Tuesday, July 17, 2018

Syncope in a 20-something woman

A 20-something was outside exerting herself.  She states that  it was hot outside and that she was probably dehydrated. At one point, she felt lightheaded and then can't remember anything until waking up in the ambulance.  Her friends saw her lose consciousness and fall on the ground.  She regained consciousness spontaneously before responders arrived. Fire department was on scene first, who noted a cyanotic color to the patient's face.  EMS arrived and also noted cyanotic color which improved en route to HCMC. She denies head pain, neck pain, back pain, abdominal pain or any pain at this time.  There was no nausea or vomiting.

In the ED her exam was normal.  All vital signs were normal, with a pulse of 65.


Here is her ECG:
Computer interpretation: borderline long QT interval
What do you think?


































Physician assessment (who apparently took the computer read as truth): "ECG had borderline prolonged QT interval, but otherwise did not have signs of arrhythmia or RH strain (Pulmonary embolism) that would be underlying cause of syncope."


Should we believe the computer's assessment?  Never!  When you have ANY suspicion that the QT is prolonged on visualizing the ECG, you must measure it.  The computer is often wrong.


Here I measure the QT:
One should measure the longest QT of the 12 leads.
I did not do that, but just chose one that looked long
See the 2 black lines at the beginning of the QRS and end of the T-wave.
This measures about 680 ms.
The heart rate is barely above 60, so correction will not change it much.
So this is a dangerously long QT (any corrected QT above 480 - 500 ms is associated with a significant risk of Torsades de Pointes--TdP)


There is actually a second hump on many of the T-waves.  Are these large U-waves?  Perhaps, but either way, it is very abnormal and puts the patients at risk for TdP.

See this post on QT correction: 

QT Correction Formulas Compared to The Rule of Thumb ("Half the RR")


Final physician assessment: dehydration.  The patient was discharged.

Outcome

Another Emergency physician was later reading the ECGs on the system and putting in final interpretations.  She immediately recognized long QT.  She called the patient back.  The patient was admitted.  

She was on no medications that would prolong the QT.  Her K was 3.4 but the ECG findings persisted after correction.  

Thus, she was diagnosed with long QT syndrome.  The electrophysiologist diagnosed it as "probable type 2" long QT (beyond the scope of this blog post and of my understanding).

Genetic testing was undertaken, results pending.

Nadolol 20 mg prescribed.  It is typical to prescribe beta blockers for congenital long QT, though that depends on the type of congenital long QT.

For more on syncope:  

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

Friday, July 13, 2018

A man in his 40s with chest pain


Case submitted and written by Alex Bracey, with edits by Pendell Meyers and Steve Smith


This ECG was tossed onto my desk on my first day of a new rotation at a community site. The technician was nowhere to be found by the time I turned to ask what the story is or where the patient is located.
Initial ECG at 1350 - are you concerned?




















- There is 0.5 mm STE in aVL, no clear STE in lead I.

- There is ST depression in II, III, and aVF.

- Nicely demonstrated here, leads III and aVL are reciprocal: STD in III is reciprocal ST depression to STE in aVL. This is diagnostic of occlusion (OMI).

- There is also some slight STD in V4-V6. Out of context, STD in V4-V6 as well as II, III, and aVF, with slight STE in aVR may make you think of diffuse supply demand mismatch ischemia as can happen with any pathology involving diminished blood flow to the majority of the heart, such as left main stenosis or severe three vessel disease. However, the morphology and STE in aVL with the morphology of the reciprocal STD inferiorly sets this case apart and identifies OMI rather than just global supply/demand mismatch.
- STEMI criteria are not met.


No prior ECGs were available.


My co-resident and I went to find the patient in the main ED. He was a man in a his late 40s who was alert but looked as though he was trying to maintain a smile through some discomfort. He told me that he had been having chest pain for ~6 hours, described as a heaviness in his chest, that started just after signing his divorce papers. He was an active smoker with hypertension and had a closely related family member that had an MI at the age of 49.


We gave him aspirin and asked for a repeat ECG.


While awaiting the repeat ECG, it was suggested that cardiology be consulted emergently for intervention. A senior team member, while concerned about the ECG wanted to wait for the troponin to result before involving cardiology. At 14:35, ~45 minutes after in the initial ECG the patient, the troponin I resulted as 0.701 ng/mL (normal range 0.000 - 0.045 ng/mL).

At this point, even if the ECG is confusing to you, the diagnosis is made: chest pain with an elevated troponin in this context is acute myocardial infarction. No matter what the ECG shows, with continued chest pain the patient must go emergently to the cath lab. In this case, you have BOTH a diagnostic ECG and a diagnostic troponin.

A repeat ECG was obtained shortly after:
Repeat ECG @ 1447

Similar to prior. The artery is still occluded.





At this point, cardiology was consulted and I described the findings and relayed concern for acute coronary occlusion in the absence of a STEMI. The cath lab was not immediately activated, but cardiology staff was sent to evaluate the patient. The patient was admitted to cardiology and underwent cardiac catheterization ~2.5 hours after presentation and initial ECG.


Prior to the publishing of the cath note, we received a phone call from the interventional cardiology who commended us and informed us, with some surprise, that he had found thrombus in the LCx second obtuse marginal, which had successfully undergone PCI with one drug eluting stent.



On the actual cath report, no initial stenosis percentage or TIMI flow were reported; rather, only the post procedure TIMI III and residual stenosis of 0% are documented.


This is the subsequent ECG taken just after PCI:
ST changes are resolving.



One day later, the troponin I peaked at 48.2 ng/mL. He was discharged home the subsequent day with a diagnosis of "NSTEMI."


TEACHING POINTS:

STEMI criteria will miss a significant number of acute coronary occlusions. While this criteria exists and is still recognized as the standard for diagnosing acute coronary occlusion, patients will continue to have delay to definitive management (e.g., PCI). As in this case, the diagnosis was made at hospital presentation, but he patient waited for 2 hours until intervention. Even then, the cardiologist was surprised to find an acute lesion. As we've said before, we must change the language to include those that will benefit from emergent intervention even though they do not manifest STEMI criteria (see this post: OMI Manifesto).

We were fortunate to have a fairly receptive interventionalist on this case; however, that will not always be the case. In such instances, serial ECGs become invaluable, as the patient may manifest worsening STE or even simply dynamic ECG changes which may be enough to convince an interventionist to emergently activate the cath lab. But notice that in this case there was no serial change; you cannot depend upon it!

Do not wait for the troponin to result before getting cardiology involved with a concerning ECG and story; the troponin plays a supporting and complimentary role in the diagnosis of OMI. Keep in mind that contemporary troponin assays will only start to manifest at the 4-6 hours mark, and many people with ACO will present well before that point. Had this patient’s troponin been undetectable, it would not have changed where this patient needed to go: the cath lab. Had it been negative, it may have delayed his time to PCI. Time is myocardium.



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Comment by KEN GRAUER, MD (7/13/2018):
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It is cases like this one that emphasize the tremendous importance and educational impact of Dr. Smith’s ECG Blog. This case should not have been delayed for several hours before being recognized for the OMI that it is. I’ll add the following points:
  • As per Drs. Bracey, Smith and Meyers  — dependence on strict STEMI criteria will miss a significant number of acute coronary occlusions. This is especially so in cases like this one, in which only lead aVL manifests ST elevation. It is important to appreciate that lead aVL is the “highest” lateral lead — and with acute occlusion of the 1st or 2nd obtuse marginal branch of the LCx — lead aVL may occasionally be the only lead to show ST elevation.
  • There is ample evidence on the rest of the initial ECG (done at 13:50) to support the conclusion that changes in lead aVL must be assumed acute until proven otherwise. As per Dr. Bracey, Smith and Meyers — this evidence includes reciprocal ST depression in each of the inferior leads, with an exact “mirror-image opposite picture” of the ST elevation in aVL seen by the shape of the ST-T depression in lead III. In addition, there is ST segment flattening with 0.5-1mm of ST depression in leads V4, V5 and V6.
  • The appearance of anterior leads V1, V2 and V3 is also worthy of mention. On initial inspection of the 1st ECG (done at 13:50) — there appears to be a QS complex in each of these 3 anterior leads. This raises suspicion of anteroseptal infarction at some point in time. The disproportionately tall (and fatter-than-expected-at-its-peak) T wave in lead V3 might raise suspicion of an acute event in the LAD distribution, if not for 2 points: ithe even more convincing ECG picture in the limb leads that suggests acute LCx Obtuse Marginal occlusion; andiithe likelihood of some chest electrode lead misplacement, given the prominent negative P wave component in V1, V2 — and, the unexpected decrease in S wave amplitude from V1-to-V2, that then unexpectedly increases again by lead V3. Sure enough, a definite initial positive deflection (r waveis seen in lead V3 of the 2nd ECG (done at 14:47) — which makes prior anteroseptal infarction less likely.
COMMENT: The presentation of this case reminds me of my experience as the provider charged with interpreting all ECGs done by the 35 practitioners at our ambulatory Family Medicine Center over the 30 years that I served in the Residency Program as full-time core faculty. In that role, I was often presented a series of tracings without any history. The challenge was determining which tracing(s) showed findings that mandated dropping whatever I was doing to immediately find out the history, because of concern for a potential acute condition. Credit to Dr. Alex Bracey for doing just that in this case! Had he not directly hunted down the patient in the ED — there is a very good chance that this patient’s OMI would not have been recognized in time.
  • MORALIt’s impossible to appropriately interpret ECGs without clinical correlation! The initial (13:50) ECG in this case might not necessarily be cause for alarm in the absence of symptoms — especially if a prior ECG was found showing similar changes. But on learning that the patient in this case had new-onset chest discomfort just a few hours earlier — acute OMI has to be assumed until proven otherwise, regardless of what serum troponin shows — and regardless of whether the 2nd ECG shows serial changes.


Wednesday, July 11, 2018

Is there a Right Ventricular MI in addition to Infero-postero-lateral MI?

A 40-something woman had sudden chest pain.  She called 911.  This prehospital ECG was recorded:


Here are limb leads:

Here are precordial leads:
Diagnosis?

















This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria.

But which myocardial walls are affected?

Inferior
Posterior (as manifested with T-wave inversion)
Lateral (subtle ST elevation)
Is there also RV MI?  Can you tell from this ECG?  (hint: no, you can't tell from this ECG)

When this was shown to me, I said "Activate the Cath Lab."

The providers had been uncertain until I gave my opinion, but then went ahead and activated.

Then this was recorded in the ED 10 minutes after the first:
Now there is massive STE
Many inferior MI are associated with RV MI.  Is there RV MI here?

The left sided 12-lead is imperfect for diagnosing RV MI.  The same week this case arrived, I submitted a revision of a manuscript that is under consideration in which we found:

1) ST depression in lead I is useless in differentiating RCA occlusion with vs. without RV MI
2) ST elevation in V1 is pretty specific (~83%) for RV MI in the setting of inferior MI.
3) ST elevation in V1 is not sensitive for RVMI, and is very insensitive if there is ST depression in V2 (posterior MI pulls the ST segment down and negates any ST elevation that might otherwise be present in V1 during RV MI).

So, if you have the time while waiting for the angiography team, you should record a right sided ECG, because RV MI have higher mortality, are more likely to be hypotensive, and are more nitroglycerin sensitive.

So we recorded a right sided ECG:
V1 = V1R = same position as V2 on left side ECG
V2 = V2R = same position as V1 on left side ECG
V3 = V3R
etc.
Now you can see that there is much STE in V4R-V6R, diagnostic of RV MI.


At angiogram, there was a culprit just distal to the RV marginal branch (not proximal), and so it was called a mid-RCA occlusion.  By the ECG, it should be a proximal occlusion, proximal to the RV marginal branch.

I saw this result the next day and it perplexed me, so I inquired with the cardiologists.

Today, they viewed the angiogram and concluded that the thrombus at the mid RCA must have extended proximally from the culprit ruptured plaque, extending proximal to the RV marginal branch and temporarily occluding it.  However, by the time of the angiogram it had embolized distally,  and had only done so after the right sided ECG was recorded.

See this case in which I saw STE in V1 and called the angiographer to suggest he look more closely at the angiogram.  He did, found the true culprit, and went back in to stent it.

Right Ventricular MI seen on ECG helps Angiographer to find Culprit Lesion



This is the ECG.  You can listen to my explanation by playing the video.





Learning Points:

1. To reliably diagnose RV MI, you need a right sided ECG.
2. In inferior MI, ST elevation in V1 is specific for RVMI.  False negatives could be partly due to misleading angiograms!
3. In inferior MI, ST elevation in V1 is not sensitive for RVMI, and is particularly insensitive when there is ST depression (due to posterior MI) in V2.
4. ST depression in lead I is NOT useful in determining the presence of right ventricular MI
5.  The condition of the coronary artery at the time of angiogram may be different than it was 30 minutes prior during recording of the ECG.


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Comment by KEN GRAUER, MD (7/11/2018):
-----------------------------------------------------------
Insightful blog post by Dr. Smith regarding ECG criteria for recognizing acute RV involvement in patients with inferior STEMI. I’ll highlight a few additional points:
  • As per Dr. Smith — the initial ECG is diagnostic of acute coronary occlusion MI (OMI). This initial tracing is a superb example of Hyperacute ST-T wave changes. By this, we mean that while there is relatively little ST segment elevation — the T waves in each of the inferior leads are extremely prominent, and much fatter-than-expected at their peak. It is almost as if you can imagine the prominent T wave peak beginning to lift up the ST segment — which then becomes dramatically obvious in the 2nd ECG recorded in the ED just 10 short minutes later! I find it humbling to appreciate how RAPIDLY acute ST-T wave changes may sometimes evolve ...
  • Hyperacute ST-T wave changes are transient. In this case, they were gone within 10 minutes. The reason it is so important to recognize hyperacute changes for the brief time they are present — is that when they are seen in “patterns of leads” (ie, in all 3 inferior leads), in association with reciprocal changes — they can be diagnostic of acute OMI before frank ST elevation occurs.
  • Confirmation that suspected hyperacute changes are real — is forthcoming once you identify mirror-image reciprocal changes (Figure-1). With acute inferior STEMI — there is an almost magic mirror-image” picture for the ST-T waves in lead III compared to lead aVL. To better appreciate this concept — I’ve placed a mirror image picture of lead III within the BLUE rectangle — and a mirror image picture of lead aVL within the YELLOW rectangle. Thus, lead aVL shows how reciprocal ST-T depression can also manifest a hyperacute picture.
  • Hyperacute changes are also seen in other leads in Figure-1. Note how lead V6 shows a disproportionately large and fatter-than-expected T wave peak. Little wonder this picture in V6 was soon to evolve into significant ST elevation in the 2nd ECG. Hyperacute changes are more subtle in lead V5 — but given the concept of neighboring leads”, they are nevertheless present. That is, the ST segment in lead V4 is clearly abnormal (ie, coved instead of concave up) — so the ST-T wave picture in V5 reflects a “transition” between what we see in neighboring leads V4 and V6.
  • Finally — leads V2 and V3 in Figure-1 manifest a similar ST-T wave shape as is seen in lead aVL. This reflects the mirror-image ST-T wave reciprocal picture in anterior leads that is so commonly seen in association with acute infero-postero OMI.
Figure-1: Initial ECG, obtained pre-hospital from this 40-ish year old woman with new-onset chest pain (See text).
Comparing the First Tracings:
It is interesting follow the evolution of the hyperacute changes seen in the initial ECG. To facilitate this comparison — I’ve put both images into a single figure (Figure-2).
  • Note that all leads showing hyperacute changes in the initial ECG (within the RED rectangle) — now show dramatic ST deviation (elevation or depression) in the 2nd tracing (within the BLUE rectangle).
  • Localization of the “culprit artery” to the RCA is suggested in the 2nd ECG by: iMore ST elevation in lead III compared to lead II (the opposite tends to be true when the LCx is the culprit artery); iimarked reciprocal ST depression in lead aVL; and iiiLess ST elevation in lead V6 compared to what is seen in the inferior leads.
  • As per Dr. Smith — right-sided leads were needed to diagnose acute RV involvement. However, once right-sided leads confirmed associated RV MI — identification of the RCA as the “culprit artery” is solidified.
Figure-2: TOP — Initial ECG obtained pre-hospital. BOTTOM — 2nd ECG obtained 10 minutes later in the ED (See text).

PS (7/15/2018): In a July 11 post to the EKG Club — Peter Calvert raised the excellent point about development of prominent J-waves in the 2nd ECG — noting that no J waves were seen on the initial ECG (Figure-2). His astute observation is worthy of brief discussion:
  • Rituparna et al document a case study report, in which J waves appeared to be induced by ischemia (Pacing Clin Electrophysiol 30(6):817-819, 2007)The proposed mechanism is complex. The “bottom line” conclusions of their case report were that transient J waves may on occasion be induced by an acute injury current from impending myocardial infarction. Recognition of such J waves may assist in localization of the likely “culprit artery”. The presence of such J waves may be associated with malignant ventricular arrhythmias.
  • In Figure-2 — prominent J waves are seen in each of the leads that show ST elevation. In addition, there is prominent notching at the onset of ST depression in lead aVR. In view of the lack of J waves in the pre-hospital tracing — it would certainly seen that these J waves were ischemia-induced, and markers of the “culprit artery”. In the future — I’ll be on the look-out for this interesting ECG sign!


Sunday, July 8, 2018

Test yourself: how many hours between your diagnosis of OMI and positive STEMI criteria?

Written by Pendell Meyers, with edits by Steve Smith

A male in his early 40s presented with intermittent chest/abdominal pain. He admitted to several episodes over the past two days, including one episode several hours prior to presentation, described as severe (8/10), substernal "burning," non-radiating, associated with diaphoresis, described as "feeling food stuck in my throat," or "like I ate too fast," but not associated with eating, relieved by belching and flatulence, relieved by lying flat. The episode on the day of presentation was similar except he had the additional new features of "burning ears" and "blurry vision," which prompted him to finally go to the ED. His history included known CAD (prior cath two years ago showed a 60% mid-LAD stenosis and 60% 1st diagonal stenosis), as well as early CAD in several close relatives.

Upon evaluation in the ED, he states that his pain had completely resolved just before arrival of EMS.

Here is his first ED ECG (no priors available):

I read this as normal. I see no evidence of ischemia, no evidence of OMI.


I would not have applied the the subtle anterior OMI vs. early repol formula to this ECG, as the formulas were not designed for cases with no STE (early repolarization, otherwise known as "normal variant STE," implies that there is STE). 

Had this been my case prospectively, I would not have identified OMI at this time. This is supported by the patient's lack of chest pain at the time of the ECG, likely meaning that the ECG changes (if present during pain) are resolving. I would strive to obtain any available EMS ECGs, and I would order q30 min serial ECGs during his ED stay and give him (and best if present, his wife or family members) my spiel about the importance of notifying staff for ANY possible returning symptoms.  I would also obtain an ECG immediately if his discomfort recurs.

The patient remained pain free in the ED, had an initial undetectable troponin, and was admitted for further ACS rule out.

Three serial troponins (not high sensitivity) were undetectable. A stress test was ordered for the next day. No serial ECGs were performed.


Day 1, 0650: Nursing report states that the patient has recurrent "heartburn." Pepcid and maalox were administered, and no further symptoms are charted. No ECG was performed at this time. 

Comment: This is a mistake. A patient was admitted for for discomfort of possible ischemic origin.  He is admitted for suspicion of coronary ischemia. The discomfort had resolved. But when the discomfort recurs, no ECG is performed.    

Furthermore, no additional troponins were ordered at that time. This also is not acceptable, unexplainable, and unfortunately I believe (without hard evidence) a common occurrence in many institutions. Practice patterns like this are the reason that we advocate even transient occlusions undergo emergent angiogram, because there is just no reliable hospital unit to monitor for reocclusion given the standard practice patterns and standard skill of ECG interpretation.

Ideally, patients at risk for recurrent ischemia should be placed on continuous 12-lead ST segment monitoring.  See these cases:

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



Case continued

His pain apparently resolved spontaneously, and later that morning he went for a regadenoson/sestamibi/SPECT imaging stress test, which revealed a "large perfusion defect involving the apex, inferoapex, anteroapex, apical septum, and mid-anterior walls." There were reportedly no electrocardiographic changes noted during the stress test.

This test result confirms that this patient is having myocardial ischemia of the LAD distribution and has a huge area at risk of infarction, or actively infarcting, or already infarcted.  This alone should prompt an emergent angiogram.

It seems that this result led the team to schedule an angiogram the next day (unclear why they chose not to perform immediate angiogram).


Day 1, 2230: Nursing reports state that the patient had "recurrent chest pain starting at 10:30pm after he reached over his head to lift the head of the bed up." Last vitals before onset of recurrent chest pain included HR 84 and BP 146/72, then repeat vitals during chest pain were HR 145 and BP 200/102. 

Another troponin was sent, and an ECG was immediately obtained:


Sinus tachycardia. There is unequivocal evidence of anterolateral OMI including STE in V2-V3 and aVL, reciprocal STD in III and aVF, even more diminished R waves and QRS amplitude in V2-V4, and hyperacute T waves in V2-V4, as well as I and aVL. To sum up all these changes in one visual description, there is a diagnostic increase in the ratio of: area under the ST-T wave (increased) to the QRS complex (decreased).


Dr. Smith often says that tachycardia should make you doubt OMI unless the patient is in cardiogenic shock. This case is NOT an exception to that rule, even if the patient has elevated blood pressure. In a patient who lacks an adequate stroke volume (in this case due to massive ischemic wall motion abnormality), the only way to maintain cardiac output is to make up for it with increase heart rate. This patient must be assumed to be in cardiogenic shock. There is no documentation of bedside ultrasound during this time, no documentation of peripheral perfusion or signs of acute pulmonary edema. The patient is in cardiogenic shock.



The anterior wall is now completely without blood supply and actively infarcting! 


But this went unnoticed, apparently because it doesn't meet STEMI criteria.

Troponin T from 22:30 returned undetectable.

It appears that they attributed his chest pain over the next several hours to his his elevated BP and HR (HR 120-130 and BP 170-190/75-90).


His pain persisted, and another ECG was ordered:

Obvious anterolateral OMI (but still not meeting STEMI criteria), with massively hyperacute T-waves in V2-V4, I, and aVL.  The HR is now less than 100.



He was given nitroglycerin several times with some intermittent improvement throughout the night, but overall his pain persisted. Around 4:20am his pain worsened with radiation to the left arm, when this repeat ECG was obtained:

Finally obvious enough to meet STEMI criteria.



A repeat troponin T at this time came back at 0.13 ng/mL (mildly elevated). The cath lab was finally activated at 4:45 am (~6.5 hours after first diagnostic ECG).

His cath images are shown below:


Non-obstructed RCA.


First obtained view of the left main and its branches. What do you see?

Normal left main. The LCX is non-obstructed, but the LAD on the top of the screen is acutely occluded (arrow). The angiogram reports this as a "99% thrombotic stenosis" with "TIMI-1 flow," however you can see for yourself that there is no flow distally. This is a complete occlusion, although it doesn't take 100% TIMI-0 flow to cause immediate, full thickness infarction.


In this view the LAD is now below the LCX on the screen. The wire is just proximal to the lesion in preparation for intervention.


Just after opening of the stent, the remainder of the LAD is starting to reperfuse.


TIMI-3 flow has been restored per report.



TIMI flow was improved to 3 after intervention, and the patient's chest pain resolved.


Repeat ECG after cath:

There is new RBBB, which is common in proximal-mid LAD occlusion, however somewhat unusual to develop after the cath unless there is no-reflow phenomenon (in which there is diffuse downstream small vessel occlusion despite open epicardial vessel on angiogram). There is persistent STE with inferior reciprocal STD, however some leads including V2 also have terminal T-wave inversion suggesting reperfusion. I would not be entirely certain of the efficacy of reperfusion therapy based on this ECG, however the resolution of chest pain would be very helpful.



See this post: Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG


Another repeat later that day:

RBBB has resolved. V1-V2 shows QS waves of anterior infarction, and V3-V4 have very diminished R-waves and QRS amplitude. There are Q-waves in 1 and aVL with persistent STE and terminally inverted T-waves. Overall this ECG confirms severe and nearly completed anterolateral transmural infarction with LV aneurysm morphology remaining.


Take a look at our OMI progression diagram below and compare the ECGs from this case with the progression, to lock in your knowledge of the progression of anterior OMI resulting in LV aneurysm morphology!




Over the next 10 hours after cath, troponin T peaked at 4.67 ng/mL (large MI).

Repeat echo showed large anterior and apical WMA and EF 45%.

Here is his repeat ECG 1 month later:
Large completed anterior infarct.


Let's reiterate some of the the many issues in this case:

1) When the patient had recurrent symptoms, no ECG or troponin was measured.

2) The team ignored the abnormal results of the stress test.

3) When they finally got repeat ECGs during recurrent symptoms, it was diagnostic for OMI but did not meet STEMI criteria. This led to at least a 6.5 hour delay to treatment of acute coronary occlusion.



Learning Points:

1) Contemporary troponin T (and likely many other similar assays) will not become positive until at least 4-6 hours of onset of persistent acute coronary occlusion. Conversely, elevated troponin does not distinguish OMI from other pathologies. Troponin should have no role in the diagnosis of OMI unless you are both unable to learn ECG interpretation and you don't mind letting the patient lie in bed with crushing chest pain and a fully occluded LAD for 6 hours without intervention.

2) This case is an excellent example of how unstable angina is alive and well. There were 4 initial undetectable troponins in a patient with symptoms and LAD thrombus. This is unstable angina that progressed to completed transmural anterior MI, likely with severe long term consequences. It is a myth that unstable angina is a thing of the past. See this post:

Unstable Angina: Dr. Braunwald asks if it is time for a Requiem


Because of cases like this and a vast body of supportive literature, we have proposed a requiem for the STEMI/NSTEMI paradigm rather than a requiem for unstable angina. For more see the OMI Manifesto.

3) STEMI criteria often misses OMI, and in many cases such as this one the delay until positive STEMI criteria causes an unacceptable delay to intervention, during which time the entire affected wall may be lost. The only way to consistently identify OMI as soon as possible is to learn expert ECG interpretation.

4) The ECG confirms reperfusion more accurately than TIMI flow on the angiogram.  (TIMI myocardial perfusion grade or "blush" is an angiographic measure of microvascular perfusion which correlates very closely with ECG measures of reperfusion)

5) You must be familiar with the progression of OMI and the features of LV aneurysm morphology in order to prevent false positives and false negative activations for this patient in the future.


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Comment by KEN GRAUER, MD (7/8/2018):
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Excellent blog post by Drs. Meyers & Smith. I’ll highlight a few additional points:
  • The History in this case is critical. The patient is in his 40s, and he has known coronary disease proved on prior cath. He has been having several prior episodes over the 2 days before admission — with no less that 8/10 chest pain that occurred several hours before he finally presented to the ED. In the context of this worrisome history in a patient with known coronary disease — I did not interpret his initial ECG as normal (Top ECG in Figure-1).
Figure-1: Original ECG at Time = 0 (Top) — and 2nd ECG (Bottom), done 37 hours after presentation. (See text).
The importance of history in interpreting ECG changes cannot be overemphasized. Clearly, the initial ECG (Top in Figure-1) is not diagnostic of OMI (acute Occlusion-related MI). But lead aVL (within the RED rectangleshows a straighter-than-usual ST segment that leads up to a T wave that looks both taller and fatter-than-it-should-beat its peak given the tiny amplitude of the R wave in this lead.
  • We are then faced with asking ourselves which of the 2 complexes in leads V2 and V3 are “the real complexes” in these leads — “A” or “B”? Due to baseline wander — we just can’t tell what the “real” QRS in these leads would look like. That said — both “A” and “B” are not totally normal. In — the ST segment is again straight, whereas there should be a gentle upsloping that gradually blends into the T wave. In — the T wave in V3 looks like it might be taller-than-it-should-be given the tiny r wave in this lead. While fully acknowledging that none of what I describe above is in any way definitive — in a patient who you KNOW has coronary disease, and who tells you he had an 8/10 severe CP episode just several hours earlier — the TOP tracing in Figure-1 is both technically inadequate, and (in my opinion) — demands repeat ECG over the next 20-30 minutes.
  • I presume an ECG was done at the scene at the time the patient contacted EMS. We are told this EMS tracing is “unavailable”. Chances are that IF that on-the-scene ECG was available for comparison with the initial ED ECG — that there would have been serial change. The point to emphasize, is that in patients with coronary disease who present with fluctuating symptoms — the presence of dynamic ECG changes is diagnostic of acute ischemia. Usually this is enough of an indication for cath, regardless of whether “stemi criteria” are or are not present.
  • As per Dr. Meyers — No ECG was done on Day #1 @ 06:50 when the patient had recurrent “heartburn”. The point is that any change in symptoms in a patient with known coronary disease who is admitted for chest pain should mandate repeat ECG.
  • As per Dr. Meyers — the 2nd ECG (Bottom tracing in Figure-1) is clearly indicative of OMI — but apparently was not acted upon because “it doesn’t meet STEMI criteria”. The point is that there are dynamic ST-T wave changes (which are actually quite dramatic!) that have occurred between the time that the 2 ECGs in Figure-1 were obtained — and that is indication for acute cath regardless of whether “stemi criteria” are or are not present.
  • I see no valid reason for doing a stress test on this patient. Had either the EMS ECG been available — or had the 2nd ECG been done in a more timely manner (rather than waiting 37 hours) — it is almost certain that dynamic ECG changes would have been seen — and that should have sufficed to prompt acute cath. The reason for considering a stress test in this patient is not to determine if there is coronary disease — because that has already been proven. And, given that there are fluctuating symptoms with dynamic ECG changes — this should be all that is needed to justify prompt cath. It is hard for me to imagine any result on stress testing that would dissuade me from that conclusion ...
COMMENT: Soul-searching cases like this one is difficult! It is one of the reasons I always strive to assess the case (and associated ECGsbefore I read what happens. That’s why I fully acknowledge how easy it is to second-guess from the comfort of my easy chair in front of my computer. But it’s important to learn from mistakes made, with goal of more optimal performance the next time out.
  • We are all learning all the time … Thanks to Drs. Meyers & Smith for presenting this soul-searching case.


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