ECG Blog #448 — A Young Man with Chest Pain ...

The ECG in Figure-1 was obtained from a previously healthy man in his early 20s — who initially presented with GI symptoms, that then evolved into CP (Chest Pain).

• The patient was thought to have anxiety.

QUESTIONS:

• Given the above history — How would YOU interpret the initial ECG that is shown in Figure-1?
• Does the patient's age infuence your interpretation?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWERS:

As emphasized in ECG Blog #205 — I favor a 2-Step Process for the interpretation of any ECG:

• STEP #1 = Descriptive Analysis — in which we simply assess the 6 KEY Parameters of Rate — Rhythm — Intervals (PR-QRS-QTc) — Axis — Chamber Enlargement — and Q-R-S-T Changes — but without yet commenting on what this assessment might mean clinically.
• STEP #2 = Clinical Impression — in which we correlate our assessment that we made in Step #1 to the clinical situation at hand. For example, considering whatever symptoms that the patient may have had (ie, chest pain, palpitations, shortness of breath, etc.) — what this might mean in view of the ECG we are looking at.

KEY Points:

• Use of this systematic 2-Step approach does not slow you down. On the contrary — it speeds you up, because once you routinely incorporate a sequential, systematic approach — you'll find you no longer go back-and-forth looking at the ECG to see if you missed anything.
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• PEARL #1: My assessment of the 6 KEY Parameters is the same — regardless of the age of the patient. That said — What (if anything) these ECG findings that you identify might mean — will depend on your clinical correlation in Step #2.
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• PEARL #2: The reason it helps to know the age of the patient and the reason the ECG was done as soon as possible — is that it greatly facilitates Clinical Correlation. For example, in today's case — Knowing the patient is a younger adult who developed chest pain immediately increases our need to consider acute myocarditis in the differential diagnosis.

Figure-2: I've labeled the initial ECG. 

MY Interpretation of Today's Initial ECG:

I've labeled key findings in Figure-2 for today's initial ECG:

• The rhythm is sinus tachycardia at ~105/minute. 
• All intervals (PR, QRS, QTc) are normal. 
• The frontal plane axis is normal at about +70 degrees. 
• Given the patient's young adult age — QRS amplitude does not satisfy criteria for chamber enlargement.

Regarding Q-R-S-T Changes:

• Small and narrow Q waves are seen in the inferior leads, and in lead V6. These are likely to be normal septal q waves. (The initial deflection in lead aVL is positive — so there is an rSr' complex, but no Q wave in this lead).
• R wave progression — is normal, with progressive increase in R wave amplitude (albeit transition is slightly delayed until lead V5, when the R wave finally becomes taller than the S wave is deep).

There are subtle-but-important ST-T wave findings:

• My "eye" was drawn first to the 2 leads within the RED rectangle (ie, leads V5 and V6 each show 2 millimeters of J-point ST elevation — which is more than is usually seen with a normal repolarization pattern).
• There is a lesser amount of ST elevation in lead V4 — but given my concern about leads V5,V6 — I thought the ST-T wave in lead V4 showed some ST segment straightening, and was disproportionately larger-than-it-should-be with respect to the modest-sized R wave in this lead (within the BLUE rectangle).
• Normally, there is slight, gently upsloping ST elevation in leads V2 and V3. While I thought the ST-T wave in lead V3 was non-diagnostic — lead V2 lacks the slight amount of gently upsloping ST elevation that is usually seen in this lead.
• In the limb leads — there is slight-but-real J-point ST elevation in the inferior leads and in lead I (BLUE arrows) — with ST segment straightening in these same leads (as shown by the light BLUE lines).

STEP #2 = My Clinical Impression of ECG #1:

I had been sent this ECG with only the information that I noted in the above history (ie, that the patient was a previously healthy man in his early 20s — who presented with GI symptoms — that evolved into chest pain thought to be the result of anxiety).

• I wrote back, "This is not a normal ECG". I then specified the findings I cite above in my Descriptive Analysis.
• The sinus tachycardia is a definite concern that something acute may be ongoing. Almost all leads show some ST elevation — with more ST elevation in leads V5,V6 than is usually seen with early repolarization and, with abnormal straightening of the ST segment takeoff in multiple leads.
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• To Emphasize: I was not at all certain about what might be going on here. But what I wrote back was the following: "This could be acute LAD occlusion (ie, acute LAD OMI). Given that this patient is having CP — more evaluation is clearly needed. Alternatively — this could represent acute infero-postero-lateral OMI. In any event — I'd repeat the ECG within 10-20 minutes (and serially thereafter) — check Troponin — and would definitely follow-up until a definite answer is forthcoming! 
• Pericarditis is rare — but myocarditis is not, so especially in this age group — more information is needed to quickly determine if this could be an acute MI, myocarditis, or none of the above. Let me know what happened".

CASE Follow-Up:

The emergency physician recognized the abnormal ECG findings that I highlight above — and sent the patient to a PCI-capable center.

• Unfortunately — the cardiologist at that center did not recognize the abnormal ECG findings. The patient was discharged without repeating the ECG.
• The patient arrested outside the hospital. He could not be resuscitated.

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There are Lessons-to-be-Learned from today's case:

• Treat the patient — Not the age of the patient!
• Acute MI can occur in a younger patient.
• There are other potentially serious causes of CP in a younger adult. Some of these other causes may also be potentially life-threatening.
• IF at all concerned by the history and/or appearance of the patient — Do not allow your decision-making to be determined by a single ECG. I fully acknowledge that I was not certain from today's initial ECG that this patient had a life-threatening problem. That said — a series of subtle but potentially concerning findings are present in today's initial tracing — and, this should signal the need for additional evaluation until a clear diagnosis is forthcominng.
• Be systematic in your ECG interpretation. If the interventionist would have been systematic — the abnormal ECG findings highlighted in Figure-2 would have been identified.
• Sometimes cardiac cath is needed to distinguish between an MI vs myocarditis.

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PEARL #3:  Acute MI Can Occur in a Younger Patient!

To quote Dr. Stephen Smith: "The worst risk factor for a bad outcome in acute MI is young age." This is because clinicians (including too many cardiologists) have trouble accepting the fact that a young patient can have an acute MI (See case discussion in the January 9, 2023 post in Dr. Smith's ECG Blog — with links at the bottom of this post to a series of more cases illustrating this phenomenon).

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I have excerpted a portion of My Comment from this same January 9, 2023 post — regarding acute MI in a younger patient:

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“Treat the patient — Not the age of the patient”

The tendency to discount new chest pain in a young adult as the 1st symptom of acute MI is understandable. Acute coronary occlusion almost always occurs in patients who are beyond their 20s. That said — acute MI does occur in younger patients.

• There is a literature on this subject (Sood et al — Cureus 15(4):e37102, 2023 — Gulati et al — Mayo Clin Proceed 95(1):136-156, 2020 — GGF van der Schoot et al: Neth Heart J 28(6):301-308, 2020 — and — Egred at al — Postgrad Med 81(962): 741-745, 2005 — to name just a few reports). 
• Acute MI in younger patients may result from acute coronary occlusion — which can be precipitated by conventional risk factors (such as smoking begun at an early age) — in individuals with special predisposition (ie, a factor V Leiden mutation — or nephrotic syndrome — both being correlated with a hypercoagulable state) — and/or in familial entities such as genetic hypercholesterolemia.
• In addition — there is a series of nonatherosclerotic potential causes of acute infarction in younger patients. These include coronary artery spasm (as may be precipitated by cocaine use or binge alcohol drinking) — myocardial bridging (that may be the cause of intermittent acute ischemia) — aberrant anatomy of a coronary artery (which may present with sudden rupture causing acute infarction or sudden death at any age!).
• Other types of nonatherosclerotic potential causes of acute infarction in younger patients include systematic inflammatory disease (ie, lupus, rheumatoid arthritis, Wegener granulomatosis) — thrombosis not due to coronary disease (ie, endocarditis, coagulation disorders) — pregnancy (with its hypercoagulable state).
• Causation of Endothelial damage is another potential mechanism of acute MI in a younger patient. This may occur as a result of blunt chest trauma or other acute stress that produces a sudden extreme shear force on a coronary artery (that can result in an intimal tear that leads to intraluminal thrombosis). Endothelial damage may also be seen with spontaneous dissection of a coronary artery — or result from “deceleration trauma (ie, from an auto or other vehicular accident).
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• BOTTOM LINE: While the above etiologies are not common causes of acute infarction in an adolescent or young adult — they do occur! And, like most diagnostic considerations in medicine — if the differential diagnosis excludes such "other potential etiologies" simply because they are not common, or because the patient is "too young to have a heart attack" — then these other potential etiologies will be missed!
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• RELEVANCE to this Case: Although the young adult in today’s case presented with GI symptoms (that were thought to be exacerbated by anxiety) — this did evolve into frank CP. So, while today's history by itself is not particularly suggestive of an acute coronary event — in association with the abnormal ECG findings and persistent CP — additional evaluation was clearly indicated.
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• P.S.: Given the history in today's case, and the abnormal ECG findings — acute myocarditis needs to be included in diagnostic considerations. There are times when distinction between acute myocarditis vs acute OMI in a younger patient with acute-looking ECG changes and troponin elevation can only be made by cardiac catheterization. At other times, when strongly suspecting acute myocarditis and not acute MI — cardiac MRI may yield a definitive enough picture to confirm acute myocarditis as the diagnosis.

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Acknowledgment: My appreciation to Kashif Aleem (from Sargodha, Punjab, Pakistan) for the case and these tracings.

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