A 50 year old with chest pain? What is going on? By Emre Aslanger.

Posted by Emre Aslanger, our newest blog Editor. Emre is a distinguished cardiologist in Turkey, and has published widely on the ECG in OMI and other areas.

Emre Aslanger Google Scholar Profile

A 50-year-old male with a 20 years’ history of diabetes mellitus treated with metformin only presents with chest pain that started 20 minutes ago. The pain radiates to left inner arm and is now about to resolve. His admission ECG is given below.

What do you think?

You can click on it to make it larger, but let's make it a bit easier to see here:

What do you think? (you can still click on it to make it larger)

Although the wandering baseline makes it a bit hard to interpret, ST-segment depression in inferior leads are quite evident. This should immediately urge the interpreter to look at high lateral (lead I and aVF) and anterior leads for subtle ST-segment elevation. There seems to be a subtle ST-segment elevation in aVL, which can be easily overlooked if interpreted in isolation. The ST-segment elevation in V1-3 is also highly suspicious. Moreover there is ST-segment depression in V4-6. All indicate a proximal left anterior descending artery (LAD) occlusion myocardial infarction (OMI), which sadly does not meet ST-elevation myocardial infarction (STEMI) criteria.

Despite this, the automated interpretation suggests acute STEMI!  

If you were use the LAD-normal variant STE formula (which is not advised when there is ST depression, which make normal variant all but impossible), you would get 18.89, which indicates LAD occlusion.

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Smith comment: This is strange because the millimeter criteria for STEMI are not met.  How did this conventional algorithm (not a neural network) diagnose STEMI?

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Smith and Meyers comment: We have posted several prior cases of STE in V1 with STD in V5, 6 due to LAD occlusion.  These seem to indicate septal MI, proximal to septal perforator (see below for other cases).  We have coined the term "Procordial Swirl" pattern based on the upward ST-segment shift usually seen in V1-V2/V3 and downward shift in V4/V5-V6, as shown in another example below. Please note: the most important mimic of the precordial swirl sign is seen in cases of LVH, which routinely have STD in lateral leads and STE in V1-V2. 

Here is another example of "Precordial Swirl":

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The clinician in charge was not sure and ordered ECG and troponin follow-up.

A second ECG was taken after 15 minutes. The patient said the pain was almost resolved. 

What do you think?

The subtle ST-segment elevation in lead I, aVL and V2 continues. The ST-segments in inferolateral leads are resolving, but there is still significant ST depression especially in lead III (this should always be considered to be reciprocal to high lateral STE, whether that STE is evident or not -- it is NOT "inferior (subendocardial) ischemia"!!  . Also note the tiny Q wave in V2. Even this ECG is highly suspicious, if not diagnostic, for anterior OMI !

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Smith comment: 

Since I started writing this blog, I have been making the point that "ST depression does not localize," meaning that ST depression in inferior, anterior, or lateral leads does NOT tell you that there is subendocardial ischemia in those leads.  This has been proven by many studies of stress ECGs.  ST depression in II, III, aVF is generally reciprocal to (often unseen) STE in aVL.

ST depression limited to Inferior leads is reciprocal to high lateral wall and represents STEMI

ST depression does not localize: 2 cases of "inferior" ST depression diagnostic of high lateral STEMI (references can be found here)

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The first troponin (hsTnT) turned out to be 9 pg/dL (normal <14 pg/dL). [This is the same as the ng/L, the units used in most of the US and Europe].  As pain was then completely resolved, they decided to wait for a second troponin. 

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Smith comment: If the ECG is diagnostic, as it is here, waiting for the troponin is only acceptable if BOTH ECG and symptoms have resolved

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The second troponin came 69 pg/dL. A diagnosis of non-STEMI was made and a search for a PCI-capable center was commenced. 

Another ECG was taken at 4th hour.

Nearly all ST segment changes returned to normal. Note spontaneous reperfusion caused T-wave inversion in aVL and relatively bulky T-waves in inferior leads ("reciprocal reperfusion T-waves".) 

The patient was transferred to PCI-capable center. A third troponin at three hours after admission turned out to be 320 pg/dL.

Angiogram showed exactly what is expected: a thrombosed stenosis just before the first septal and diagonal artery. 

LAD lesion was successfully stented. The next day echocardiogram showed mid and apical anterior and septal dyskinesia with an ejection fraction of 40%. 

 

Take home messages:

• A subtle ECG does not mean a mild, unimportant lesion.
• Troponin lags and does not reflect the seriousness of the situation. 
• Although this lesion is spontaneously reperfused, the risk of reocclusion is quite high and if it occurred, a significant amount of myocardium would be lost before reaching to catheter laboratory. These patients should urgently be taken to catheterization laboratory.

Research on the ECG in OMI:

If this case were in one of our studies, it would be considered a false positive EKG!!  Our methods in determining retrospectively if the artery was occluded at the time of the ECG recording require EITHER 1) TIMI 0/1 or sometimes 0/1/2 flow OR a culprit PLUS a very high troponin, which for high sensitivity Troponin T is above 1000 ng/L.  In this case, reperfusion was so fast that the peak was at 320 ng/L, and this case would be considered a false positive in one of our studies!!

See these other cases with precordial swirl sign:

A man in his 50s with "gas pain"

A man in his 60s with shockable arrest, then ROSC, and no STEMI - what will you do?

A 49 year old man with chest pain. Is it OMI? is it pseudonormalization?

35 yo woman with LAD occlusion manifesting with only hyperacute Ts and inferior ST depression, also missed by computer

Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB

Very subtle anterior STEMI, TIMI II flow with thrombus

What will you do for this patient transferred to you who is now asymptomatic?

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.

A man in his sixties with chest pain at midnight with undetectable troponin

A 40 year old man with chest pain since last night

A man in his sixties with chest pain, tachypnea, and hypertension

What is the culprit vessel?

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Comment by KEN GRAUER, MD (9/25/2022):

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We welcome Dr. Emre Aslanger as our newest Associate Editor to Dr. Smith's ECG Blog! The problem he addresses in today's case relates to a "theme" well known to our readers: Recognizing subtle signs of an acute OMI that does not meet "STEMI criteria" — but which nevertheless needs prompt intervention.

For clarity and ease of comparison — I have reproduced the 3 serial tracings in today's case in Figure-1.

• I find it easiest to appreciate the serial ECG findings highlighted by Dr. Aslanger — by lead-to-lead comparison — in association with close correlation to the clinical history.

Figure-1: Comparison of the 3 serial ECGs in today's case.

MY Thoughts on the Serial ECGs in Today's Case:

As is so often true — the History in today's case is KEY: The patient is a 50-year old man with the longstanding risk factor of diabetes. He presented to the ED with new-onset chest pain that began just 20 minutes prior to ECG #1. 

• Not only does the presentation of today's patient immediately place him in a "high-prevalence" group for a likely coronary event — but the fact that he presented to the ED so soon (ie, within 20 minutes!) after the onset of symptoms: i) Makes it quite possible that any ECG findings found on his initial tracing will be subtle and not yet fully evolved; and, ii) Makes this patient an optimal candidate for maximum benefit from prompt intervention IF it turns out that he is in the process of evolving an acute cardiac event.

ECG #1:

The rhythm in ECG #1 is sinus arrhythmia at ~90/minute. The axis is normal at +15 degrees. The PR, QRS and QTc intervals are normal. No chamber enlargement.

• Q waves — A tiny, narrow q wave is seen in lead aVL.
• R Wave Progression — Transition (ie, where the R wave becomes taller than the S wave is deep) — is slightly delayed, occurring between leads V5-to-V6. Of NOTE (and potentially relevant given this patient's clinical course!) — is the fact that the R wave increases from lead V1-to-V2 — but then decreases from V2-to-V3 — increasing again in lead V4 — but inexplicably decreasing one more time from V4-to-V5. I thought this repetitive increasing-then-decreasing R wave progression strongly suggested one or more errors with chest lead electrode placement.

Regarding ST-T Wave Changes in ECG #1:

I counted ST-T wave abnormalities in no less than 11/12 leads!

• I thought the most "eye-catching" ST-T wave abnormality was in lead V2. Although slight ST elevation is commonly seen as a normal finding in anterior leads V2 and V3 — this usually does not attain 2 mm, as seen in lead V2 of ECG #1. Even more remarkable is the disproportionately enlarged T wave in lead V2 (with respect to the QRS complex in this lead) — that in a patient with new-onset chest pain strongly suggests a hyperacute change.
• 
  
• Neighboring leads V1 and V3 also manifest taller-than-they-should-be T waves — that I interpreted as a continuation of the hyperacute change seen in lead V2.
• Leads V4 and V5 manifest the unusual appearance of an initially downward-sloping ST segment — that evolves into disproportionate taller-and-fatter-than-they-should-be T waves.
• This appearance of the ST-T waves in leads V4 and V5 made more sense to me when I considered anterior neighboring leads V1,V2,V3 (all of which show hyperacute T waves) — and the neighboring lateral chest lead V6, which shows primarily reciprocal ST depression (ie, leads V4 and V5 being obviously acute — manifest an intermediate picture to its anterior and lateral neighboring leads).
• 
  
• As per Dr. Aslanger — the overall picture of ECG #1 in this patient with new-onset chest pain strongly suggests acute proximal LAD OMI. This impression of proximal LAD occlusion is further supported by the subtle-but-real ST elevation in high-lateral leads I and aVL — and the reciprocal ST depression in all 3 of the inferior leads. 
• 
  
• QUESTION: How might the appearance of the acute ST-T wave changes seen in all 6 of the chest leads been altered — IF chest lead electrodes had been correctly placed?
• 
  
• BOTTOM LINE: Even before troponin results come back positive — this high-risk clinical presentation in today's patient with new-onset chest pain + abnormal ST-T waves in 11/12 leads, including multiple leads with hyperacute T waves — clearly justifies prompt cath after this 1st ECG.

ECG #2:

It's important to emphasize how optimal it is that the initial ECG was repeated in just 15 minutes! The need for quickly repeating the initial ECG became especially important in today's case when the patient's clinical condition changed! (ie, His chest pain had almost resolved within 15 minutes after ECG #1 was done!).

• Interpretation of ECG #2 is best accomplished by direct lead-by-lead comparison (which is facilitated by side-by-side viewing of the first 2 ECGs in today's case, as shown in Figure-1).
• Although subtle — there is definitely less ST elevation in lead V2 of ECG #2 — and there is no longer any ST elevation at all in lead V3. The T waves in these 2 leads clearly look less hyperacute.
• In lead V1 — Not only has the ST elevation completely resolved in ECG #2 — but instead of the straight ST segment takeoff seen in the 1st ECG, the ST segment is now distinctly flat.
• In the lateral chest leads (V4,V5,V6) — although T wave size has not appreciably changed — there is no longer ST segment flattening or depression in any of these leads.
• In the inferior leads — the reciprocal ST depression previously seen in ECG #1 has now almost resolved.
• In lead aVL — the T wave has become smaller in ECG #2.
• The only lead not to show any ST-T wave change is lead I.

Putting It All Together:

Although only 15 minutes passed between the time that ECG #1 and ECG #2 were recorded — the patient's chest pain virtually resolved during this period and at the same time, there was improvement in ST-T wave morphology in 10/11 leads that showed abnormalities in ECG #1. This qualifies as clear evidence of "dynamic" ST-T wave changes in a patient who presented to the ED for new chest pain less than 1 hour earlier.

• As per Dr. Aslanger — Acute proximal LAD OMI should be assumed until proven otherwise. Although relief of chest pain and resolution of acute ST-T wave changes suggests spontaneous reperfusion of the occluded vessel — the risk of reocclusion remains high.
• Troponin may not become significantly elevated if the period of vessel occlusion is very brief (ie, when there is rapid spontaneous reperfusion). The decision to perform cardiac catheterization should not have to wait for troponin to become elevated.
• Clinically in Today's Case — Conditions could not have been better for potential optimal benefit from prompt cath with PCI of the "culprit" vessel to prevent reocclusion.

ECG #3:

To Emphasize — Prompt cath was indicated in today's case, if not immediately (after ECG #1) — then 15 minutes later after ECG #2.

• Although ECG #3 was not needed for diagnostic purposes — interpretation of this 3rd tracing adds further support to the conclusions drawn from review of the first 2 ECGs. As per Dr. Aslanger — Chest lead ST-T wave changes have essentially normalized in ECG #3 — with reperfusion changes evident in the limb leads (ie, T wave inversion in lead aVL — and flat ST segments with bulky inferior T waves).