A man in his 70s with chest pain during a bike ride

Case written and submitted by Ryan Barnicle MD, with edits by Pendell Meyers


While vacationing on one of the islands off the northeast coast, a healthy 70ish year old male presented to the island health center for an evaluation of chest pain. The chest pain started about one hour prior to arrival while bike riding. It was a constant ache on the left side of his chest that forced him to stop cycling and call for an ambulance. It was radiating to his bilateral upper arms. It was associated with nausea but he denied dyspnea, dizziness, and headache.

He explained that he had the same chest pain the day prior as well, on and off. That episode started while climbing a long set of stairs from the beach to the parking lot. His pain radiated to his shoulders throughout the evening and the night but it did not prompt him to seek medical attention.

The patient stated he had a long history of well-controlled hypertension for which he was compliant with his ACE-inhibitor. He was also treated for erectile dysfunction but had not taken any medications recently. He had no prior MI and recalls a “negative” stress test in the recent years.

His vital signs on arrival were HR 77, BP 148/95, RR 16, SpO2 95%. He was in obvious discomfort.

Below was his first ECG, obtained within minutes of arrival.

What do you think?

Meyers comment: Ryan texted me this ECG with no information and my response was "Tough one. I'm worried about inferior posterior OMI but not convinced yet. Would get serial ECGs to help. Is there active pain at the time of this? Tell me more."

I later sent this same ECG without any context to Dr. Smith who replied: "Super subtle inferior OMI, and posterior. Great case."


First, you will likely notice the small amount of ST depression in V2-V6, seemingly maximal in V3-V4. It is even more subtle in I and aVL. The morphology in V2 is also concerning and it appears that the ST segment is being pushed down, as in ST depression. In lead III there is the tiniest possible amount of STE which is difficult to measure due to the very low-voltage. These findings are concerning for inferior wall ischemia with possible posterior wall involvement.


Repeat ECG minutes later (one shown below) showed no significant change.

No significant changes, ongoing pain.

Fortunately, we were able to obtain a copy of his only known prior ECG from his cardiologist (from another state) via facsimile remarkably fast. It was from four years prior.

All the noted abnormalities are proven new in comparison. At baseline, the patient has some expected, normal STE in lead V2, further demonstrating that the STD morphology in the presentation ECG above is "true" and diagnostic.

You will note that it is essentially an unremarkable electrocardiogram except for some PACS. This raised our concerns that the findings on his initial one were real. At the same time, his point-of-care labs came back and were most notable for a cardiac Troponin-I of 8.7 ng/mL.

The case was discussed with the cardiology fellow at the nearest tertiary care center and arrangements were made to fly the patient via HEMS. He was expected to arrive at the tertiary care center within 60 minutes of the call. He was loaded with aspirin, ticagrelor, and heparin. No arrhythmias occurred en route.

The patient’s ECG on arrival at the emergency department is shown below. Note the slightly more obvious ST elevation in III with more distinct ischemic morphology.

His initial cTnI at the receiving hospital was 27 ng/mL, and no further troponins were measured thereafter. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent.

In the available view, the RCA appears fully occluded.

To our knowledge, the patient did well. Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. No further follow up information is available.


Learning Points: 

Everything is proportional. A very small QRS complex can only mount a very small amount of STE. This patient had a full RCA occlusion with the smallest visible STE.

Baseline and serial ECGs make you much more likely to identify OMI.

Using the STEMI paradigm would have resulted in significant delays for this patient, which correspond with the doubled mortality and morbidity of NSTEMI Occlusions seen in over 50,000 subjects in NSTEMI trials.

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MY Comment, by KEN GRAUER, MD (9/30/2019):

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Our THANKS to Dr. Ryan Barnicle for sharing this case — with excellent commentary on the key features by Dr. Meyers. ECG findings in this case are subtle — and worthy of repetition. To this, I’ll add a few additional points — with focus on the 1st and 3rd ECGs shown above in this case.

• For clarity — I’ve put these 2 tracings together in Figure-1.

Figure-1: The initial ED ECG ( = ECG #1) — with comparison to the patient’s baseline ECG done 4 years earlier ( = ECG #3).

MY THOUGHTS: It is precisely because ECG findings are subtle — that we need to pay special attention to the details in this case:

• The History states that this patient presented to medical attention for “evaluation of chest pain”— and that these symptoms had begun ~1 hour prior to being seen. BUT — the history also states that he had the same chest pain the day before. Duration of symptoms for at least 24 hours may account for the finding of ECG changes that did not look overly acute.

When confronted with subtle ECG changes that almost make me question IF they are real — I like to: i) Look for 1 or 2 leads that I KNOW are abnormal; and then, ii) See HOW MANY leads I can find that also show subtle abnormalities. In a patient with worrisome chest pain — the more leads that manifest abnormal findings, even if subtle — the more likely these findings are real.

• The ECG finding that I KNOW is real in ECG #1 is the mirror-image appearance of ST-T waves in leads III and aVL. We have often referred to this almost magical mirror-image relationship for ST-T waves in leads III and aVL — which when present, means acute inferior OMI until you prove otherwise (See My Comment on the 8/9/2018 SSmith Blog Post). While ST elevation is minimal (barely perceptible) in lead III of ECG #1 — a mirror-image reflection of the coved (“frowny”-configuration) ST segment in lead III is seen in lead aVL. When you invert the scooped ST segment in lead aVL (as I have done in the magnification placed just above lead III in ECG #1) — Doesn’t this coved ST segment shape now look virtually the same as the ST coving that we see in lead III?
• In support that the ST coving in lead III of ECG #1 is real — Don’t we see this same coved shape in lead aVF?
• The other high-lateral lead ( = lead I) — also shows slight-but-real ST segment flattening and depression (0.5 mm).
• Dr. Meyers highlighted the slight-but-real J-point ST depression in leads V2-thru-V6. Even before the prior ECG ( = ECG #3) was found — the point to emphasize is that the J-point in these chest leads looks like it is slightly depressed below the PR segment baseline, even though the amount of this depression is minimal.
• Putting This All Together — In this patient with worrisome chest pain, we have in ECG #1 mirror-image ST-T wave changes in leads III and aVL + subtle-but-real ST-T wave abnormalities in no less than 9 of the 12 leads (ie, leads I, III, aVL, aVF and V2-thru-V6). Add in the fact that symptoms began at least 24 hours ago — and these subtle-but-real ECG findings suggest a recent event until we can prove otherwise.
• Availability of this patient’s baseline ECG (done 4 years earlier) — added support that findings in ECG #1 are new. As per Dr. Meyers — the scooped ST segment in lead V2 of ECG #3 was clearly higher than in ECG #1 — and, the J-point in leads V3-thru-V6 of ECG #3 was not depressed. The magical reciprocal relationship for ST-T waves in leads III and aVL was also not seen in the baseline ECG.
• Beyond-the-Core: Did you notice that the R wave becomes predominant in lead V3 of ECG #1 — whereas transition did not occur until later in the patient’s baseline tracing. Early transition (with a predominant R wave by lead V3) could be another sign of posterior infarction in this patient.

QUESTION: What Was the Rhythm in ECG #3?

• HINT: If you said either sinus or sinus with PACs — Take another look!

ANSWER: Doesn’t P wave size and morphology, as well as the PR interval and the R-R interval change with almost every beat in the long lead II rhythm strip? P waves preceding beats #1, 3, and 4 are notched — the P wave preceding beat #6 is tiny — P waves preceding beats #8 and 9 are peaked — and P wave amplitude is not constant for the other rounded, upright P waves. I never see 2 P waves in a row with the same morphology. Given minimal artifact on this tracing — I believe this variation in P wave morphology is real!

• BOTTOM LINE: This is not a sinus rhythm. It is also not a wandering pacemaker — because change in atrial pacing site is gradual with that disorder. Instead, given the change in P wave morphology and PR interval from one-beat-to-the-next — this would suggest MAT (Multifocal Atrial Tachycardia) — except that the rate is clearly not tachycardic!
• Some cardiac rhythms do not read the textbook! Having observed this phenomenon over many years — I’ve noticed that rather than black-or-white classifications for rhythms such as wandering pacemaker; sinus with many PACs; and MAT — that there is a spectrum for these rhythm disorders. (CLICK HERE — for my detailed discussion of this subject).
• Clinically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia. A majority of patients with MAT have longstanding pulmonary disease. Rather than antiarrhythmic medication — optimizing pulmonary function is the best treatment approach. Beyond-the-Core: There are a number of findings on ECG #3 consistent with pulmonary disease (ie, an incomplete RBBB pattern; relatively low voltage in the limb leads; numerous S waves [ie, in leads I,II,III and in all chest leads]). The rhythm we see in the long lead II is not a common one. Therefore — I’d like to know if this patient had pulmonary problems, a smoking history, or some other significant systemic disorder at the time ECG #3 was obtained ...
• PEARL: Over the 3+ decades that I've been teaching ECG interpretation — the most common error I've observed even experienced interpreters to make — is to overlook a non-sinus rhythm. The temptation is great to assume sinus rhythm, and jump to the "interesting" findings on the tracing. Guaranteed, it will take no more than 3 seconds for your "educated eye" to begin the interpretation of each and every ECG you are given with a QUICK SCAN of the long lead II rhythm strip under the 12-lead — in order to assess IF each QRS complex is preceded by an upright P wave with a constant PR interval. IF it isn't — then a simple sinus rhythm is not present ...

Our THANKS to Drs. Barnicle and Meyers for presenting this case!