EXTRA COPY- Should Prompt Cath be Done? (4-21.1-2029) - EXTRA COPY

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The ECG in Figure-1 was obtained from an older woman — who presented following an episode of severe epigastric pain, associated with nausea, vomiting and dyspnea. This ECG was obtained a number of hours after the episode had subsided.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  

Figure-1: The initial ECG in today's case — obtained from an older womman following an episode of severe epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 shows a fairly regular sinus rhythm at ~90/minute. The PR and QRS intervals are normal — and the QTc is at most borderline prolonged. The frontal plane axis is normal at about 0 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: None.
• R Wave Progression: Delayed. Transition (where the R wave becomes taller than the S wave is deep) does not occur until between lead V5-to-V6. That said — at least a small R wave is present in each of the chest leads, with gradual increase in R wave size until transition occurs.

Regarding ST-T Wave Changes:

As highlighted in Figure-2 — ST-T wave appearance is clearly of concern — with abnormal findings in almost all leads.

• ST segments in multiple leads are flat. Most remarkable is the shelf-like ST depression that is maximal in leads V2,V3,V4 (within the RED rectangle in Figure-2). 
• A lesser degree of flat ST depression is seen in the remaining chest leads (ie, in leads V1;V5;V6).
• There is terminal T wave positivity in all 6 chest leads.

In the Limb Leads:

• There is nonspecific ST-T wave flattening with slight depression in high-lateral leads I and aVL (BLUE arrows in these leads).
• In the inferior leads — leads II and aVF show nonspecific ST-T wave flattening. KEY Point: The 3rd inferior lead (which is lead III) — shows ST segment coving, with a hint of ST elevation.
• The remaining limb lead (which is lead aVR) — shows a very slight amount of ST elevation. 

My Impression: 

If today's patient had presented with the ECG in Figure-2 and a history of new-onset chest pain — then this tracing would be especially worrisome.

• Instead — this patient presented with severe epigastric pain, associated with nausea, vomiting and dyspnea. That said — in view of the fact that the symptoms reported could represent a CP (Chest Pain) “equivalent” syndrome — Consideration has to be given to the possibility of an acute ongoing cardiac event.
• ST depression is seen in 8/12 leads in Figure-2 (leads I,aVL; and the 6 chest leads). Even without any more than the minimal ST elevation in lead aVR — these findings suggest DSI (Diffuse Subendocardial Ischemia). As discussed in ECG Blog #483 and ECG Blog #400 — DSI may be the result of either non-cardiac causes (ie, anemia, GI bleeding, marked hypotension, "sick" patient, etc.) and/or significant underlying coronary disease, which could be acute.
• As suggested by the RED arrows (within the RED rectangle in Figure-2) — ST depression appears to be maximal in leads V2,V3,V4 — which strongly suggests the possibility of acute or recent posterior OMI.
• In this context — the ST segment coving with slight ST elevation in lead III could reflect associated inferior OMI in the setting of underlying multi-vessel disease (ie, similar to an Aslanger Pattern — as described in detail below).
• 
  
• BOTTOM Line: Although more information is urgently needed to better define what is going on — one needs to consider the possibility of an acute occlusion infarction (ie, an "OMI") until proven otherwise.

Figure-2: I've highlighted key findings in today's ECG.

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CASE Follow-Up:

Clinical details are unfortunately lacking in today's case — But from what I am aware of, the possibility of an acute MI was not considered until a serum Troponin came back markedly elevated.

• At that point — the MI was declared a NSTEMI (Non-ST Elevation Myocardial Infarction). In the absence of ST elevation — cardiac catheterization was not deemed necessary.
• An Echo was not done until later. It showed an inferolateral wall motion defect with significant LV dysfunction. At this point — cardiac cath was finally recommended, but not performed because the patient feared the procedure.
• The patient's condition deteriorated — but she still refused cardiac cath. Eventually, after a complicated hospital course — her condition improved and the patient was discharged from the hospital.
• The patient never underwent cardiac catheterization. A number of weeks later on follow-up — she appeared stable on her new medical treatment regime for heart failure.

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COMMENT:

There are lessons to be learned from this case.

• It is well established that not all patients with an acute MI have CP (Chest Pain). Some patients have other "CP-equivalent" symptoms (ie, epigastric pain, dyspnea) —
• That today's patient had a recent (ongoing) MI was not appreciated until her Troponin came back markedly elevated. This possibility should have been realized as soon as her initial ECG (shown in Figure-1) was recorded. Yet a few days passed before this possibility was considered.
• Given the less typical presentation (ie, epigastric rather than chest pain) — I would interpret today's initial ECG as suspicious but non-diagnostic. The diffuse ST depression (present in 8/12 leads in Figure-2) — clearly indicates DSI (Diffuse Subendocardial Ischemia). As noted above — DSI often (but not always) indicates severe underlying coronary disease.

The situation of having to determine if a patient with a non-diagnostic initial ECG is having an acute MI is common. 

• "Time is Muscle (myocardium). If the cause of an acute MI is acute occlusion of a major coronary vessel (ie, an "OMI" = Occlusion-associated Myocardial Infarction) — then we need to appreciate that the more time that passes until the occluded vessel is reperfused (either by cardiac cath with PCI or by use of thrombolytic agents) — the greater the amount of myocardium that will be lost.
• As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — the most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in up to 60% more myocardium infarcted).

There are 2 main types of acute myocardial infarction:

• Type 1 MI's — which are caused by a ruptured plaque that results in acute occlusion of a major coronary vessel. 
• Optimal treatment of Type 1 MI's consists of reopening the acutely occluded artery (ie, reperfusion by cardiac cath with PCI — or with use of thrombolytic agents). 
• Sometimes (if not often) — the acutely occluded artery will spontaneously reopen (which is why the patient's symptoms and ECG abnormalities may suddenly improve, even without treatment).
• But what spontaneously reperfuses — may just as easily spontaneously reclose (which is why with a Type I MI, even if symptoms and the ECG suddenly normalize — definitive treatment with PCI may be needed to prevent subsequent reclosure).

• Type 2 MI's — which are not the result of a ruptured plaque, but instead are due to an oxygen supply-demand mismatch (which may be seen with "high-demand" states, in which the heart requires more oxygen than it receives — as may occur with marked stress states, septicemia, severe anemia, sustained tachyarrhythmias,  or shock, among other causes).
• Optimal treatment of Type 2 MI's is to find and "fix" the cause of the supply-demand mismatch (Neither PCI nor thrombolytics benefit a Type 2 MI).
• If not clear from history and serial ECGs — Cardiac cath may occasionally (not often) be needed to distinguish between a Type 1 vs Type 2 MI.

Today's ECG was called a NSTEMI (Non-ST Elevation Myocardial Infarction) — because Troponin was significantly elevated but no ECG satisfied sufficient ST elevation criteria to qualify as a STEMI.

• It was on this basis (ie, that no STEMI was present) that the recommendation for acute cardiac catheterization was delayed for more than a day. As discussed above — the patient consistently refused cardiac cath — so this delay did not influence the ultimate outcome. BUT — in reviewing today's case — it is still important to consider the rationale for delaying the recommendation for cardiac cath.
• Practically speaking — the diagnostic designation, "NSTEMI" — serves no useful purpose. On the contrary — the "default diagnosis" of calling cases such as the one in today's case a NSTEMI is potentially harmful because of the false sense of security that it gives to providers, which therefore results in significant delay until cardiac cath is finally done.
• Up to 35% of NSTEMIs are found on their delayed cath to have had acute coronary occlusion despite a lack of ST elevation (Chi-Sheng Hung et al- Critical Care 22:34, 2018 — Khan et al- Eur Heart J 38(41): 3082-3089, 2017 — and — Avdikos, Michas, Smith- Arch Acad Emerg Med 10(1), 2022).

PS - today's MI was called a NSTEMI because no ST elev. Practically speaking — the commonly used description of an NSTEMI is useless. Worse than that — Px often worse because "only a NSTEMI" induces a false sense of security, therefore delay (ME TO LOOK FOR REF on SSmith !!!

Features in today's initial ECG that should immediately suggest the possibility of an acute Type I MI include the following:

• XXXX  - max st dep in V2,3,4 - ST coving and sl elev. in lead III (similar to Aslangers - but not quite since no st elev. in V2

What to do if you encounter a suspicious but non-diagnostic initial ECG like Fig. 1:

• repeat ecg within 10-20 minu
• Echo at bedside (echo done days later had marked lv dysfunction - had that been done immediately - would have been enough to confirm need for acute cath
• prior ecg as soon as trop came back - should have been indication for cath

How to apply this to today's case?

• This patient refused cath with informed consent. Sometimes patients know something. I long ago learned it's best never to "force" a procedure on a patient - but although doing fairly well on follow-up - pt had resultant HF - who is to know how much myocardium might have been preserved had reperfusion treatment had been started shortly after ECG #1 done ... 

Type 2 Myocardial Infarction (Type 2 MI or T2MI) is a heart attack caused by a mismatch between oxygen supply and demand, rather than a plaque rupture (which is Type 1). It occurs when the heart muscle requires more oxygen than it receives due to stress, such as sepsis, severe anemia, tachyarrhythmias, or severe blood pressure issues. 

Key Aspects and Characteristics

• Mechanism: It is a "demand ischemia," where coronary arteries may not be acutely blocked, but cannot supply enough blood to meet high oxygen demands.
• Triggers/Causes: Common causes include sepsis (infection), operative stress, rapid arrhythmia (e.g., AFib), anemia, and extreme hypertensive/hypotensive crises.
• Patients Affected:
   Type 2 MI is very common in hospitalized patients, often affecting older patients with multiple comorbidities (like renal failure or heart disease).

go over Aslanger — OMI —  

As per many other posts — stemi criteria miss many acute occlusion MIs = OMIs — several interventions can facilitate determining if OMI was present

NSTEMI is not a helpful diagnosis ...

cath was indicated - but patient refused - although safe in hands of experienced operators, adverse effects can occur (so patient informed consent decision should be respected). I have to believe that had reperfusion been performed/cath — myocardium could have been saved - and her heart failure may not have been severe. but who 

MY REPLY:

Thanks for this follow-up — which does teach us something, namely that even though doing a cath offered potential for saving myocardium — who is to say that this patient might not be now doing equally well without having had her cath?

 

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Acknowledgment: My appreciation to Ahmed Marai (from Anbar, Iraq) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (4/XXX/2026):

• XXXX 

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From ECG Blog #258 — on ASLANGER Pattern!

https://ecg-interpretation.blogspot.com/2021/10/ecg-blog-258-mp-70-how-to-date-mi.html

Also from ECG Blog #322  

https://ecg-interpretation.blogspot.com/2022/07/ecg-blog-322-71yo-with-1-week-of-chest_26.html

I added the following to Blog #322:

NOTE: Other than the finding of ST depression in lead V2 — the initial ECG in today's case satisfies the other above-cited features of Aslanger's Pattern. 

• I can't help but wonder if the fairly deep, symmetric T wave inversion in lead III represents a reperfusion T wave from recent occlusion.

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ADDENDUM (10/28/2021) — There are elements of this case that closely resemble Aslanger's Pattern (This pattern is very nicely described by Dr. Smith in his January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

The above said — additional features to consider in today's case include: i) There is also marked LVH; and, ii) The infero-postero MI is probably at least 10 hours old, and is now showing prominent reperfusion T waves in the posterior distribution (ie, tall, peaked anterior T waves). 

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