A woman in her 50s with acute chest pain

Submitted and written by Anonymous, edits by Meyers and Smith

A 50s-year-old patient with no known cardiac history presented at 0045 with three hours of unrelenting central chest pain. The pain was heavy, radiated to her jaw with an associated headache.

Triage VS: 135/65 mmHg, 95 bpm, 94% on room air, 16/min, 98.6 F

Triage ECG:

ECG Interpretation:

Sinus rhythm with normal QRS. There is slight STE in V1, V2, and aVR, with STD in V3-V6, I, aVL, and II. There are T waves in lead III which are suspicious for hyperacute T waves, with reciprocal negative large T wave inversions in aVL. I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia), but comparison to a previous might reveal this ECG as diagnostic of OMI.

Smith comment: However, with the STD in I, II, and V4-6, it is diagnostic of ischemia [the question is whether that ischemia is due to 100% occlusion [OMI, with subepicaridal (full thickness) ischemia], or whether it is incomplete ischemia [subendocardial only].

Here is her prior ECG (4 months prior) on file:

Now, with comparison to prior ECG, the findings are new and concerning for inferior OMI, subendocardial ischemia, or both (which is essentially Aslanger's pattern).  

Smith comment: There is a change in V2 as well, with less normal STE and a smaller T-wave with some inversion.  This is likely to be due to high lead placement (as evidenced by a negative P-wave -- should always be upright in V2).  Nevertheless, this suggests that the OMI involves the posterior wall as well.

Initially, the patient was tearful and unable to provide much history secondary to severe pain. The patient had no respiratory distress and was not diaphoretic. Additionally, the patient vomited once prior to arrival which was felt to be indigestion and reported a black stool earlier in the evening. The patient was given 0.4mg SL nitro x 3 with no appreciable change in chest pain (though the headache worsened) and 162mg ASA given the questionable GI bleed. Because of continued chest pain, opioids were given which took the edge off allowing the patient to add they experienced similar pain after dinner for the past 1-2 weeks. Tonight’s episode did not improve with simethicone and Tums as it had previously. The patient vomited once and given the more intense pain decided to come to the ED. On further review of symptoms, there was epigastric and bilateral lower abdominal pain for days. No history of GIB, dysuria, or GU symptoms.

Two repeat ECGs done at 15-minute intervals were unfortunately not captured, however demonstrated no dynamic changes.

Cardiology interpretation of the initial ECG: “ST depressions laterally.”

Smith comment: Cardiology should know, by its own guidelines, that ischemic ST depression that is refractory to medical therapy, is an indication for emergent cath lab, with angiography at < 2 hours.  Unfortunately, they follow their own guidelines only 6% of the time!!
Lupu L, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Clin Cardiol 2022;

https://onlinelibrary.wiley.com/doi/10.1002/clc.23781

Labs included: hsTnI 156 ng/L, Hb 12 g/dL, WBC 12x10^9/L, Cr. 0.9 mg/dL, K 3.5 mmol/L.

The patient’s abdomen was benign and no gross blood on rectal exam. A CT was completed to rule out dissection, PE, or aneurysm, and this was unremarkable.

Another 162mg ASA and heparin were given at this point. The pain recurred and was severe at times, and the patient was started on a nitro drip and given Dilaudid. It was difficult to tell if the nitroglycerin was helping, but 1mg Dilaudid did resolve or nearly resolve the pain.

Smith comment: We have shown that use of opiates is associated with worse outcomes in ACS: 

Bracey, A.  Meyers HP.  Smith SW.  Wei L. Singer DD.  Singer A.  Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion Myocardial Infarctions.  SAEM 2020.  Academic Emergency Medicine 27(S1): S220. Abstract 556.

2-hour hsTn: 615 ng/L; bedside ED echo (without contrast) did not show a clear wall motion abnormality (WMA).

Smith comment: Point of Care ultrasound is not adequate to rule out wall motion abnormality; moreover, diffuse subendocardial ischemia often has no wall motion abnormality because the epicardium is still contracting.  You can't use absence of  WMA to rule out need for emergent angiography!

Repeat ECG:

The cath lab at our nearest referral center was contacted while the patient was in CT and again following the results and repeat labs. The facility was not pressed to activate emergent transfer for PCI since the pain was improving and suggested we optimize pain control and admit to the Cardiac ICU.

Serial troponins continued to rise "greater than 1,000 ng/L" and were still rapidly rising when measurements were stopped.

The patient remained hemodynamically stable, was admitted to the CICU, and went to cath early in the morning which showed 100% distal RCA occlusion, with thrombus and TIMI 0 flow. Most other arteries had scattered 20-30% stenoses. A single DES stent was placed, and the patient did well post-procedure. Formal echo showed mild inferior wall hypokinesis and EF 50%.


Immediate post-cath ECG:

T-waves are no longer hyperacute.  Negative T-wave in aVL is resolved.

No further ECGs were recorded.

The patient did well and was able to be discharged.

Learning Points:

Comparison with prior ECG can help a difficult ECG become diagnostic of OMI.

T wave inversion in aVL usually accompanies hyperacute T waves in lead III.

Opioids in ACS may reduce the pain score, but do not provide reperfusion for ongoing ACS. Thus, they obscure the last possible indication for emergent reperfusion in "NSTEMI" (all guidelines recommend emergent cath for refractory ischemia in NSTEMI). We believe this is why increased mortality and increased delay to cath has been associated with opioids in NSTEMI patients. After the decision to perform emergent reperfusion has been made, then opioids can be given for pain without any such risk.

OMI is not just an ECG diagnosis. When the patient has ACS, with ongoing ischemic symptoms despite maximal medical management, you must consider ongoing acute coronary occlusion MI regardless of your certainty of the ECG findings.

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My Comment by KEN GRAUER, MD (1/6/2023):

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I found today's case interesting for the fact that despite a lack of being able to "localize" a specific culprit artery — the initial tracing from this 51-year old woman who presented with 3 hours of "unrelenting central chest pain" — should have been enough to prompt cardiac cath with no more than minimal delay.

• Dr. Meyers has highlighted the essential ECG findings in this initial tracing. To this, I'll add an additional perspective of why I thought ECG #1 (that for clarity I've reproduced in Figure-1) — to be indicative of an acute process until proven otherwise.

Figure-1: The initial ECG in today's case.

My Thoughts on the Initial ECG:

ECG #1 in Figure-1 — shows sinus rhythm at ~80/minute — normal intervals (PR,QRS,QTc) — a normal frontal plane axis (of +45 degrees) — and no chamber enlargement. Regarding Q-R-S-T Changes:

• There are Q waves in leads III and aVF — but not in lead II. The Q wave in lead III is deep, but not wide — so the significance of these Q waves is uncertain (ie, possibly — but not definitely indicative of inferior MI at some point in time).
• R wave progression appears appropriate (albeit the larger-than-expected QRS amplitude of the complex in lead V2 compared to the complexes in leads V1 and V3 — raises the possibility of some lead malposition).

Regarding ST-T Waves:

• As per Dr. Meyers — In a patient with severe, new chest pain, the T wave in lead III looks like it may be hyperacute (ie, almost as if this T wave in lead III is "trying" to lift up the ST segment in this lead).
• Support that this T wave change in lead III is acute — is forthcoming from the mirror-image opposite ST-T wave depression shape in lead aVL. That said — the ST-T wave in lead aVF does not look hyperacute. And although there is some ST segment flattening with slight depression in lead II, the T wave does not look hyperacute in this lead.
• 
  
• KEY Point: I thought the ST-T wave shape in lead I to be decisively abnormal. This is the finding that convinced me that the ST-T wave changes in leads III and aVL have to be considered acute until proven otherwise in this 51-year old woman with new, severe chest pain!

In the Chest Leads — the ST depression in leads V4,V5,V6 is clearly of concern in this patient with new chest pain. But it was the decisively abnormal shape of the ST-T wave in lead V2 — that convinced me that the composite of ST-T wave changes seen in multiple leads from ECG #1 have to be considered acute until proven otherwise.

• The normal ST segment in lead V2 is typically slightly elevated and gently upsloping, as it imperceptibly blends into a normal upright T wave. Instead of this picture — the ST segment in lead V2 of ECG #1 is flat — and there is no T wave to speak of. Given that T waves in the remaining 4 chest leads are all upright — there should be no doubt that the above described ST-T wave appearance in lead V2 is abnormal.
• In support of this finding — is the ST-T wave appearance in neighboring lead V3. Normally, the ST segment in lead V3 is also slightly elevated and gently upsloping. Instead — there is no ST elevation in lead V3 of ECG #1, and the ST segment in this lead is flat. In a patient with new chest pain and suspected inferior infarction — these findings in leads V2 and V3 should strongly suggest associated posterior OMI.

BOTTOM Line: The main "decision point" in today's case, given the clinical presentation of new-onset, severe chest pain — is whether prompt cath is indicated — and if so, at what point this indication is established. I thought it was established after seeing ECG #1.