Case from Cody Pinnow (KG- Done)

A previously healthy 70 something y.o presented to the ER with 1 hour of dull, retrosternal chest pain radiating to the left shoulder. He reports no cardiac history and actually underwent a stress test (unclear type) 6 days prior which was normal and the patient was given a clean bill of health by his cardiologist. An ECG was obtained at time 0000, no priors were available.

This ECG was triaged as “No STEMI” and the patient was placed in a room. The patient’s doctor recognized the ECG as being concerning for OMI, most notably a hyperacute T wave in V2, less so in V3 and V4.

Retrospectively, the ECG was ran through the Queen, who agrees.

On evaluation, the patient had continued 8/10 pain. The patient was loaded with aspirin and given sublingual nitroglycerin. With improving pain, a repeat ECG was obtained at time 0058.

V2 appears less hyperacute, and there are now terminal T-wave inventions in V3-V5, suggestive of reperfusion and consistent with the patient’s history of improving ACS symptoms. The Queen again recognizes this as high confidence OMI, without having any information on the patient’s pain.

A nitroglycerin drip was started and interventional cardiology was called. Interventional agreed with the dynamic changes, however requested the patient’s cardiology group be consulted before the catheterization was performed given the recent reassuring stress test. The patient’s pain continued to improve on nitroglycerin. 

As discussed on this blog previously, stress tests are practically USELESS for emergency department risk stratification of chest pain.

1. Stress tests have not been shown to catch at risk plaques

1. Smith SW.  Jackson E. Hanson K. Bart B. Incidence of MI in ED Chest Pain Patients with a Recent Negative Stress Imaging Test.  Academic Emergency Medicine 2005; 12(Suppl 5):51. 

2. Walker J, Galuska M, Vega D. Coronary disease in emergency department chest pain patients with recent negative stress testing. West J Emerg Med. 2010 Sep;11(4):384-8. Erratum in: West J Emerg Med. 2018 Nov;19(6):1065. doi: 10.5811/westjem.2018.10.41206. PMID: 21079714; PMCID: PMC2967694.

3. Meyer MC, Mooney RP, Sekera AK. A critical pathway for patients with acute chest pain and low risk for short-term adverse cardiac events: role of outpatient stress testing. Annals of emergency medicine. 2006; 47(5):427-35. PMID

2. Stress tests have bad sensitivity for obstructive CAD, as low as 45%. 

1. Froelicher VF, Lehmann KG, Thomas R, et al. The electrocardiographic exercise test in a population with reduced workup bias: diagnostic performance, computerized interpretation, and multivariable prediction. Veterans Affairs Cooperative Study in Health Services #016 (QUEXTA) Study Group. Quantitative Exercise Testing and Angiography. Ann Intern Med. 1998;128:(12 Pt 1)965-74

An excellent review of the pitfalls and weaknesses of stress tests from an emergency department perspective: https://first10em.com/stress-test-accuracy/

Back to the case:

The patient’s primary cardiologist recommended obtaining a troponin to help decide on catheterization “as the initial ECG was relatively unremarkable”. The initial high-sensitivity troponin returned at 92 (upper limit for men 22) which convinced the cardiology teams that catheterization was appropriate. The patient was started on heparin and went for catheterization (pain free) at time 0400. He was found to have severe triple vessel disease including 50% stenosis of the left main, complex stenosis of various parts of the LAD with 80% stenosis of the distal LAD. No immediate culprit lesion was identified. 

Cardiothoracic surgery was consulted and the patient successfully underwent CABG x4 the following day. The troponin was not trended further. Patient’s hospital course was complicated by atrial fibrillation and volume overload, however he is now doing well.

An ECG several months later for comparison makes the hyperacute changes of his first ECG more obvious.

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MY Comment, by KEN GRAUER, MD (6/8/2025):

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As I reviewed today's case in the comfort of my home office relaxing chair — I thought, "the Devil is in the Details ... ".

• The patient in today's case is a previously healthy 70-something man who presented to the ED (Emergency Department) with "1 hour of dull, retrosternal CP (Chest Pain) radiating to the left shoulder".
• Of note, the patient underwent a stress test (unclear type) 6 days earlier — which was reported as "normal". He was therefore "given a clean bill of health" by his cardiologist.

The "Details" in this History:

As noted above in Dr. Smith's discussion — Interventional cardiology was called to see this patient, but was reluctant to perform cardiac catheterization despite ECG changes because of the "reassuring" stress test.

• Detail #1: There are a series of "stress tests" that might have been performed so decision-making will clearly depend on the specific type of stress test that was done (ie, treadmill exercise — echo stress — nuclear stress test — cardiac MRI, etc.).
• Detail #2: What were the specific results of the test? For example — an exercise treadmill test might be "negative for ischemia" — but if an insufficient exercise workload was achieved, significant cardiac disease may still be present. Or body habitus or other factors may have resulted in a "negative" but suboptimally visualized test.
• Detail #3: WHY was a stress test ordered in the 1st place, just 6 days before this patient presents with new-onset CP? If the reason was for a history of angina — then depending on the type of stress test and its results — a "negative" result might not have negated the risk of underlying heart disease.
• Detail #4: Most stress tests assess for the presence of flow-limiting coronary stenosis. But a majority of infarcts arise from non-flow-limiting (less severe) coronary stenoses that harbor an unstable plaque that ruptures and results in acute coronary occlusion (Fearson — Circulation: Cardiovasc Interven 4(6): 539-541, 2011).

The "Details" in Today's ECGs:

For clarity in Figure-1 — I've placed side-by-side the first 2 ECGs in today's case.

• The initial ECG (TOP tracing in Figure-1) — was classified in triage as, "No STEMI". The treating physician did however recognize the hyperacute T wave in lead V2 (less so in leads V3,V4).
• About an hour later — the patient was doing better (much less CP after ASA and SL followed by IV NTG). A repeat ECG was obtained — and it was noted that lead V2 looked less hyperacute, with now terminal T wave inversions in leads V3,V4,V5.
• Disposition: At this point — Cardiology recommended obtaining a Troponin "to help decide on catheterization" — as the initial ECG was "relatively unremarkable".

What additional details should be noted in the interpretation of ECGs #1 and #2?

• How should these details have influenced management decisions?

Figure-1: Comparison of the initial ECG — and the repeat ECG in today's case.

Answers: The details in the interpretation of these 2 ECGs:

Given the history of new-onset CP in this 70-something man — the diagnosis of acute OMI should have been made as soon as ECG #1 was seen.

• The rhythm in ECG #1 is sinus. There is LAHB. But in a patient with new-onset CP — our "eye" is captured by the 2 leads within the RED rectangle. The hyperacute T wave in lead V2 is large enough (and "fat" enough) to swallow the small QRS complex in this lead.
• Support that hyperacuity in lead V2 is real — is forthcoming from the ST-T wave in lead V3, which shows distinct straightening of the ST segment takeoff and subtle-but-real terminal T wave inversion.
• Similar findings of concern are seen in other leads in ECG #1. These include: i) ST segment straightening (in leads V4,V5 — with ST segment flattening in lead V6) — and, ii) Terminal T wave inversion (BLUE arrows in leads III,aVF; V4,V5).
• Impression: Given the history — ECG #1 is diagnostic of an acute OMI, with clear ST-T wave abnormalities in at least 7/12 leads. The terminal T wave inversion that is seen in 5 leads suggests there has been some degree of spontaneous reperfusion of the "culprit" artery. But what spontaneously reopens — might just as easily (at any moment) spontaneously reclose — which is why prompt cath is indicated on the basis of this initial ECG. Regardless of what an initial Troponin might show — prompt cath is indicated!
• PEARL: In isolation — I might not be certain that the inverted T waves in leads III and aVF represent reperfusion T waves (because the T wave may at times be normally inverted when the QRS is predominantly negative in leads III and/or aVF, as it is in ECG #1). However, the subtle-but-real T wave inversion in leads V3,V4,V5 is important to appreciate because it confirms reperfusion and that this patient has an acute evolving OMI.

Learning Point: Isn't it much easier to appreciate the dynamic ST-T wave changes in Figure-1 when we view the 2 tracings we are comparing side-by-side?

• Note that the patient's CP is much less at the time ECG #2 was recorded. As a result — we should expect improvement in this repeat ECG.
• Although subtle — all 3 inferior leads show signs suggestive of reperfusion (ST flattening and beginning T wave inversion in lead II — and deeper T inversion in leads III,aVF).
• The hyperacute T wave in lead V2 has clearly deflated.
• The T waves in high-lateral leads I and aVL have both improved (deflation of the T wave in lead I — and the T wave in aVL is less pointed). Retrospectively — this comparison suggests that lead I in ECG #1 was also a hyperacute T wave.
• ST-T wave morphology has evolved in leads V3,V4,V5,V6 (ST segment straightening has evolved into ST segment coving with deeper terminal T wave inversion).
• Impression: No less than 10/12 leads show "dynamic" ST-T wave changes in ECG #2 compared to ECG #1. There can be no doubt that this patient had an acute OMI — which fortunately is now showing ST-T wave changes of spontaneous reperfusion in 10/12 leads.
• Learning Point: It should not be surprising that when cardiac cath was finally performed (4 hours after the initial ECG) — that this patient did not have a "culprit" lesion identified on cath. That's because the reason the patient was completely pain-free at the time cath was performed is (as ECGs #1 and #2 have told us) — that there has been spontaneous reperfusion of whichever of his multivessel disease arteries had been occluded, but had reopened by the time cath was finally done.