Quiz post: 2 similar patients with similar ECGs. Which, if any, or both, are OMI? Will you outperform the Queen of Hearts?

 Written by Pendell Meyers

Two adult patients in their 50s called EMS for acute chest pain that started within the last hour. Both were awake and alert with normal vital signs. Both cases had an EMS ECG that was transmitted to the ED physician asking "should we activate the cath lab?"

What do you think? Here they are:

Patient 1, ECG1:

Zoll computer algorithm stated: "***STEMI***, Anterior Infarct"

Patient 2, ECG1:

Zoll computer algorithm stated: "ST elevation, probably benign early repolarization..."

Queen of hearts interpretations:

Patient 1, ECG1:

Patient 2, ECG1:

Patient 1 Clinical Course and Outcome:

The EM physician did not see that the S wave voltage has been truncated and squared off at 10 mm, thereby greatly limiting the assessment of proportionality. He diagnosed anterior "STEMI" and activated the cath lab. 

On arrival to the ED, while waiting for cath lab team, he obtained another ECG:

You can now see the full voltage of the high-voltage QRS, likely with some degree of LVH. Now that you can appropriately judge proportionality (one of the many key features that the guidelines totally ignore), you and the Queen can see it is much less concerning. But still, low confidence should not be dismissed, and still requires emergent evaluation.

This new ECG was still interpreted as STEMI and the patient was taken to the cath lab where the angiogram showed completely normal coronary arteries throughout. 

Smith: this ECG is definitely not OMI, but could be mistaken for Swirl pattern, which is a septal OMI with STE in V1 and STD in V6.  

See these cases: 

Precordial Swirl -- 20 cases of Swirl or Look-Alikes

Subsequent serial high sensitivity troponin I measurements were all below the level of detection. AMI was ruled out altogether. Serial ECGs remained unchanged.  Echo showed normal EF and no wall motion abnormalities, and no pericardial effusion. Of course the patient was saddled with the erroneous "pericarditis" diagnosis after CTs ruled also ruled out PE and dissection. But he did well.

Patient 2 Clinical Course and Outcome:

This patients first ECG was sent to the EM physician who said it did not meet STEMI criteria, but wisely agreed with EMS to get serial ECGs during transport.

25 minutes later, EMS called back with this new ECG:

Super obvious STEMI(+) OMI. The cath lab was now activated. 

The patient was found to have total "mid" LAD occlusion which was stented:

Pre-PCI.

Post-PCI.

The initial troponin resulted at less than the level of detection! (less than 6 ng/L)

Subsequent troponins were:

10,054 

greater than 25,000 x 2

none further measured

Next morning ECG:

Reperfusion pattern.

Unfortunately no echo was available.

Learning points:

Because proportionality is key to ECG interpretation, any ECG system that limits or cuts off voltage display is a critical human-induced error in ECG interpretation which can lead to bad decisions. Most commonly, it causes false positive cath lab activations due to inflated STE/S proportions. In this case, it was likely a factor causing the physicians and the Queen of Hearts to cause a false positive cath lab activation. 

We are trying to work with the EMS monitor companies to fix this, and also trying to specifically train the Queen to interpret "through" this, or despite this limitation.

"Precordial swirl pattern" LAD OMI is an important pattern to learn, and it is mimicked by LVH. Seeing these side by side and correlating to the outcome will allow you to learn this pattern and discriminate if from mimics. 

Initial troponin in full blown LAD OMI is not infrequently undetectable even in the age of high sensitivity troponins, if the patient has had very short duration of OMI symptoms.

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

MY Comment, by KEN GRAUER, MD (11/29/2023):

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

Important post by Dr. Meyers — with an “EASY Fix” — as well as “My Take” on some more subtle but essential concepts.

• For clarity in Figure-1 — I’ve reproduced and labeled the initial EMS Tracings for the 2 patients in today’s case. 
• To Emphasize: Both of these patients presented with new-onset CP (Chest Pain).
• 
  
• My Initial Thoughts: In view of the history of new CP — I fully acknowledge that I initially found it difficult to decide if one (or both) of these patients were in process of evolving an acute OMI.

Figure-1: I've labeled the initial EMS tracings from Patient #1 and Patient #2 (See text).

The “EASY Fix” in Figure-1:

There is a limit to the amount of voltage that prehospital ECGs in most EMS systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit (which is 10 mm for the deepest S wave and tallest R wave in today's tracings).

• Once aware of this automatic truncation of ECG amplitudes in most EMS systems in the United States — it becomes easy to spot. The dotted BLUE lines in the initial EMS tracing for Patient #1 — show truncation of the S waves in leads V2,V3 and V4 — and truncation of the R wave in leads V5,V6. (I put ?? for the S wave in lead V1 — because I wasn't certain if the S wave in this lead was precisely 10 mm, or perhaps slightly truncated).
• The greater the distance between the ascending/descending arms of the R wave or S wave at the 10 mm cutoff point — the larger the actual amplitude of the S wave or R wave is likely to be. For example, in Patient #1 — I suspect that the largest actual S wave will be in lead V3, given the large opening at the 10 mm cutoff.
• The "truncation effect" — is clearly less significant in the initial EMS tracing for Patient #2 — being present only in leads V2,V3 (and most probably not marked given virtual closure of ascending-descending arms of the S wave at the 10 mm cutoff in these leads).
• 
  
• As per Dr. Meyers — significant truncation of either S wave or R wave amplitude may markedly distort ST-T wave appearance, rendering the important concept of "proportionality" as useless. And, as was demonstrated in today's Case for Patient #1 — the repeat ECG in the ED revealed that the reason for truncation was the presence of greatly increased QRS amplitudes, as a result of marked LVH (and in the context of LVH — the elevated anterior ST-T waves seen in the initial EMS tracing for Patient #1 were consistent with the appearance of LV "strain" in anterior leads).
• 
  
• PEARL #1: It's important to be aware of this automatic truncation effect so commonly seen in EMS ECGs — because one might otherwise misinterpret the seemingly "large" ST-T waves as disproportionate to a short S wave, and therefore presume this to represent a hyperacute T wave (Please see My Comment at the bottom of the page in the June 20, 2020 — the February 6, 2020 — and November 14, 2023 posts in Dr. Smith's ECG Blog).
• 
  
• PEARL #2: The automatic EMS truncation effect is most likely to cause confusion in chest pain patients who manifest marked LVH with deep anterior S waves (just as we saw for Patient #1 in today's case — and as I describe in the December 27, 2018 post, as well as in the above posts that I cited in Pearl #1).
• 
  
• PEARL #3: As per Dr. Meyers — The 3rd KEY concept to be aware of in the interpretation of EMS tracings of CP patients with LVH — is "Precordial Swirl". The October 15, 2022 post in Dr. Smith's ECG Blog features no less than 20 ECG examples by Drs. Meyers and Smith of what is and what is not "Precordial Swirl" from proximal LAD occlusion (In My Comment at the bottom of the page in this Oct. 15 post — I consolidate KEY features to facilitate identification of this Precordial Swirl Pattern).

PEARL #4: How to "Put It All Together" re Today's CASE ...

Despite me being aware of each of the points I outline above — I still initially had difficulty determining whether or not Patient #1 and/or Patient #2 were "in process" of evolving an acute OMI. My thoughts were as follows:

• For Patient #1: I instantly recognized truncation of the S wave in leads V2,V3,V4 (and possibly also in lead V1) — as well as truncation of R wave height in leads V5,V6. Especially in view of the wide opening between descending and ascending arms of the S wave in lead V3 — I was virtually certain there was marked LVH — and, that this might account for all of the ST-T wave findings seen in this initial EMS tracing.
• The above said — I was not 100% certain that LVH explained everything in the initial EMS ECG from this middle-aged adult with new CP. I thought the peak of the T wave in lead V2 seemed "fatter"-than-expected — the base of the T wave in lead V3 seemed "wider"-than-expected — the J-point depression in lead V6 was with a flattend ST segment (not typical for LV "strain") — and there was subtle ST flattening in leads III and aVF — with ST coving and shallow T wave inversion in lead aVL.
• 
  
• My BOTTOM Line for Patient #1: I would not have activated the cath lab on the basis of this initial tracing. I suspected LVH as the main issue here — but felt the need for additional evaluation, including a look at the initial ED ECG to better appreciate the true proportionality of ST-T waves. And as shown by Dr. Meyers in his above discussion — the repeat ECG in the ED without truncation — strongly supported the premise that abnormal findings were the result of marked LVH and not acute OMI.
• 
  
• 
  
• For Patient #2: I again instantly recognized truncation of the S wave in leads V2 and V3 — albeit lack of significant "opening" between descending and ascending arms of the S wave in these leads suggested that S wave depth was less likely to be deep enough to account for the surprisingly tall T waves, with "fat" peak and wide base in these leads.
• KEY Point: There is no truncation in lead V1 of the initial Patient #2 EMS tracing! (BLUE arrows in these leads showing S wave amplitude clearly below the 10 mm cutoff point!). Given that there is no truncation in lead V1 — there is NO WAY that the straightening of the elevated ST segment takeoff, with disproportionately tall and "fat" T wave (considering the tiny amplitude of the S in V1) could possibly be normal. In this patient with new CP — acute LAD OMI has to be assumed until proven otherwise.
• 
  
• My BOTTOM Line for Patient #2: Once I realized that lead V1 (within the BLUE rectangle) was definitely abnormal — I became more convinced that the T waves in neighboring leads V2,V3,V4 were hyperacute until proven otherwise. It was no surprise to learn that this patient evolved total mid-LAD occlusion. 

Chest pain and new regional/reciprocal ECG changes compared to previous ECGs: code STEMI?

 Written by Jesse McLaren

 

A 45 year old presented with two weeks of recurring non-exertional chest pain, now constant for an hour. Below is old and then new ECG (old on top; new below). What do you think?

Both ECGs have normal sinus rhythm, normal conduction and normal voltages. There’s a change in axis that may interfere with direct lead-to-lead comparison, but there appear to be larger T waves in I/aVL and new TWI in III/aVF. But do they represent acute coronary occlusion?

 

Because of the ECG changes in a patient with chest pain, and with inferolateral hypokinesis on POCUS, the cath lab was activated. But coronaries were normal, and serial high sensitivity troponin was undetectable. Formal echo showed EF 55% with mild inferolateral hypokinesis without any prior for comparison. Based on ECG changes and echo findings, the patient was diagnosed as coronary vasospasm. Below is the discharge ECG, which showed the baseline ECG without any reperfusion T wave inversion.

The admission and discharge diagnosis both attributed the ECG changes and echo findings to ischemia. But the echo findings could have been old (especially with undetectable troponins), and the ECG changes could have been non-ischemic. This brings up questions around hyperacute T waves and reciprocal changes, dynamic ECG changes, and the ability to identify preventable cath lab activations.

 

OMI vs not OMI: what’s hyperacute and where’s the reciprocal change?

 

Leads III/aVL are reciprocal to each other, so any ST/T wave in one will elicit the opposite in the other. But interpreting which is the main change, and which is the reciprocal change, can be challenging.

 

 

 

Looking back at the ECG that led to the cath lab activation, the emergency physician interpreted the tall T wave in I/aVL as hyperacute, and therefore the inferior TWI as the reciprocal change. It was good to look for hyperacute T waves that are tall relative to the QRS, which can be small in absolute terms in leads with small QRS like aVL. But these T waves do not fit the other features of hyperacute T waves: wide based, symmetric and inflated, with a large area under the curve. Here, the lateral T waves have a very concave ascent to a narrow peak, with a small area under the curve. Instead it is the inferior leads that have discordant and asymmetric TWI, similar to LVH type strain pattern, and this produces reciprocally tall T (but not hyperacute) T wave in the high lateral leads.

 

Here’s a comparison with patient with a 100% ramus occlusion, with lateral hyperacute T waves and inferior reciprocal STD/TWI:

ECG changes: ischemic vs fluctuating baseline

 

The other challenge for this case was the change from previous ECG, which in a patient with chest pain leads us to think of ischemic change. But looking back in the chart, the patient had prior visits for a variety of complaints with fluctuating ECG changes similar to the more recent ones, and with troponin levels always undetectable. Here are the ECGs from two prior visits, the top with chest pain and the bottom with abdominal pain. Comparison of these two ECGs could also be interpreted as “dynamic” inferior/lateral changes, when it was fluctuating baseline changes unrelated to ischemia

 

 

Similarly, patients with early repolarization or LVH can have fluctuating ECG changes over time, which can be mistinterpreted as dynamic ischemic changes if patients present with chest pain. For this reason, ECGs need first to be interpreted in isolation, and then applied to the patient.

 

Could this false positive cath lab activation been prevented?

 

The biggest problem with STEMI criteria are false negatives – because this costs patient’s myocardium, with greater mortality and morbidity. But the resource cost of false positives is not insignificant, and the ideal goal would be to identify both false negatives in need of emergent reperfusion as well as false positives that don’t need cath lab activation. Coronary vasospasm that mimics OMI should not be prevented because this is an angiographic diagnosis of exclusion, but what about vasospasm as a retrospective diagnosis based on an ECG that did not mimic OMI?

 

I sent both ECGs to Dr. Smith, with the only information that these were prior vs new ECG. Despite the ECG changes, he immediately replied, “not OMI.” I also sent the new ECG to the Queen of Hearts App, which replied with the same answer as its teacher: Not OMI, high confidence. 

 

 

Patients can still have OMI in the absence of ECG changes – and ischemic symptoms with regional wall motion abnormalities is a compelling reason for cath lab activation. But having the reassurance that this ECG in isolation does not represent acute coronary occlusion might have given pause to cath lab activation, and to the discharge diagnosis.

 

Having this expert-trained AI widely available could dramatically improve the identification of both false negatives and false positives, saving myocardium and resources at the same time.

 

 

Take home

1.     when there are changes in reciprocal leads, consider which is the main changes and which is the reciprocal change: hyperacute T waves can produce reciprocal TWI, and TWI can produce reciprocally tall T waves

2.     hyperacute T waves are tall relative to their QRS, as well as bulky/inflated with a large area under the curve

3.     baseline ECGs may fluctuate over time, and not necessarily represent dynamic ischemia

4.     the QoH can help identify both false negative and false positives

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  

For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

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

MY Comment, by KEN GRAUER, MD (11/27/2023):

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

Superb commentary by Dr. McLaren — that addresses a number of truly challenging aspects regarding ECG assessment of patients who present with new chest pain. I'd add the following to Dr. McLaren's thoughtful and insightful commentary.

• It is highly likely that the 45yo in today's case will have one or more recurrences in the future. Given the accumulating "data set" of serial ECGs from this admission — and, from prior visits — apparently always with undetectable Troponin — and, with cardiac cath on this admission not showing any significant coronary disease — future disposition decision-making is simplified. As long as Troponin is negative and ECGs continue to show the similar pattern of ST-T wave variation seen on this admission — future cardiac catheterization should be avoidable. 
• Dr. McLaren's description of serial ECG assessment of the first 2 tracings in today's case ( = the "old" then "new" ECGs) — is a model for clinicians to emulate. Lead-by-lead comparison is tremendously facilitated by Dr. McLaren's technique of putting the 2 ECGs to be compared side-by-side. All too often I observe clinicians look entirely at 1 tracing, not seeing anything — and then looking entirely at the 2nd tracing without ever putting both tracings next to each other. This faulty technique renders it very easy to miss potential "dynamic" ST-T wave changes between these 2 tracings — that if interpreted separately, would not raise suspicion.
• Dr. McLaren astutely points out the difference in frontal plane axis between the first 2 tracings — which must be taken into account when assessing whether ST-T wave appearance in serial tracings is truly changed vs simply different due to a change in frontal plane axis. I completely agree with Dr. McLaren that the changes between the "old" and "new" ECG seem more than what might be explained solely by a shift in frontal plane axis.
• There are some subtle ST-T wave changes also in the chest leads. While I suspected the small changes in QRST morphology in leads V1,V2,V3 in the first 2 tracings were unlikely to be significant (if real at all — given slight difference in R wave progression) — I thought there clearly was change from the upright T waves in leads V4,V5,V6 in the top tracing — to the ST segment flattening, with slight ST downsloping in lead V6 of the bottom tracing that looks typical for LV "strain" (despite lack of voltage criteria for LVH).
• I would want to know formal Echo specifics as to whether this patient has LVH (as per Dr. McLaren — patients with LVH are more prone to fluctuating ECG changes over time, that are more likely to be misinterpreted as dynamic ischemic changes). As a side note — I occasionally do see LV "strain" in patients with Echo-confirmed LVH, who do not satisfy LVH voltage criteria.
• 
  
• Finally — I think it important to point out that while the serial ECGs in today's case were not indicative of acute OMI — neither ECG is "normal". The essential "immediate" decision to be made in "zero time" in the ED, is whether or not prompt cath and reperfusion is needed. That said — I like to look for an explanation as to WHY a given ECG looks the way it does in patients who present for chest pain. Today's patient clearly has variable ST-T wave appearance over time — and, despite normal coronary arteries and a respectable EF ~55% on formal Echo — there is at least mild inferolateral hypokinesis. It may be in this case that no satisfying explanation can be found beyond determination of "not being ischemic" — but additional information may be insightful.
•  
• BOTTOM Line: Our confidence is enhanced from today's case that future visits by this patient with a similar presenting history, negative troponin values and similar variations on serial tracings — will not indicate OMI (and should not need cardiac cath). That said — IF I was charged with evaluating a 45yo with a 2-week history of non-exertional chest pain, now constant — with inferolateral hypokinesis on POCUS and similar initial and prior tracings as shown at the beginning of today's case without the benefit of previous visits with prior ECGs to compare — I would have trouble being 100% certain that the ECG appearance with serial ST-T wave changes were not ischemic. While "fake" rather than OMI may seem the more likely interpretation (as per Drs. McLaren and Smith and the QOH no OMI interpretation) — I would probably favor a cath to be certain (with the knowledge that performing an anatomy-defining cardiac catheterization should facilitate and expedite future decision-making and avoidance of repeat cath on future visits).

GREAT case by Dr. McLaren! 

Infection and DKA, then sudden dyspnea with chest pain while in the ED

A 63 year old male with PMH of CAD and peripheral vascular disease from type I DM presented to clinic and was found to have a very high blood sugar and so was sent to the ED.

Patient stated that he has had glucose over 400 even though he has not missed any doses of insulin.  He also endorses fatigue, upset stomach, frequent urination, increased thirst, and decreased appetite over the past 2 days. 

Pulse was 115, BP 140/65, and afebrile

He was found to have cellulitis and to be in diabetic ketoacidosis, with bicarb of 14, pH of 2.27, glucose of 381, anion gap of 18, and lactate of 2.2 mEq/L.

He was treated for infection and DKA, and admission to hospital was planned.

While in the ED, patient developed acute dyspnea while at rest, initially not associated with chest pain. He later developed mild continuous chest pain, that he describes as the sensation of someone standing on his chest. 

This ECG was recorded: 

What do you think?

There is widespread ST depression.  This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was also tachycardia prior to development of chest pain.

Bedside echo showed no evidence of reduced EF, no signs of right heart strain, no regional wall abnormality. Lung exam showed diffuse B lines bilaterally. Xray was consistent with pulmonary vascular congestion. 40 mg of furosemide was given.

Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present.  See this post: What do you think the echocardiogram shows in this case?

Shortly thereafter, the troponin came back at 3,129 ng/L (very high).  Aspirin was given and cardiology was consulted.  But due to the absence of significant ST elevation, the cath lab was not activated.  They agreed ischemia was likely in the setting of demand given DKA and infection. EKG showed sinus rhythm at 100 BPM with a normal axis and diffuse ST depressions.

That this is all demand ischemia is unlikely.  The patient had no chest symptoms until he had been in the ED for many hours and had been undergoing management of his DKA.  

Another ECG was recorded:

What do you think?

This is diagnostic of Occlusion MI (OMI) as Aslanger's pattern (Diagnostic of OMI).  Aslanger's is a combination of inferior OMI with widespread ST depression and is due to BOTH occlusion of one artery (usually the circumflex, but sometimes the RCA) AND simultantous 3 vessel disease.  

Because there is an ST depression vector towards leads V5 and II, leads aVF and II cannot manifest ST elevation or hyperacute T-wave from the inferior OMI.  The ST depression vector includes these leads and cancels out the STE of the inferior OMI.  Only lead III can have STE (and, of course, aVR, which is opposite, reciprocal to, the ST depression in I, II, V5).

Not knowing anything about the patient, I saw this ECG on our system just as I was leaving the dept.  The patient was under the care of another ED physician.

Here was the interpretation I put into the system, and told the physicians about it:

Inferior Occlusion MI with diffuse subendocardial ischemia.  Aslanger's pattern.  Hyperacute T-wave in lead III, with reciprocal findings in aVL -- single lead OMI in the setting of multivessel disease.

Aslanger's pattern (Smith was co-author on this): A new electrocardiographic pattern indicating inferior myocardial infarction

The next troponin returned at 8822 ng/L.

The emergency physicians advocated for the cath lab but she was not taken until the morning because this was a "NonSTEMI."

Here is the troponin profile:

Here is the Queen of Hearts assessment:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  

For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

Case continued

After about 8 hours of pain, the patient's pain resolved spontaneously, probably aided by the aspirin and heparin.  Here is the ECG at that point in time: 

The ischemia is mostly resolved.  One would expect that the angiogram would show open arteries with normal TIMI-3 flow and culprit lesions.  20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later.

So the presence of an open artery does not tell you anything about the state of the artery at the time of the ECG.

Angiogram:

Severe two-vessel coronary artery disease with possible co-culprits (90% proximal circumflex, 70% mid/distal RCA) in the setting of non-ST elevation myocardial infarction. 

Previously placed stents in the LAD (multiple) and mid circumflex and patent

Formal echocardiogram:

Normal left ventricular size and wall thickness.

Mildly decreased left ventricular systolic function with an estimated EF of 48%.

Regional wall motion abnormality--basal to mid inferior and inferolateral hypokinesis.

This was the previous echo just 3 months before

Normal left ventricular chamber size. Normal left ventricular wall thickness. 

Ejection fraction of 66%. 

No regional wall motion abnormalities. 

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

MY Comment, by KEN GRAUER, MD (11/21/2023):

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

Today's case provides an excellent example of Aslanger's Pattern — as well as an astute test in the "art" of comparing serial ECGs. 

• For clarity in Figure-1 — I've reproduced the first 2 ECGs in today's case. It could be all-too-easy to overlook the subtle-but-real ECG changes that occurred during the 4 hours that passed between the recording of these 2 tracings.

Figure-1: Comparison of the first 2 ECGs in today's case.

Comparison Between ECGs #1 and #2:

As per Dr. Smith — ECG #1 shows sinus tachycardia with the pattern of DSI (Diffuse Subendocardial Ischemia) — in that there is ST depression in multiple leads with ST elevation in lead aVR>V1.

• PEARL #1: The BEST way to compare 2 serial ECGs — is to put both tracings next to each other — and then to compare lead-by-lead to note any subtle changes that may have occurred. 
• It is all-too-easy to overlook subtle changes if you simply look at one entire tracing — and then look at the 2nd tracing, but without specifically looking lead-by-lead to see if there are any changes.

Applying this technique to the 2 tracings in Figure-1:

• Lead III in ECG #2 now shows a Q wave — as well as ST segment coving with slight ST elevation that replaces the ST depression that was seen in ECG #1.
• Lead aVL in ECG #2 now shows subtle-but-real coved ST depression, that is the mirror-image opposite picture of the new coved ST elevation that we now see in lead III.
• 
  
• In the chest leads in ECG #2 — there is now a definite increase in R wave amplitude in leads V1,V2,V3 and V4 — compared to relative R wave amplitude that was previously seen in these leads in ECG #1

IMPRESSION: As per Dr. Smith — the findings now seen in ECG #2 are perfectly consistent with Aslanger's Pattern — which in today's case, strongly suggests an acutely evolving infero-postero OMI. The reason these ECG changes are so challenging to recognize — is that this patient has severe underlying multi-vessel coronary disease that masks some of the acute findings.

• Inferior OMI — is suggested by the new ST coving with elevation in lead III, in association with mirror-image opposite reciprocal ST depresstion in lead aVL.
• Posterior OMI — is suggested by the increased R wave amplitude in leads V1-thru-V4.
• The combination of new persistent chest pain + the above-described ECG changes between the 2 tracings shown in Figure-1 — constitute "dynamic" ECG changes.

PEARL #2:  = Aslanger's Pattern:

Examples of Aslanger's Pattern appear in a number of cases in Dr. Smith's ECG Blog (This pattern is very nicely described by Dr. Smith in the January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

 

Isn't it interesting how closely ECG #2 in today's case follows the above description of Aslanger's Pattern!