Saddleback ST Elevation. Is it STEMI? Is it type II Brugada?

A 50-something presented with epigastric and chest pain.

Here is his ECG:

What do you think?  QTc 388 ms.

Computer interpretation:

SINUS RHYTHM
INCOMPLETE RIGHT BUNDLE BRANCH BLOCK
ST ELEVATION, CONSIDER SEPTAL INJURY
***ACUTE MI***








There is a saddleback, which is rarely due to MI.  V2 has the morphology of type II Brugada, as there is a relatively large beta angle, described here:

Explanation
1. Draw a horizontal line from top of r' wave (black line 1)
2. Draw a horizontal line 5 mm below this (green line 2)
3. Extend the downsloping r'-ST segment (black line 3) until it intersects the green line
4. Measure the base.  
If greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree beta angle)

However, whenever you see an rSR', especially with a saddleback, think of lead placement.

Then look at the P-wave in V2.  Is it fully upright?  If not, then there is probable high placement of lead V2.

I went back to look and, indeed, V1 and V2 were placed too high.

I put them in the correct position and we recorded another ECG:

Now the P-wave in V2 is upright.  The lead is placed correctly.
Looks like typical normal variant ST elevation (otherwise known as early repolarization)
QTc 384

You can use the LAD-Early Repol Formula to differentiate this from LAD occlusion:

ST elevation at 60 ms after the J-point, relative to PQ junction (STE60V3), = 2.5mm
QTc by computer = 384
R-wave amplitude in V4 (RAV4) = 19mm
Total QRS amplitude in V2 (QRSV2) = 17.5mm

Any of these calculators work:
Use the iPhone app: SubtleSTEMI
Use the Android app: ECG SMITH
Use the link at the top of the blog.
Use MDcalc.com: https://www.mdcalc.com/subtle-anterior-stemi-calculator-4-variable

4-variable formula: 15.1 (A value less than 18.2 favors early repol.  This value is very low.)

The patient was diagnosed with reflux

Learning Points:

1. Saddleback ST Elevation is almost never STEMI
2. Saddleback STE may be type II Brugada syndrome
3. A Type II mimic may result from leads V1 and V2 placed too high
4.  An inverted P-wave in lead V2 implies lead misplacement too high


Saddleback in STEMI:

Here are the only 2 ECGs with V2 "saddleback" that I have ever seen which really represented an LAD Occlusion:

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

A Very Subtle LAD Occlusion....T-wave in V1??

Here are other cases of saddleback STE:

Is this Saddleback a STEMI??

Epigastric pain, Syncope, and Saddleback ST Elevation

A 65 Year Old Man with Chest pain and Precordial ST Elevation

Non-Vagal Syncope and Saddleback Morphology in V2

Is this STEMI? Pattern Recognition is Key

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My Comment, by KEN GRAUER, MD (11/28/2018):

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Great case for illustrating a number of important concepts — albeit it raises a series of questions without definite answer. For clarity — I put both tracings together in Figure-1. For the purpose of fostering discussion — I’ll play “Devil’s Advocate” with my comments below:

Figure-1: TOP ( = ECG #1) — Initial ECG in this case. BOTTOM ( = ECG #2) — Repeat ECG after verifying correct lead placement. The lead V1 and V2 electrodes had been placed too high on the chest in ECG #1 (See text). 

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ECG #1: ( = the Initial Tracing):

The initial concern at the time ECG #1 was obtained was whether the ST elevation in leads V1 and V2 was indicative of acute OMI. As it turned out — leads V1 and V2 were placed too high on the chest, so that ECG #1 was not a valid tracing for such assessment. That said — I think it worthwhile to specify reasons why even if lead placement had been correct, acute OMI would still be unlikely on the basis of this initial ECG:

• The shape of the ST elevation in leads V1 and V2 in ECG #1 is concave up, which is usually a benign morphology. As per Dr. Smith — the “saddleback” configuration (seen best here in lead V2) is rarely due to acute MI.
• Apart from leads V1 and V2 — there really is no abnormal ST segment deviation. The slight ST elevation seen in lead V3 does not exceed the 1-2 mm of concave-up ST elevation commonly seen in leads V2 and/or V3 with normal repolarization variants. No other lead shows any ST elevation. There is no reciprocal ST depression. So, even if all leads had been correctly placed in ECG #1 — I would not have suspected acute OMI.

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Assessing for a Brugada-2 ECG Pattern:

A “saddleback” (ie, Brugada-2) ECG pattern is assessed for by applying the criteria in the Figure explained by Dr. Smith above. I illustrate application of these measurements in the magnified insert of the middle complex in lead V2.

• In ECG #1 — the base of the triangle (horizontal PINK line) formed by drawing lines from the peak of the r’ in lead V2 looks to be extremely close to 3.5 mm, which is right at the upper limit qualifying for a Brugada-2 pattern.
• Criteria for a Brugada-2 ECG pattern disappeared once the V1 and V2 electrodes were correctly positioned (See ECG #2 in Figure-1). While disappearance of the saddleback pattern in lead V2 after repositioning of the V1, V2 electrodes is comforting — it should be appreciated that in some patients with Brugada patterns, the ECG abnormality may only be seen with higher-than-usual electrode lead positioning (ie, in the 2nd or 3rd interspaces). This is because the abnormal electrical activity leading to a Brugada ECG pattern arises from a very limited zone located in the RVOT — and in some patients this electrical zone requires higher lead placement for detection. This raises the difficult-to-answer clinical question of when to do additional ECGs on a patient with placement of leads V1,V2 in the 2nd and/or 3rd interspaces?
• When associated with appropriate clinical features (ie, personal history of cardiac arrest, polymorphic VT, non-vagal syncope, positive family history of sudden death at an early age, etc.) — then spontaneous occurrence of a Brugada-1 ECG pattern is diagnostic of Brugada Syndrome. On the other hand — isolated occurrence of a Brugada-2 pattern is non-diagnostic, although when associated with other features, it may raise clinical suspicion and warrant pharmacologic challenge and/or referral to EP cardiology.

For More on Brugada ECG Patterns:

• Dr. Smith’s March 26, 2015 post has great illustrations reviewing assessment for a Brugada-2 ECG pattern.
• My 29-minute ECG Video on the topic reviews the basics of recognizing Brugada-1 and Brugada-2 patterns, with detailed discussion of Brugada Syndrome.

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Regarding Malposition of Leads V1 & V2:

Dr. Smith’s suspicion of lead malposition in this case was invaluable for accurate diagnosis. He then confirmed his suspicion by checking the patient himself to see where the V1, V2 electrodes had been placed — and followed this up by repeat ECG that revealed the patient’s “true” ECG.

• We’ve previously reviewed clues to quickly Recognize V1, V2 Misplacement (Click HERE).
• I was admittedly less suspicious about lead V1,V2 misplacement in this case — because: i) The negative component of the P wave in lead V2 is relatively modest; ii) The P wave and QRST morphology in leads V1 and V2 looks quite different from the all-negative P wave and QRST complex appearance in lead aVR; and, iii) The distinct terminal S waves in both leads I and V6 suggested to me that the r’ in leads V1 and V2 might simply be explained by the presence of incomplete RBBB. That said, Dr. Smith’s suspicion was correct — and the saddleback pattern disappeared on the repeat ECG.

ECG #2: Some Unusual Findings:

As discussed by Dr. Smith — this patient’s “true ECG” ( = ECG #2) no longer manifests a saddleback pattern, and does not show any acute changes. Nevertheless — there are some additional ECG findings worthy of mention.

• There is a surprising amount of fragmentation of the QRS complex in ECG #2. For example, the QRS complex shows a 4-component (rSr’S’ ) QRS deflection in lead III. Multi-fragmented complexes are also evident in leads aVL and aVF. S waves are present in 11 of the 12 leads on this tracing. Clinically — the significance of these unusual findings is uncertain — though “fragmentation” often indicates “scar”, and might reflect underlying cardiac disease. Whether to explore this possibility further would depend on clinical correlation.