Acute MI, pain onset 24-48 hours ago. Should the patient go for emergent angiogram/PCI?

Case 1.

A 60-something man with HTN, DM, and hyperlipidemia presented stating he had chest pain starting 48 hours prior to arrival. It was substernal, non-radiating and associated with diaphoresis.  

He stated that he had the symptoms throughout the day. He didn't think much of the pain at the time and took some acetaminophen without much relief.  

He had similar discomfort 1 day prior to presentation.  

Apparently the pain was not continuous.


Patient denies of having any chest pain previously before this episode. No cardiac history.

The patient had no chest pain at the time of arrival.

Here was his triage ECG:

What do you think?

There is inferior ST elevation with reciprocal ST depression in aVL and I. There is ST depression in V2-V4.  So this is an infero-posterior STEMI.

However, there are deep QS-waves in II, III, aVF and very tall R-waves in V1-V3.  Why?

This ECG correlates perfectly with the history of 48 hours of pain, as this is a classic subacute STEMI.  There is completed infarction.  The tall R-waves are really Q-waves of the posterior wall as recorded from anterior leads.  [For purists, these tall R-waves actually represent "lateral" infarction, (see Bayes de Luna; Journal of Electrocardiology 41 (2008) 413–418.)]

The initial troponin I returned at 11.0 ng/mL. This is a very typical initial troponin for a subacute STEMI. One expects that, after the artery is opened and the trapped troponin is released, that the post PCI troponin will be much higher.

There is significant ST Elevation.

The cath lab was activated even though symptoms were resolved.  Is that necessary?

Angiogram

There were 2 culprits ("co-culprits"):

1. 99% stenosis in the mid RCA with 90% long stenosis in the ostial and proximal RPDA.

2. Also 99% long stenosis in the distal Left Circumflex and 2nd obtuse marginal (OM2).

These were both opened and stented.

Post PCI ECG, next day:

There is less ST Elevation

48 hours

Less STE still.

Echocardiogram:

Significantly reduced LVEF (35-40%) on TTE with large inferior and inferolateral (+ apical) regional dysfunction. 

A STEMI with early reperfusion may have these echocardiogram findings due to reversible myocardial stunning, and then recover much or most its function over the ensuing weeks. 

On the other hand, in a case of completed transmural infarction, as evidenced by Q-waves (and tall R-waves which signify lateral MI), the poor function and wall motion abnormalities are likely to be permanent. 

Fortunately, he did not develop any overt heart failure signs or symptoms while in the hospital, but was initiated on an ACE inhibitor.

Case 2.


A 70-something y.o. male w/PMH HTN, HLD, DM2 presented with malaise. On the day prior, he experienced "crushing" chest discomfort and profuse diaphoresis between 1330-1500, accompanied by some lightheadedness. He went home to rest.

On the day of admission, he experienced occipital headache and some vague epigastric abdominal pain and two episodes of non-bloody emesis.

At triage, this was his ECG:

He was chest pain free on arrival.

An ECG was recorded at triage:

This again shows inferior Q-waves and large R-waves in V2 and V3.
There has already been significant infarction, completed.
The "coving" (upward convexity with slight STE and inverted T-wave) in inferior leads is diagnostic of inferior MI, and with Q-waves and inverted T-waves, is typical of subacute MI.

The initial troponin I (which also turned out to be the peak) was 39.5 ng/mL.

Angiogram next morning

Because the infarct had happened the previous day, and the patient was asymptomatic at presentation, he was not taken for emergent angiogram.  He was taken the next day.

There was a 100% mid circumflex subacute occlusion.  It was opened and stented.

Echo:

Decreased left ventricular systolic performance-mild.
The estimated left ventricular ejection fraction is 40-45%.
Regional wall motion abnormality-inferior.
Regional wall motion abnormality-inferolateral.



Discussion

Which subacute STEMI should go to the cath lab?

Simplified:

IF there is subacute STEMI by ECG or other criteria AND:
1. Symptoms onset is within 48 hours AND
2. There are persistent symptoms OR persistent ST Elevation

Then the patient should go for emergent angiogram/PCI.

I think it makes sense to extend this beyond 48 hours because ischemia can be so intermittent.

Schomig et al. randomized patients with STEMI and:

12-48 hours of symptoms
No persistent symptoms
Persistent ST Elevation
No hemodynamic or electrical instability, no pulmonary edema

The patients who received emergent PCI had significantly smaller median left ventricular infarct size (8% vs. 13%, p=0.001) measured by single-photon emission computed tomography study, as well as non-significant but underpowered decrease in the composite of death, recurrent MI, or stroke at 30 days (4.4% vs. 6.6%, p=0.37).


The first patient had no symptoms but did have persistent ST Elevation (and ST depression of posterior MI, which is reciprocal to posterior ST Elevation), so emergent angio was indicated.  The wisdom of this is somewhat demonstrated by the dramatic rise in troponin after opening the artery and the resolution of ST Elevation after PCI.

The 2nd patient had BOTH resolved ST segments (no ST deviation) and no persistent symptoms, so angiography could be delayed.  That emergent angio was not indicated is retrospectively supported by the absence of a rise in troponin after artery opening.

Summary: if there is EITHER symptom or ECG evidence of ongoing ischemia, subacute STEMI should go emergently to the cath lab.  
If there is any hemodynamic or electrical instability, or pulmonary edema, the patient should go emergently.
If neither, it is ok to wait.

Reference:

Schomig, A., J. Mehilli, D. Antoniucci, G. Ndrepepa, C. Markwardt, F. Di Pede, S. G. Nekolla, et al. 2005. “Mechanical Reperfusion in Patients with Acute Myocardial Infarction Presenting More than 12 Hours from Symptom Onset: A Randomized Controlled Trial.” JAMA: The Journal of the American Medical Association 293 (23): 2865–72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15956631.




For those wanting even more detailed ECG Analysis, See Below comments below by Ken Grauer:

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Comment by KEN GRAUER, MD (7/5/2019):

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The 2 cases in today’s ECG blog post illustrate how much correlation with the History facilitates clinical interpretation of the ECGs in this Case.

• I focus my attention on ECG interpretation of the initial ED tracing in each Case (Figure-1).

Figure-1: The initial ECG in each Case (See text).

Extra CHALLENGE: YOU should be able to identify at least 4 different and important ECG findings in assessment of ECG #1. What are they?

• HINT: You are likely to miss at least one of these important findings IF you fail to use a systematic approach ...

My THOUGHTS on ECG #1 — The patient in Case #1 was a 60-something man with hypertension and diabetes, who presented with intermittent chest pain over the 48 hours preceding his arrival in the ED. He was not having chest pain at the time of his initial ED tracing ( = ECG #1 in Figure-1):

• The rhythm is sinus at ~95/minute.
• The PR interval is normal — and the QRS complex is narrow. The QTc appears at least slightly prolonged, although assessment of QTc duration is more challenging (and often less helpful) at heart rates over 90-100/minute.
• There is marked LAD (Left Axis Deviation) — as evidenced by all negative complexes in each of the inferior leads.
• There is definite voltage for LVH. This is most evident in lead aVL (R wave amplitude is obviously much greater than the criterion of R≥12 mm) — but increased voltage is also evidenced by the very tall chest lead R waves. (CLICK HERE — for the LVH criteria I favor).

Regarding Q-R-S-T Changes:

• As already noted — there are deep QS complexes in each of the inferior leads. No other Q waves are seen.
• There is a Tall R Wave in Lead V1. I measure 13 mm for the predominant R wave in lead V1 — vs only 3 mm for the S wave in this lead. (CLICK HERE — for Review of Common Causes of a Tall R in Lead V1).
• Regarding ST-T wave Changes — Each of the inferior leads manifest coved ST elevation of 2-3 mm, followed by fairly deep, symmetric T wave inversion. Reciprocal ST depression is seen in lead aVL > lead I. In the chest leads — ST depression is maximal in lead V2 — but also present in leads V1, V3, V4 — with ST-T wave flattening (and shallow T inversion) in leads V5,V6.

COMMENT / Clinical Impression: To answer the CHALLENGE I posed earlier — the 4 important findings in ECG #1 are: i) Recent acute MI; ii) Marked LAD (that is consistent with LAHB = Left Anterior HemiBlock); iii) LVH; and, iv) Tall R Wave in Lead V1.

• Each of these findings is important and relevant to this case. Considering the History ( = new chest pain that began 48 hours earlier, and which has been intermittent since — but which was not present at the time ECG #1 was recorded) — the overall clinical picture makes sense.
• It is quite unusual to see such deep QS complexes in each of the inferior leads as appear in ECG #1. Much more often, you’ll see at least some R wave activity in at least one or two of the inferior leads (as we see in ECG #2). That said — the inescapable conclusion is that there is most likely both LAHB and inferior MI in ECG #1.
• R wave amplitude far surpasses criteria for LVH in lead aVL (as well as being quite generous across the precordial leads). Without seeing a prior tracing on this patient — I find it impossible to discount a component of LV “strain” (or a strain equivalent) for the ST depression that we see in lead aVL. Given the history of diabetes and hypertension — the inescapable conclusion is that there is LVH.
• Recognition of the finding of a predominant R wave in lead V1 should prompt consideration of the differential diagnosis that we have REVIEWED PREVIOUSLY. Given new chest pain (of 48 hour duration at the time of presentation) and the limb lead findings described above — we have to presume the Tall R in V1 is the result of associated posterior infarction.
• BOTTOM Line: As per Dr. Smith — the findings in ECG #1 are consistent with a subacute infero-postero STEMI. Although it is possible for Q waves of acute infarction to form in as little as 1-2 hours — formation of the deep inferior lead QS complexes and the predominant R wave of posterior MI that we see in lead V1 generally take more time than that to develop (ie, typically at least 12-48 hours). Similarly, the fairly deep inferior lead T wave inversion seen here typically also takes some time to develop. Yet significant ( = 2-3 mm) ST elevation persists in the inferior leads of ECG #1 — which (as per Dr. Smith) was the reason for taking this patient to cath even 48 hours after likely onset of his acute event.
• P.S. — As I’ve emphasized many times in these ECG blogs — the most common reason I see for capable clinicians overlooking important findings is simple failure to regularly use a Systematic Approach in the interpretation of every tracing they encounter (CLICK HERE — for the System I favor).

My THOUGHTS on ECG #2 — The patient in Case #2 was a 70-something man who experienced “crushing” chest pain the day before he presented to the ED. He was not having chest pain at the time of his initial ED tracing ( = ECG #2 in Figure-1):

• The rhythm is sinus bradycardia at ~55-60/minute.
• All intervals (PR/QRS/QTc) are normal.
• There is a leftward frontal plane axis — but not leftward enough to qualify for LAHB. That is — since the QRS complex in lead II appears to be at least slightly more positive than negative — the frontal plane axis is less negative than -30 degrees, which is the minimum required to qualify LAD as LAHB. In addition — QRS morphology (with a QR rather than an rS) in lead II is consistent with inferior infarction, but not with what is typically seen in LAHB.
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are large Q waves in each of the inferior leads. The deep Q waves in leads III and aVF appear to be followed by a tiny r wave. Considering how small QRS amplitude is in lead II — the 2 mm deep Q wave in this lead (which comprises ~40% of the R wave in lead II) qualifies as a “large” Q wave.
• Transition occurs early in ECG #2 — with abrupt development of a predominant R wave as soon as lead V2. While there is no predominant R wave in lead V1 — the dramatic change in transition seen here should prompt consideration of similar entities as were mentioned in Case #1 for a Tall R in lead V1.
• Regarding ST-T wave Changes — Each of the inferior leads in ECG #2 manifest ST segment coving — but with no more than minimal ST elevation. This is followed by shallow T wave inversion. Lead aVL manifests ST segment flattening — but really no ST depression. Similarly, there is ST-T wave flattening in leads V4-thru-V6 — but no ST segment deviation. And, although the T waves in leads V1 and V2 look a little-more-peaked-than-expected given QRS morphology in these leads — these are not acute changes.

COMMENT / Clinical Impression: There has been inferior MI. In addition, abrupt early transition with a surprisingly tall R wave already in lead V2 suggests associated posterior involvement. That said — the History (ie, severe new-onset chest pain the day before — that has since resolved) + the non-acute nature of the ST-T wave changes described above — suggest that the onset of this acute MI most probably corresponds to the onset of chest pain 1 day earlier.

• Lack of ongoing symptoms, and lack of acute ST-T wave changes in Case #2 — were the reason cardiac cath was not done until the following day.