Cardiac arrest with anterior-inferior STEMI: Guess the value of the initial ED high sensitivity Abbott troponin I

A ~40 year old woman started having chest discomfort.  She called 911 after an uncertain amount of time.  EMS arrived and recorded this prehospital ECG:

Obvious Anterior and Inferior STEMI, consistent with LAD occlusion

After recording this ECG, the patient went into ventricular fibrillation.

She was rapidly defibrillated.

The cath lab was activated by the paramedics.

She arrived complaining of chest pain, with a BP of 110/70.

An ED ECG was recorded:

It looks worse still

Aside: Should the patient receive antidysrhythmics to prevent recurrent VT/VF?  See discussion below on both beta blockers and other anti-dysrhythmics.

The patient went to the cath lab.

22 minutes after leaving for the cath lab, the initial High Sensitivity Troponin I returned (Abbott Architect, Limit of detection by FDA guidelines at 4 ng/L, 99% Upper Reference Limit for Women = 16 ng/L).  It had been drawn at arrival.

Result: Below 4 ng/L (below the level of detection)

Angiogram/Intervention

100% Distal LAD occlusion due to coronary dissection was found and opened and stented.

Repeat ECG next day:

The 2nd troponin, drawn 3 hours, 25 minutes after arrival, returned at 803 ng/L.

Here is the troponin profile over 7 blood draws (more than is necessary!).  You can see that the highest value (which may or may not be the peak) was over 16,000 ng/L.  

16,665 ng/L roughly correlates with a level of 16.665 ng/mL on the older, contemporary (4th generation) Abbott troponin I assay.  It is typical for STEMI to have a troponin I of greater than 10 ng/mL.  A large anterior MI typically has a level over 30 or 40 ng/mL.

However, we do not know much about the high sensitivity assay, and if that really correlates to a level greater than 10,000 ng/L.  Time will tell.

What is the initial high sensitivity troponin I in STEMI? New ARTICLE.

I co-authored this article with the authors of the HIGH-STEACS trial, and it was published last month in a research letter in JAMA Cardiology.  

Click on this link for the full text: High-Sensitivity Cardiac Troponin Concentrations at Presentation in Patients With ST-Segment Elevation Myocardial Infarction 

We studied 925 STEMI, and showed that the median initial hs troponin I (Abbott Architect) was 196 ng/L.  20 of 925 (2%) had a level less than 5 ng/L.  26.8% had a level below the European Society "Rule-In" level of 52 ng/L.  Patients presenting less than 2 hours (216 of 809) were more likely to have the initial value below the 99th percentile (26.4%, or 57 of 216)[16 ng/L for women; 34 ng/L for men], compared to those presenting later (14.1%, or 95 of 674)

This shows that whether the patient presents at less than, or greater than, 2 hours, the initial hs troponin I below 5 ng/L does not rule out STEMI, and it certainly does not rule out OMI.  This is even more true for the 99th percentile (16 ng/L for women, and 34 ng/L for men).  And it is even more true for the Rule in level of 52 ng/L.

Why is this important for the ECG?

If you are wondering if the ECG you are reading is positive for Occlusion MI, then a very low troponin does not definitively answer the question for you.

Another Great article from the HIGH-STEACS group:

[By the way, this group just published the groundbreaking HiSTORIC study on medrxiv.org. High-sensitivity cardiac troponin on presentation to rule out myocardial infarction: a stepped-wedge cluster randomised controlled trial]  

Beta blockers in acute Anterior MI.

See extensive discussion and references in this post: https://hqmeded-ecg.blogspot.com/2018/10/anterior-stemi-and-multiform-pvcs-with.html

Anterior MI patients treated with PCI (not fibrinolytics) without contraindications to beta blockers, who are anticipated to undergo PCI within 6 hours of onset, who have a BP greater than 120 systolic, appear to benefit from three 5 mg doses of IV metoprolol given prior to PCI.  All patients without contraindications benefit from oral metoprolol after PCI.

If there are no contraindications (no heart failure, SBP at least 120, no tachycardia, no AV block), metoprolol 5mg IV x 3, with oral metoprolol given later if tolerated, seems to convey benefit prior to PCI in anterior MI.  Esmolol is probably a safer choice.

With a BP of 110/70, this patient would not be eligible for beta blockade.

How about other anti-dysrhythmics?   Not indicated.

VT/VF in Acute MI (this is what we wrote in the Tachydysrhythmias chapter of the EmRap compendium):

• Acute MI, particularly ST-elevated MI (STEMI), may present primarily as sudden death due to VT/VF, or these rhythms may occur during ED evaluation for ACS.
  • Note that VT in the setting of cardiac ischemia is usually polymorphic rather than monomorphic.
• Recurrence of VTs in these settings is common.※
• Recent studies suggest that lidocaine, procainamide, and the class III agent amiodarone do not improve the neurologic outcome or mortality to hospital discharge when administered acutely to prevent recurrent or refractory VF after sudden cardiac death.※ Amiodarone, however, improves survival to hospital admission, possibly due to suppression of subsequent events.※
• There is ample evidence that beta blockade lowers the risk of VTs and mortality both acutely and chronically in the setting of acute MI.※
• However, beta blockade can be detrimental in patients with CHF or a low ejection fraction.※
• Reperfusion is the best treatment for prevention of VT.

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MY Comment by KEN GRAUER, MD (9/19/2020):

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As emphasized by Dr. Smith — Today’s case dramatically illustrates how even a high-sensitivity troponin will not always be positive if obtained early in the course of acute OMI.

• The other reason I like this case — is because it shows that even after a very large infarction — the next day’s ECG will not always show obvious signs of a large OMI from the day before!

The patient in today’s case was a 40-year old woman who called 911 because of new-onset chest pain. Shortly after EMS arrival — she developed VFib. After successful defibrillation — the paramedics promptly activated the cath lab on recognizing an extensive STEMI on her pre-hospital ECG.

• I thought it would be insightful to Take Another Look at the 2nd and 3rd tracings obtained in this case (Figure-1).

Figure-1: The 2nd and 3rd ECGs done in this case (See text).

As per Dr. Smith — the ECG in the field and the initial ECG in the ED show an obvious ongoing acute STEMI.

• Taking Another Look — WHAT are the ECG findings YOU see in ECG #2?
• In the ECG done the following day (ie, 1 day after PCI) — WHAT evidence of the MI from the day before do YOU see in ECG #3?

MY Thoughts on ECG #2: The rhythm is sinus at a rate just under 100/minute. The PR and QRS intervals are normal. The QTc looks slightly prolonged. The frontal plane axis is normal. There is no chamber enlargement. Regarding Q-R-S-T Changes — I found it easiest to assess this by looking at lead areas:

• In the Inferior Leads (ie, leads II, III, aVF) — there appear to tiny-but-present Q waves in each of the inferior leads. This may be significant given the 2-3 mm of ST elevation with hyperacute T waves in these leads.
• Mirror-image opposite (reciprocal) ST depression to the ST elevation in lead III is seen in lead aVL. Reciprocal ST depression is also seen in the other high-lateral lead (ie, lead I), albeit less prominent than what we see in lead aVL.
• In the Chest Leads — there are hyperacute T waves in leads V2-thru-V6. ST elevation begins in lead V2 — is maximal in lead V3 (at least 3 mm!) — and persists until lead V4.
• Of Note — R wave progression in ECG #2 is normal — with preservation of anterior R waves, and transition occurring normally between lead V2-to-V3.

IMPRESSION of ECG #2: In this patient with new-onset chest pain (not-to-mention her episode of VFib moments earlier) — these findings are consistent with an acute, extensive inferior and anterior STEMI. Incrimination of the LAD as the “culprit” artery is suggested by ST elevation in leads V2-thru-V4, with hyperacute T waves extending through to lead V6.

• In favor of a mid-to-distal (rather than proximal) location for LAD occlusion are: i) Lack of ST elevation in lead V1, with less-than-maximal ST elevation occurring in lead V2; ii) Lack of ST elevation in lead aVL; iii) Marked inferior lead ST elevation without hint of any inferior reciprocal changes; and iv) Lack of any conduction defect (RBBB & LAHB being common accompaniments of acute proximal LAD occlusion).
• In association with the acute anterior STEMI — acute involvement of the inferior wall in ECG #2 (including high-lateral lead reciprocal changes) — strongly suggests a component of LAD “Wraparound” (in which the LAD is an especially large vessel that “wraps around” the LV apex to involve a portion of the LV inferior wall).

WHAT do We See the Next Day? As per Dr. Smith — Cardiac cath was promptly performed after hospital arrival, and revealed 100% distal LAD occlusion, which was stented. The next day — ECG #3 was obtained:

• The rhythm in ECG #3 is sinus at 85-90/minute. All intervals (including the QTc) are normal.
• There is some change both in the frontal plane axis, as well as in QRS morphology in the chest leads. However, rather than being due to lead placement — I suspect the changes we see in QRS morphology are more likely the result of the large infarction.
• There is now a large Q wave in lead III, with no more than a tiny terminal r wave in this lead. In addition — there is a hint of residual ST elevation in lead III, finishing in shallow T wave inversion.
• QRS amplitude in lead aVF is minuscule (no more than 2 mm total). I don’t think there is a Q in aVF — but the QRS is too tiny to be certain.
• QRS amplitude in lead II in ECG #3 is also reduced compared to ECG #2.
• Regarding the Chest Leads in ECG #3 — No Q waves have formed! That said, compared to ECG #2 — R wave amplitude is clearly reduced! Although the initial septal r wave is preserved in lead V1 — R wave amplitude does not surpass 3 mm until lead V6, and even then, the R in V6 is small.
• Regarding overall ST-T wave appearance in ECG #3 — There is barely any ST-T wave deviation anywhere on this tracing. Instead, there is relative ST-T wave flattening in virtually all leads.

IMPRESSION of ECG #3: I thought it of interest to note that one would never guess from looking at ECG #3 — that this patient had experienced an extensive infero-anterior MI just 1 day earlier.

• The large Q in lead III is a marker of her inferior MI — as is loss of inferior lead R wave amplitude.
• Loss of chest lead R wave amplitude is the marker of her anterior MI. No anterior Q waves formed.

Lessons from Today’s Case:

• An initial negative high-sensitivity troponin value does not necessarily rule out acute OMI if obtained early in the course.
• Follow-up ECG done the day after a large acute MI will not always show obvious ECG findings indicative of the large MI that occurred just 1 day before.