen in leads V2 and V3 — with subtle-but-real ST-T wave abnormalities in no less than 10 (if not 11) of the 12 leads. As was recognized by the astute triage physician — acute LAD occlusion must be assumed until proven otherwise!

Figure-2: I've labed the initial ECG in today's case.

Extra CREDIT:

Did YOU notice that the rhythm in ECG #1 was not sinus?

• Why do I say this?

ANSWER:

We recognize sinus rhythm by the presence of an upright P wave in lead II. The reason for this finding, is that the path of the electrical impulse as it travels from the SA Node toward the AV Node — will be oriented very close to +60 degrees in the frontal plane when the rhythm is sinus. This is why the P wave should normally be tallest in lead II (compared to P wave amplitude in leads I and III).

• Suspect either a non-sinus rhythm or LA-LL Lead Reversal if ever the P wave is clearly upright and larger in lead I compared to lead II (as is the case in ECG #1).
• As per the August 28, 2020 post in Dr. Smith's ECG Blog (Please see the Addendum I wrote at the bottom of the page of that post) — among the changes that occur with LA-LL Lead Reversal are: i) Leads I and II switch places (which is why a sinus P wave will look larger in lead I with this type of lead reversal); ii) Lead III becomes inverted; and, iii) Leads aVL and aVF switch places.
• Since the repeat ECG during chest pain recurrence in today's case showed a normal-appearing upright P wave (much larger than the P wave in lead I at that time) — but without inversion of lead III — we can conclude that the reason for the small P wave in lead II of ECG #1 is not LA-LL lead reversal — but instead simply reflects a Low Atrial Rhythm.
• 
  
• To Emphasize — A low atrial rhythm is often not a pathologic rhythm, and in today's case, the fact that there is a low atrial rhythm has no impact on either treatment or the clinical course of this patient. But the most common mistake I've seen even experienced interpreters make when interpreting arrhythmias — is the failure to spend the 3-5 seconds it takes for your "educated eye" to look in front of each beat in the long lead II rhythm strip to ensure that you always see a clearly upright P wave with constant PR interval before each beat. IF you don't — then something else is going on!
• 
  
• As noted above, among the changes seen when there is LA-LL Lead Reversal — are that lead III will be inverted — leads I and II switch places — and leads aVL and aVF switch places. Failure to recognize this lead reversal in the above referenced August 28, 2020 post completely changed the location and appearance of acutely-evolving ST-T wave changes in the follow-up ECG of that case. PEARL: Be on the alert that IF the P wave in lead I is clearly larger than the upright P wave in lead II — that it's important to find out why!