A 65 year old with chest pain, ECG recorded at 50 mm/sec

This case was sent by Peter Hammarlund, from Stockholm, Sweden:

Hi Steve,

What would you say about this ECG?

A 65 yo smoking man with a prior MI 15 years ago who lives in Stockholm, but who was in southern Sweden on vacation. There was no other known previous illness. 

He suddenly experienced central chest pressure, 9/10, without radiation, but with associated nausea. 5/10 after sublingual NTG.

This prehospital ECG was sent to the Hospital and I was on the night shift and reviewed the ECG. What do you say?

This is recorded at 50 mm/sec on the left (12-lead), and 12.5 mm per sec on the right (for rhythm).
That's the way they do it in Sweden.
For an image that may be easier to interpret, I have horizontally compressed the ECGs at the bottom.

Peter,

Good to hear from you!

LAD occlusion.  Could be a D1 occlusion.

V2 with hyperacute T-wave

II, III, aVF with STD

Tell me!

Steve

Peter:

"But you were of course right, Steve!

I saw this and I immediately recognized the hyperacute T wave in V2 and the reciprocal ST segment changes in the inferior leads as well as the subtle STD in the lateral leads." 

"The ECG was highly suspicious for LAD occlusion (however, a couple of years ago before I started reading your blog I probably wouldn’t have picked this up)." 

"Our cath lab is currently only available during office hours so I had to decide if the patient was in need of immediate coronary angiography and in that case he would have to be transported to Lund University Hospital (30 minutes by ambulance). Since I know that these patients sometimes are difficult ”to sell” and the ambulance wasn’t far from our ED, I called the paramedics and told them to transport to our ER (with highest priority) for a rapid evaluation and probably an immediate transfer to Lund." 

"When the patient arrived ~10 minutes later a new ECG was obtained about 35 minutes after the first:" 

This again is recorded at 50 mm/sec on the left, and 12.5 mm per sec on the right.
For an image that may be easier to interpret, I have horizontally compressed the ECGs at the bottom.

Peter: "Now there are T waves of hyperacute appearance in both V2 and V3, with some new STE in V3."  

"The patient wasn’t in apparent distress, but stated that he was having continuous chest pressure (5/10). I performed a rapid bedside echo where I saw an RWMA in the apical-septal region. Within 10 minutes from arrival in our ED I called the cardiologist on call in Lund who accepted the patient and activated their cath lab." 

"The patient was immediately transported to Lund. A subtotal occlusion in mid-LAD (99% stenosis with TIMI-2 flow) was opened and stented. Hs-TnT rose from 44 to ~450 ng/L. The patient had a great outcome with EF in the lower normal range and hypokinesis of the apico-septal wall on formal echo. He was discharged two days later." 

"What I found interesting is that both the 3- and 4-variable formula predicts this to be BER (I get 22.80 and 18.02 on the 1st ECG, respectively; the latter being quite close to the "STEMI” cut-off). I usually rely on my visual impression so I must admit that I don’t use the formulas that often." 

"However, I guess the formulas are not applicable in this case because of the STD? Exactly correct, Peter!    To my understanding the exclusion criteria were a sum of 1 mm STD in the inferior leads (I’m not sure that he fulfills that criteria) or STD in the lateral leads (any STD?).  I don’t recall reading any millimeter cut-off defining significant STD in the lateral leads) so I guess this case would have been excluded in your studies? (At least based on the lateral STD)." 

Yes!! ANY ST depression in precordial leads is an exclusion and the first ECG has STD in V4 and V5.  Normal variant ST elevation is never associated with ST depression on other precordial leads; thus, the STE in V2 must be ischemic until proven otherwise.

"I guess this case is a reminder that one should pay attention to hyperacute T waves and be aware that the formulas shouldn’t be used (or at least should be used with great caution) if the patient fulfills one of the exclusion criterias. Also, echo is super useful in these borderline cases, as you’ve mentioned several times on your blog!" 

Here I have compressed ECG 1 horizontally so it looks more like a 25 mm/second ECG:

Here is ECG 2 compressed horizontally:

Learning points:

1. Recognise hyperacute T-waves
2. ST Elevation in precordial leads is not normal variant (early repol) if there is any ST depression in precordial leads
3. ECGs that are recorded at "paper" speed that is different from what one is accustomed to can be very difficult to read.

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Comment by KEN GRAUER, MD (9/26/2018):

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As an American physician — I had not in the past been exposed to ECG formats other than those used in the United States. Now that I’m actively participating in multiple internet ECG forums with a large international audience — I’ve become well aware that other countries do some things differently ...

• NOTE: In addition to recording the ECGs shown in this case at 50mm/second speed (instead of at 25mm/second, as is standard in the U.S.) — the Cabrera Format was used (Figure-1). In this recording format — the vertical limb lead display begins with lead aVL (within the small BLUE rectangles) — and, reversed polarity is used for lead aVR (= -aVR, as shown within the small PURPLE rectangles). For additional details regarding the Cabrera Format that is used in certain other countries — CLICK HERE—

Figure-1: Side-to-side comparison of the 2 ECGs included in this case. Note that the Cabrera Format was used. Note also that instead of the original ECGs presented by Dr. Hammerlund, I show the 2 tracings that Dr. Smith compressed horizontally, so that their morphologic appearance looks more like a 25mm/second ECG (See text).

CONFESSION: I have difficulty interpreting 12-lead ECGs that have been recorded at 50mm/second speed. I believe the reason for this is interesting:

• Although I teach and religiously employ in my own interpretation a Systematic Approach to ECG interpretation — engrained in my brain from the past 45+ years of regular exposure to countless ECGs are the data from pattern recognition of all tracings that I have ever seen. This is the experiential process that allows near instant recognition by experienced interpreters of the most important ECG findings for almost any tracing.
• All of this “data” in my brain is invalidated the moment I am shown a tracing recorded at 50mm/second speed. Other clinicians may be far better than me at making the transition from a 25mm/second tracing to one recorded at 50mm/second — but no matter how hard I try, I find myself in the uncomfortable position of no longer being able to draw on my “internal data bank” of what looks to be normal vs abnormal. Instead, I feel like a novice interpreter once again … (This is why I so greatly appreciate Dr. Smith’s compression of the 2 tracings in this case — as shown in Figure-1).

Comment on Figure-1: There are subtle abnormalities in multiple leads in both tracings — with progression of findings, at least in leads V1, V2 and V3 in ECG #2 obtained 35 minutes later.

• As per Drs. Hammarlund and Smith — the principal initial finding in ECG #1, obtained from this 65yo man with severe new-onset chest pain is the hyperacute ST-T wave (taller and fatter-than-it-should-be) in lead V2 — that occurs in association with subtle inferior and lateral chest lead ST depression.
• I would add that lead V1 in ECG #1 also looks distinctly abnormal. The ST segment takeoff in this lead is straight, with slight J-point ST elevation and a coved shape to the ST segment. This is not the usual ST-T wave appearance in lead V1.
• As astutely picked up by Dr. Hammarlund — there has been progression in the amount of ST elevation and the hyperacute appearance for leads V2 and V3 in ECG #2.
• I would add that there has also been progression in the amount of ST elevation and the hyperacute appearance of the ST-T wave in lead V1 in ECG #2. And, without change in the relative size of the R wave-to-S-wave in lead V4 between ECG #1 and #2 — the T wave is now relatively taller in this 2nd tracing (it is now almost 2/3 the height of the R wave in this lead).
• NOTE: Although the T wave in lead III of ECG #2 is now clearly inverted — the significance of this change is difficult to assess given slight variation in the frontal plane axis (the QRS complex in lead III is now predominantly negative — whereas it was predominantly positive in ECG #1). However, since QRS morphology in all chest leads for both tracings is virtually unchanged — there is no doubt that the above noted progressive ST-T wave findings in this patient with new chest pain are real and significant!

Our THANKS to Drs. Hammarlund and Smith for presentation of this superb case!