What happens when a patient with LAD OMI does not go immediately to the cath lab?

This patient was extremely elderly, and although the diagnosis was recognized, she did not go to the cath lab for reasons related to age and patient/family choice.

Nevertheless, there is a lot to learn from the ECGs.


I was shown this ECG without any information:

QTc = 431 ms


What was my response?

I immediately said: "Acute LAD occlusion.  Occlusion MI (OMI)"  (And sinus rhythm with a PVC.) (Not quite a STEMI, but same effect.)

Why did I diagnose LAD occlusion?

There is ST elevation in V2-V4 that does not quite meet "STEMI criteria."  Is it normal ST elevation?  No!  How do I know?  First, there is reverse R-wave progression.  The R-wave in V3 is smaller than the R-wave in V2.  Thus, there is reverse R-wave progression, and even a Q-wave in V4. This never happens in normal ST elevation. 

There are hyperacute T-waves in V2-V4.

The 4-variable formula can be used: http://hqmeded-ecg.blogspot.com/p/rules-equations.html
Also see free apps: iPhone: "SubtleSTEMI" Android: "ECG SMITH"
www.mdcalc.com: https://www.mdcalc.com/subtle-anterior-stemi-calculator-4-variable

Here, the QTc = 431
STE60V3 = 1.5
RAV4 = 4
QRSV2 = 13.5.
Formula value = 20.89, which is much higher than the cutpoint of 18.2 and makes this LAD occlusion until proven otherwise.

You might think it is "Old MI with persistent ST Elevation" (otherwise known as "LV aneurysm" morphology.")    That is a reasonable thought, but we have shown that if there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is STEMI, not LV aneurysm.


"What's the story?"

History: An extremely elderly patient who lived independently presented with acute "oppressive" chest pain 7/10 in severity that was not positional, pleuritic, or reproducible.  Exam was benign and VS were normal.

Here is her previous ECG from 7 years prior:

Normal

This previous ECG shows that the poor R-wave progression is new.

Does this mean that there was an intervening infarct since 7 years ago?  No!  Just one hour of acute LAD occlusion can result in acute Q-waves or loss of R-wave amplitude.

Reference: Raitt, M. H., C. Maynard, G. S. Wagner, Cerqueira, R. H. Selvester, and W. D. Weaver. 1995. “Appearance of Abnormal Q Waves Early in the Course of Acute Myocardial Infarction: Implications for Efficacy of Thrombolytic Therapy.” Journal of the American College of Cardiology 25 (5): 1084–88.


Case continued:
All the physicians were very worried about LAD occlusion and recorded a couple bedside ultrasounds:



This shows a profound apical and septal wall motion abnormality, perfectly consistent with LAD OMI.


Speckle Tracking Strain Echo was also done:
https://hqmeded-ecg.blogspot.com/search/label/Speckle%20Tracking%20Strain%20Echocardiography



Again, it shows an obvious severe wall motion abnormality.  Only one echo segment on this video is moving adequately, and that is the high lateral wall on the right (on the graph to the right, it is the only segment that shows a dip below -5.0)


These ultrasounds confirm LAD occlusion.

I want to show the first ECG again, followed by serial ECGs:

30 minutes after the above ECG, the first troponin I returned at 0.147 ng/mL, confirming acute MI.

She was treated with aspirin and heparin.



This ECG was recorded at 105 minutes

This shows more ST Elevation, especially in V3.
Further evidence of evolution of LAD OMI

Apparently, the pain was improving, and another ECG was recorded at 140 min:

ST elevation is resolving, further confirming the LAD is/was(?) occluded.
Is this a transient STEMI? (spontaneously reperfused without lytics or PCI?)
Remember the Q-waves !!
There is not only resolution of ST elevation and hyperacute T-waves.
When Q-waves have developed, it cannot be assumed to be a transient STEMI.

Pain will resolve with completed infarct or with resolution of ischemia.
This looks like infarct completion.

Patient was placed on a nitro drip and pain remained under control.  For several reasons, they did not go to the cath lab.  One of these was the absence of active pain and that the ST elevation had disappeared.


ECG recorded at 7 hours

All active ischemia is gone.
There is only a completed anterior infarct remaining.
Thus, the patient may be pain free from infarct alone, even without spontaneous reperfusion.

10.5 hours

No major change.

Troponin Profile:

99% reference value = 0.030 ng/mL

Unfortunately, the patient suddenly died the next day.


Learning Points:

1. Pain will resolve not just with resolution of ischemia, but with completion of infarction.  Beware.

2. Q-waves may form early after LAD occlusion.  When they are present, it should not dissuade you from reperfusion therapy.   It should also tell you this is not a transient STEMI (OMI)

3. If there is a long enough delay to treatment of acute OMI, it will become a completed Q-wave MI.

4. Even if this were a Transient OMI, treatment of Transient STEMI (or OMI) with emergent angiogram is prudent.  Because of occasional catastrophic outcomes in patients with transient STEMI, I recommend that it be managed just like a persistent STEMI.  A recent randomized trial showed no difference in outcomes between immediate vs. delayed angiography, but there were a handful of patients who needed to go suddenly and emergently due to reocclusion, in spite of maximal medical therapy.  If emergent PCI is not undertaken, then extremely close monitoring with 12-lead ST segment monitors is essential to detect reocclusion.

--Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

--Wellens' syndrome, no culprit, what happened?

See this post:

Timing of revascularization in patients with transient STEMI: a randomized clinical trial

Here is a terrible case of transient STEMI:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

5. This was an LAD occlusion that was evolving from OMI to Q-wave MI, and pain resolution was due to infarction, not to restoration of perfusion.

6. Anyone can die of LAD occlusion, but especially the very elderly and especially if they are not reperfused.  When I heard she had not undergone immediate angiogram, my first question was, "Did she die?"

===================================

Comment by KEN GRAUER, MD (4/3/2019):

===================================

Insightful case presented by Dr. Smith — of an elderly woman with acute LAD OMI. I’ll add a few thoughts on the initial ECG that Dr. Smith was asked to interpret without the benefit of any clinical information ( = ECG #1 in Figure-1).

Figure-1: The initial ECG in this case — which Dr. Smith was asked to interpret without the benefit of any clinical information (See text).

=================

COMMENT: From the perspective of being shown ECG #1 without the benefit of any clinical information — there are a number of clues that suggest an acute event is likely to be ongoing:

• The rate of this sinus rhythm is relatively fast (ie, ~95/minute).
• There are frequent PVCs (on this tracing — 3 PVCs in the space of 10 seconds = beats #3, 9, 14).
• In a patient with PVCs and a relatively fast heart rate — the ST-T wave appearance in lead V4 in Figure-1 has to be assumed acute until proven otherwise! Features that tell us the ST-T wave in this lead is hyperacute are: i) The T wave in lead V4 is disproportionately tall, compared to the very small r wave amplitude in this lead; ii) This T wave is clearly fatter-at-its-peak than it should be; and, iii) This T wave is much wider-in-its-base than it should be.
• In support of presumed acute LAD OMI — are hyperacute T waves also in leads V2 and V3 — and possibly also in leads V1 and V5 (See below).

=================

Beyond-the-Core: I thought a number of other findings on this initial ECG in Figure-1 were worthy of mention. NOTE: These are advanced concepts.

• I suspect there is some lead malposition of either lead V2 and/or V3. I say this because progression of both S wave depth and T wave appearance in anterior chest leads is not as expected. The S wave becomes considerably larger (deeper) from lead V1-to-V2 — and then becomes much smaller by V3. By itself, this change in S wave appearance would not necessarily indicate lead malposition — BUT — the T wave becomes significantly taller from V1-to-V2 — then significantly smaller from V2-to-V3 — and then once again significantly taller from V3-to-V4. This T wave progression sequence does not make physiologic sense.
• We see the ST-T waves for only 2 sinus-conducted beats in leads V1,V2,V3; and for only 2 sinus-conducted beats in leads V4,V5,V6. Did YOU notice a change in ST-T wave appearance for these 2 sinus-conducted beats? Specifically — Doesn’t the ST-T wave appearance of beat #10 in leads V1 and V2 ( = “A”) look more ominous than the ST-T wave of beat #11 in these leads ( = “B”)? There are 2 possible reasons that may account for this difference in ST-T wave appearance: i) Artifact/respiratory movement (and we can see a definite dip in the baseline in beat #10 in the long lead II rhythm strip at the bottom of the tracing); and, ii) There is a post-ectopic phenomenon, in which unrelated to ischemia, the ST-T wave of the beat following a PVC will often be altered. To a lesser degree — Doesn’t the ST-T wave of beat #15 in leads V4 and V5 ( = “D”) look more ominous than the ST-T wave of beat #13 in these leads ( = “C”)? Which complex (A or B? C or D?) is the “correct” one? It’s impossible to tell from this single tracing that only shows 2 sinus-conducted beats to choose from in these leads ...
• Despite suspected lead malposition of lead V2 and/or V3 — I agree with Dr. Smith that there is “telltale” loss of r wave as one moves from lead V2-to-V3 — which strongly suggests there has been anterior infarction at some point in time.
• Look at the QRS for the 3 sinus-conducted complexes in lead V4 (= beats #13, 15 and 16). The QRS manifests a qrS pattern. Even though the size of this q wave in lead V4 is small — it is significant (ie, indicative of anterior infarction) — because it is simply not normal to have an initial negative deflection (q wave) followed by a positive deflection (r wave), that is then followed by a deep S wave in a mid-chest lead. This adds support regarding our concern about the loss of r wave from lead V2-to-V3 — and it confirms that there has been anterior infarction at some point.
• Note that despite evidence of anterior infarction — there is an initial small position deflection (r wave) in lead V1. The 1st part of the ventricles to depolarize is the ventricular septum — and the direction of normal septal activation is from left-to-right. At least in theory — when right-sided lead V1 writes an initial positive deflection (r wave) — this implies that septal activation is occurring normally (ie, from left-to-right) — which suggests isolated anterior infarction (and not “antero-septal” infarction). Electrocardiographically — antero-“septal” infarction would be suggested by complete absence of any positive deflection in leads V1, V2 and V3.
• As a semantic point — I was “on the fence” as to whether there is or is not 1st-degree AV block in Figure-1. The PR interval seems different depending on the lead in which you measure. Low amplitude for P waves and baseline artifact complicate assessment in this tracing. I generally accept up to 0.21 second in duration as a “normal PR interval”, especially in an older individual — and that’s what I measured in the long lead II rhythm strip. That said, 0.21 second is probably long given the relatively rapid heart rate in ECG #1. That said, even if slightly prolonged — 1st-degree AV block is unlikely to be of clinical significance here as an isolated conduction defect.

=================
FINAL POINT: When did the anterior infarction occur? Dr. Smith makes the very important point that as little as 1 hour of acute LAD occlusion can result in either acute Q waves or loss of R wave amplitude! Therefore, it certainly is possible that this evidence of anterior infarction that we see in ECG #1 is acute and associated with this ongoing event.

• But, the most recent prior ECG available on this patient was from 7 years ago. R wave progression in the chest leads was normal at that time. This means that anterior infarction occurred at some time between 7 years earlier — and when ECG #1 in Figure-1 was done.
• The Framingham studies showed that at least 1/4 (if not, up to 1/3) of all MIs are “silent” (ie, not associated with chest pain — and in their study, only incidentally discovered after-the-fact on routine ECG done a year or two later). “Silent” MIs were most common in elderly patients — and the patient in this case was said to be “extremely elderly”.
• A shortcoming of the Raitt study that is referenced above — is that it failed to account for a lack of baseline ECGs on patients in their study group. Instead, they accepted the patient and medical record account of “no past history of MI”. This acceptance on their part overlooks the concept (and possibility) of interim “silent” MI.
• BOTTOM LINE: I have no doubt that the overall conclusion of the Raitt study is accurate — namely that Q waves may develop in some patients as soon as within the 1st hour of acute coronary occlusion. But because of how common “silent” MI is (especially in the elderly) — we have no way to distinguish between a prior “silent” MI having occurred sometime during the past 7 years, now presenting with a 2nd event in the form of another anterior MI, this time with symptoms — vs — new Q waves from this current acute LAD occlusion episode that is this patient’s 1st event.

Our THANKS to Dr. Smith for this highly insightful case!