Thursday, December 29, 2016

Only the ECG Diagnoses Acute Coronary Occlusion. Do not be Fooled by a Negative High Sensitivity Troponin.

This case was sent by Peter Hammarlund, 2nd year Internal Medicine/Cardiology resident (and self-proclaimed ECG nerd) at Helsingborg Hospital, Sweden.  

Peter frequently sends me great cases like this, but I never post them because the Swedish standard, explained below, is very difficult to interpret.

This time I could not resist.

Especially interesting is the troponin data and the manipulated images seen below.


Hi Steve,

I was involved in this highly interesting case just the other week.

A previously healthy young man (in his 20s), who smokes two cigarettes a day and has a family history of MI (his father had his first MI in his early 50s), was brought to our ED by ambulance with severe central chest pain without radiation for one hour. The pain was not relieved by Nitroglycerine and only slightly relieved by morphine. 

Smith comment: do NOT use morphine until you are either: 
1) committed to the cath lab (or other definitive diagnostic modality, such as CT for dissection or PE)
2) CERTAIN that the pain is not due to serious pathology. 

Case continued

He was tachycardic, but his vitals were otherwise initially normal. 

The initial high sensitivity troponin T was 5 ng/L.
(99% reference is 14 ng/L, or less than 15 ng/L; Level of detection is 5 ng/L).

I was working in our CCU when the cardiology consultant (who was sitting right next to me) got a phone call from the ED doctor taking care of the patient. While he presented the case to the consultant we looked at the prehospital ECG (attached as EKG1, time 7.53 am) and the ED ECG (attached as EKG2, time 8.10 am). 

At the moment (time 10.45 am) the patient was in the radiology department performing a CT aorta, but right after the CT he developed shortness of breath and only had a saturation of 88% with 15 L/min of O2.

I was immediately very worried about the patient when I saw the ECGs.

What do you say? My answer is below.

Note on technique: These are recorded at the Swedish standard of 50 mm/second.  So all intervals appear twice as wide as you are accustomed to!  Furthermore, there is only one average complex per lead.
What do you think?

Here is my answer, after a quick glance:

Hyperacute T-waves are developing over 17 minutes in V2-V4.  LAD occlusion or at least dynamic thrombus.

As an afterthought just this minute before posting, I compressed the ECGs to 25mm/sec.  The difference becomes much more obvious to me:
Peter's Detailed Comment on the ECG interpretation:

The ECG at t = 0 (prehospital ECG) shows sinus rhythm with a minimal ST depression in V3-V4 as well as minimal ST depression in the lateral leads. No significant ST depression is seen in the inferior leads although there is a TWI in lead III that could be non-specific. However, the T wave in V2 looks abnormally large with a hyperacute appearance. Young people might indeed have large T waves in the anterior leads, but the T wave is in fact as large as the whole QRS complex. The positive T wave in V1 could indicate an early sign of anterior ischemia. Although many of these findings may be considered non-specific the appearance is highly unusual in a previously healthy 28 yo man. With a complaint of ongoing chest pain, this is worrisome.

The ECG at t = 17 min (1st ECG in the ED) shows no significant change in V2, but the T wave in V3 is now also hyperacute and the T wave in V4 is also a bit taller. Since the QRS complexes don’t look exactly the same, some of the ST-T changes may be due to different lead placement, but the dynamic change in V3 is too abnormal to ignore. The ST depression in the lateral leads are now gone – could this be pseudonormalisation? There might even be a tiny bit of ST elevation in aVL, and development of slightly downsloping ST segment in the inferior leads (at least aVF and III). Although neither of these ECGs are clearly diagnostic of MI alone, the dynamic changes in combination with a presentation consistent with ACS is highly worrisome.

Smith comment: The ST depression is due to early, and possibly incomplete, LAD occlusion, which is often called "de Winter's T-waves" a type of hyperacute T-wave.  17 minutes later the artery is completely occluded and the ST depression has become ST elevation.  

There should NEVER be ANY ST depression in the precordial leads of a young man.

Peter's response:

You are of course spot on. Me and my colleague saw this immediately, and since these ECGs were recorded 2½ hours before the consultant got the phone call we were very worried about the patient. 

EKG3 (not shown) was recorded 2.5 hours later (Smith comment: treatment was very delayed!) during the consultation and the diagnosis was now obvious with a huge anterolateral STEMI.  The providers had not noticed the ST depression nor the diagnostic T-waves.

Echo hadn't been performed initially, but showed EF 40% and akinesis of the anterior wall. CT of the aorta was of course normal. CT of the lungs showed bilateral infiltrates with gravitational distribution, that initially were interpreted by the radiologist as infectious, but in retrospect were considered to be flash pulmonary edema. 

The patient went for coronary angiography that showed an almost complete occlusion in the distal part of LM with a stenosis extending into the proximal part of the LAD

During PCI the patient needed CPAP and small doses of norepinephrine. He was fully revascularized and was initially admitted to the ICU, but could be moved to the coronary care unit the next day. A formal echo a couple of days later showed EF 50%. The hospitalization was prolonged, due to the development of fever and a small pericardial effusion (postinfarction syndrome?), but otherwise the patient did OK. 

This case was up for discussion the next day in our clinic, and I pointed out the subtle, but real dynamic changes, that might have been picked up, not delaying the diagnosis for another 2½ hours.

Many of my colleagues still considered the initial ECGs to be practically normal, although I pointed out that these findings might be considered non-specific if the patient was presenting with e.g. cellulitis in the leg, but highly worrisome in this particular case, since the patient was having ongoing chest pain. 

Another thing that made the case a bit more complicated was that the initial hs-Troponin T was only 5 ng/L (positive at < 15 ng/L, level of detection at 5) i.e. not positive, but just above the level of detection. This was when the chest pain had been going on for a little more than one hour. 

I think that the ED physician might have been fooled by this. The next troponin measurement in the ICU (6 hours after the onset of chest pain) showed a level of >9998 ng/L. 

In retrospect this was indeed a tricky case, but as I pointed out to my colleagues we should learn from it rather than just call it tricky and convince ourselves that it was unavoidable. 

Regarding the use of your formula: I believe if you use it on the 2nd ECG it comes out positive with a value of 23.678 (if I measured correctly using 2.5 mm of STE at 60 ms, QTc of 428 and RV4 of 14 mm) clearly indicating subtle STEMI.  (A value greater than 23.4 is nearly diagnostic of LAD occlusion in the right circumstances)

Here I have superimposed the ECGs so that you can see the evolution more clearly.  The darker lines are the second ECG at time = 17 minutes after the first:
Notice the significant increase in T-wave amplitude in V3 and V4.
Notice also the new but subtle ST Elevation in I and aVL, with reciprocal ST depression in lead III.

The formula is negative in the 1st ECG due to minimal STE at 60 ms after the J-point in lead V3.
(Remember that 60 ms in this recording format is 3 little boxes, not 1.5)
The formula is positive in the 2nd ECG.
Referring to: Formula for differentiating normal STE from STE due to LAD occlusion

Here it is compressed:

Take home points: 
1) Young people do have MI.
2) Beware hyperacute T-waves
3) Beware any ST depression in precordial leads
4) Do not mask your diagnosis with Morphine (or other opiates)
Serial ECGs would probably have made the difference in this case. 
5) Echo is very helpful in these situations.
4) Don't rely on the first troponin, even if high sensitivity (if there is a short time from the onset of chest pain to the blood testing) 


Comment on the formatting:

In Sweden the different leads usually are presented in the so called Cabrera sequence, which basically means that lead aVR is replaced by -aVR (i.e. aVR with switched polarity, which gives the lead an “up-side-down” appearance) and that the limb leads are presented in a anatomically contiguous order (aVL = -30°; I = 0°; -aVR = 30°; II = 60°; aVF = 90° and III = 120°). This means that the inferior leads are presented next to each other (vertically) and that the high lateral leads (aVL and I) are placed next to each other with -aVR in between. This makes it easier to spot ST-T-changes localized to a specific anatomic area of the heart (at least if you are used to the formatting).

In this case the recordings also have another feature. The tracings that are recorded with a paper speed of 50 mm/s are so called signal-averaged ECGs. There is only one complex presented in each lead, which is an artificially created “mean value” of several ECG complexes. The point of this is to eliminate artifacts. 

On the right side (not shown here) we display short rhythm strips at a paper speed of 12,5 mm/s (thereby looking twice as fast as usual if you’re accustomed to a paper speed of 25 mm/s).  


  1. What's the thought behind avoiding morphine?

    1. It masks the symptoms, makes you believe that you have helped the underlying problem. That is why it is associated with increased mortality.

    2. Hmm, never thought of it that way! Would that mean fentsnyl would have the same effect and be equivalent to morphine for cardiac related chest pain?

    3. Theoretically, but not studied, as morphine has been:

      Meine, T. J., et al. (2005). "Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative." Am Heart J 149(6): 1043-1049.
      see pdf at clinical pathway/myocardial infarction/morphine.pdf

      BACKGROUND: Although intravenous morphine is commonly used for the treatment of chest pain in patients presenting with non-ST-segment elevation acute coronary syndromes (NSTE ACS), its safety has not been evaluated. The CRUSADE Initiative is a nonrandomized, retrospective, observational registry enrolling patients with NSTE ACS to evaluate acute medications and interventions, inhospital outcomes, and discharge treatments. METHODS: The study population comprised patients presenting with NSTE ACS at 443 hospitals across the United States from January 2001 through June 2003 (n = 57,039). Outcomes were evaluated in patients receiving morphine versus not and between patients treated with morphine versus intravenous nitroglycerin. RESULTS: A total of 17,003 patients (29.8%) received morphine within 24 hours of presentation. Patients treated with any morphine had a higher adjusted risk of death (odds ratio [OR] 1.48, 95% CI 1.33-1.64) than patients not treated with morphine. Relative to those receiving nitroglycerin, patients treated with morphine also had a higher adjusted likelihood of death (OR 1.50, 95% CI 1.26-1.78). Utilizing a propensity score matching method, the use of morphine was associated with increased inhospital mortality (OR 1.41, 95% CI 1.26-1.57). The increased risk of death in patients receiving morphine persisted across all measured subgroups. CONCLUSIONS: Use of morphine either alone or in combination with nitroglycerin for patients presenting with NSTE ACS was associated with higher mortality even after risk adjustment and matching on propensity score for treatment. This analysis raises concerns regarding the safety of using morphine in patients with NSTE ACS and emphasizes the need for a randomized trial.

  2. Great case by Peter (who is known to us for his periodic contributions to various ECG forums). While a similar display format (with no more than minor variation) is used for ECG recording throughout the United States — variations in format are used in many countries. Since many of us only rarely (if ever) see ECG recording formats that differ significantly from our own — it is easy to miss important findings when other formats are used. Given the exponentially increasing use of the internet for international medical correspondence (with now literally scores of international Facebook ECG forums) — plus ever expanding daily use of smart phone photographs for rapid remote consultation with experts regarding problematic ECGs — the clinical reality is that virtually ALL clinicians will from time-to-time encounter ECG formats that differ from a format we are used to. Thus, it clearly IS beneficial to post at least occasional tracings with Cabrera format and/or 50mm/second recording speed (as is used in a number of countries). I fully admit that the “picture” of 25mm/second recordings is etched ever-so-unforgettably in my brain. This is why after viewing numerous thousands of tracings over the past 40+ years — I am usually able within no more than a few seconds (if not instantly) to recognize all key abnormalities. However, with Cabrera format + 50mm/second speed recording — I am back to “square one” as a beginner — simply because of unfamiliarity (and without my brain’s picture reservoir of what is or is not “normal”). That is why it is so GOOD to continue being exposed to ALL ECG formats — because in this world made so much smaller by instant internet availability — we ALL will certainly see more tracings sent to us from countries using formats that differ to the one we are most accustomed to. — P.S. — Compression of 50mm/sec recordings to half their width is a PEARL that immediately put my brain “at ease”, and tremendously facilitated my confidence in that what I thought I was seeing (at 50mm/sec) was indeed real, and highly suggestive of a DeWinter T wave pattern. THANKS again to Drs. Steve Smith & Peter Hammarlund for this intriguing post!

  3. Hi Dr Smith Thanks for a brilliant concise post. I'm a junior doctor. One of my consultant only looks at first trop. Is there any role for 2nd or even 3rd (4..5.. etc.) trops in cardiac sounding chest pain? Thanks.

    1. Only a repeat troponin with a very short interval (30 minutes, or 1 hour) will detect such an infarct quickly enough to prevent much loss of myocardium.

  4. As I said before, EKG cycle is going much faster than any hyperSensitive Troponin Cycle!!!

  5. The present case is really excellent from the learning point of view. I learned constantly from this blog to beware hyperacute and large T waves. Despite my initial troubles with the Cabrera format, I highly appreciated the entire case. Thanks for posting!

  6. Correct me if I am wrong but wouldn't it be inappropriate to use the formula for differentiating normal STE from STE from LAD occlusion due to obvious signs of occlusion on these ECGs (ST depression and TWI)?

    1. You are correct!! But it is fun to do it anyway.

  7. This is a great case! Thanks for sharing. My only question is regarding usage of the equation to differentiate benign STE from STE from LAD occlusion. Correct me if I am wrong but I do not think it would be appropriate to use the equation in this case as there are signs of ischemia (TWI and ST depression).


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