A 34 yo Man with chest pain and Zero ST Elevation

Written by Hans Helseth

A 34 year old man with no known medical history presented to the ED after an hour of chest pain. He described the pain as a mid sternal "burning sensation" and rated it 8.5 out of 10 at onset, but on presentation to the ED, reported that the pain had improved to 4.5. His first EKG is shown below, with a lead II rhythm strip:

EKG 1, 1645

A provisder who is looking for STEMI would not see much in this EKG. 

Despite zero ST elevation, however, the T waves in the inferior leads are symmetrical and large in proportion to their QRS complexes. This is the classic morphology of hyperacute T waves. This EKG coupled with the patient's story is highly suggestive if not diagnostic of inferior OMI.

I interpret this as manifesting active inferior OMI, although the patient's improving pain suggests at least some reperfusion. It is possible that the T waves in this EKG are of an intermediate morphology between full-blown STEMI and inferior reperfusion. It is also possible for hyperacute T waves to remain somewhat stable during either a sustained period of occlusion or partial reperfusion.

Here is the interpretation of the PMCardio Queen of Hearts AI Model:

Smith: The Queen does not know if the patient has active pain, resolving pain, or pain completely gone.  Although to me this is diagnostic of Acute ACTIVE Inferior OMI, I think the Queen says "reperfused" OMI because she thinks that there are reperfusion T-waves in aVL, with reciprocally hyperacute upright inferior T-waves.

Nevertheless, as you can see, she recommends cath lab activation if there are ongoing symptoms.  Patient has 4.5/10 chest pain.  So he needs the cath lab.

Case Continued

This EKG was interpreted as normal by the clinicians overseeing this patient's care.

A high sensitivity troponin I resulted at 336 ng/L (Upper limit: 76) after which the clinical suspicion changed from reflux/gastritis to "NSTEMI". The patient was given nitroglycerin, but his blood pressure dropped to 70 systolic, he became dizzy, and he still had chest pain. An EKG was repeated about an hour after the first:

EKG 2, 1745

The inferior T waves have inflated tremendously. 

A small amount ST elevation has developed, although still not enough to meet STEMI criteria. There is also diagnostic evidence of posterior OMI in V2 and lateral OMI in V6.

Cardiology was consulted at a PCI-capable hospital. The cardiologist agreed to accept the patient for transfer, but did not accept the patient for direct admission to the cath lab because the EKG was not felt to represent "STEMI".

Smith: This was a cardiologist who made this statement!!!  Hans has not even been to medical school.  

One's training has NOTHING to do with one's OMI ECG interpretation skills.

The QoH now correctly sees active OMI:

A CT scan to rule out aortic dissection was performed (Smith: why???) before transferring the patient to the cath facility. It was without evidence of dissection. When the patient finally arrived to the PCI-capable hospital, his pain had reportedly improved, but not resolved. Another EKG, shown with a V1 rhythm strip, was recorded in the emergency department:

EKG 3, 1930

There appears again to be some reperfusion since the last EKG, as the T waves in inferior leads have deflated slightly. The Q waves in the inferior leads have deepened. 

This EKG was interpreted as showing "T wave inversion in aVL, otherwise no significant ST elevation or depression." 

The patient waited another three hours in the ED until the cath lab was ready to accept him.

6 hours after his initial presentation, he went to the cath lab:

There is a filling defect consistent with thrombus in the distal RCA. There was TIMI 2 flow distal to the thrombotic occlusion. The thrombus was aspirated and the distal RCA was stented. 

The rest of the patient's hospital stay was uneventful. A formal echo the next day showed an estimated EF of 55-60% with no definite regional WMA.

Learning Points:

• Hyperacute T waves can be present for a long period of time, especially if serial EKGs are not recorded frequently enough to observe their evolution.
• Hyperacute T-waves frequently NEVER progress to diagnostic ST Elevation
• Patients with ACS and pain refractory to anti-ischemic therapy should be sent emergently for catheterization, regardless of the ECG.
• Some OMI have zero ST elevation
• OMI can happen in young patients with no known medical history

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MY Comment, by KEN GRAUER, MD (1/28/2025):  

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There is a lot to be learned from today's post. In Figure-1 — I facilitate comparison of the 3 ECGs in today's case by putting them together.

• Although tempting to seek false reassurance from the relatively young age (34yo) of today's previously healthy patient — the history of new CP (Chest Pain) lasting an hour of sufficient severity to prompt an ED visit does place this patient in a higher risk category, pending other factors.

As per Hans Helseth — the initial ECG is clearly worrisome:

• My "eye" was immediately drawn to the inferior leads (within the RED rectangles) — each of which show disproportionately enlarged T waves that exceed R wave amplitude in the same lead (The huge T wave in lead aVF literally dwarfs the tiny QRS in this lead). In a patient with cardiac-sounding CP — T waves that are clearly taller-than-they-should-be — "fatter"-at-their-peak and wider-at-their-base than expected — have to be interpreted as hyperacute T waves until proven otherwise.
• Removal of any doubt that these inferior lead ST-T wave changes are significant — is forthcoming from the abnormal ST segment coving and surprisingly deep T wave inversion in lead aVL ( = reciprocal ST-T wave change). 
• NOTE: The T wave in lead aVL may at times be normally inverted. The physiologic reason for this finding — is that the T wave axis in the limb leads generally follows the QRS axis. As a result: i) The QRS complex will typically be predominantly negative in lead aVL when T wave inversion is benign; — ii) The ST segment in this lead should not be coved; — and, iii) The appearance of the inverted T wave should not be nearly as "bulky" as it appears to be in Figure-1.
• Impression: In this patient with new CP — ST-T wave findings in these 4 limb leads are diagnostic of acute inferior OMI until proven otherwise. 

Other findings in ECG #1 are more subtle. 

• There appears to be an IRBBB (Incomplete Right Bundle Branch Block) pattern in the form of an rsr' in lead V1 with terminal S waves in lateral leads I and V6. That said — typical IRBBB should not manifest ST segment coving with slight ST elevation in lead V1 (BLUE arrow in lead V1). Instead — there should be slight ST depression in association with IRBBB. In this patient with suspected inferior OMI — this raises suspicion of acute RV involvement.
• The ST-T wave in leads V2 and V3 normally manifest gently upsloping, slight ST elevation in leads V2,V3. Although the ST-T wave in lead V3 looks unremarkable in ECG #1 — the ST segment in lead V2 is isoelectric with a suggestion of ST segment flattening. In addition, the R wave in lead V2 is significantly taller-than-expected (given the tiny r wave in neighboring lead V1) — which in a patient with suspected inferior OMI — raises suspicion of associated posterior OMI.
• Finally, while not taller than the R wave in the same lead — the peak of the T wave in lead V6 appears "fatter"-than-expected — which in this patient with suspected inferior OMI, suggests this is a hyperacute T wave.
• 
  
• To Emphasize: These findings in leads V1,V2 and V6 of ECG #1 are subtle — and in isolation would be nondiagnostic. But in the setting of a patient with new CP and suspected acute inferior OMI — these findings add concern for an acute evolving event. The cath lab should be activated.
• At the least — ECG #1 should be repeated within 15-20 minutes after the initial tracing.
• Failing that — return of the initial significantly elevated Troponin value given new CP and this abnormal ECG should have sufficed for activation the cath lab.

NOTE: This patient's BP dropped to 70 systolic on receiving NTG. He continued to have CP.

• In a patient with suspected inferior OMI — a marked hypotensive response to NTG strongly suggests acute RV involvement.
• Right-sided chest leads should be obtained to assess for acute RV MI, especially given suggestion of ST segment coving with slight elevation in lead V1.

The repeat ECG is the MIDDLE tracing in Figure-1:

• As per Hans Helseth — the inferior T waves in ECG #2 appear even more hypervoluminous than they were ECG #1. In addition — there are now Q waves in leads III and aVF — whereas there previously was an rSRs complex in ECG #1 in these leads.
• Support that the increase in inferior lead T wave hyperacuity is real — is forthcoming from the deeper T wave inversion in lead aVL of ECG #2, along with subtle-but-new ST depression in lead I. 
• There has been little change in the chest leads.
• KEY Point: It would be easy to miss these subtle-but-real changes in limb lead ST-T wave appearance in the repeat ECG if these 2 tracings were looked at separately. This highlights the importance of putting both tracings you are looking at together — and comparing both tracings lead-by-lead.
• The fact that this patient still has ongoing CP — and now demonstrates "dynamic" ST-T wave changes compared to the initial ECG is but one more indication of the need for prompt cath.

As noted by Hans Helseth — the patient was finally transferred to a PCI-capable facility.

• Cardiac cath was delayed a number of additional hours because, "the ECG did not show a STEMI". This unfortunately is faulty reasoning. As per Dr. Smith (See his comments in the January 24, 2025 post, among many other cases on Dr. Smith's ECG Blog): i) Up to 40% of OMIs do not meet STEMI criteria despite TIMI-0 flow. Delay in reperfusion of such patients by as little as 1-2 hours may reduce potential benefit from myocardial salvage by as much as 50%; — and, ii) The findings of new and now ongoing CP in association with localized hyperacute T waves — and now with "dynamic" ST-T wave changes is diagnostic of an acute ongoing cardiac event — especially in association with already significant Troponin elevation.

The 3rd ECG in today's case was obtained on arrival at the PCI center — and is the BOTTOM tracing in Figure-1. 

• Although there is not a lot of ST-T wave change since ECG #2 — what is new (and what once again is BEST noticed by comparing serial tracings when put next to each other) — is a significat increase in heart rate. While not quite "tachycardia" (ie, the rate in ECG #3 is ~90/minute) — in association with evidence of ongoing CP and acute infero-postero-lateral OMI, possibly with RV involvement — a significant increase in heart rate should prompt reassessment to ensure that the patient is not developing shock.

Figure-1: Comparison of the 3 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).