Friday, December 13, 2019

"Pericarditis" strikes again

Written by Pendell Meyers

A man in his late 40s with several ACS risk factors presented with a chief complaint of chest pain.  Several hours prior to presentation, while driving his truck, he started experiencing new central chest pain, without radiation, aggravating/alleviating factors, or other associated symptoms. On review of systems the patient reported back pain for approximately 1 week which he was treating with NSAIDs with minimal relief. On exam the patient was well appearing, with normal vitals signs other than BP 155/82, no murmurs or rubs, normal pulses, no reproducible chest pain.

Here is his triage ECG:

What do you think?

Sinus rhythm
Normal QRS morphology
Diffuse STE, including leads V2-V6, I, II, III, aVF (with obligatory reciprocal STD in aVR)
Perhaps a tiny bit of PR depression (up to 0.8 mm has been described in normal subjects)

Overall impression: In my opinion and experience, this ECG most likely represents a normal baseline ECG, but with a small chance of pericarditis instead. I do not believe there is any finding here suggestive of OMI.

I texted this to Dr. Smith without any information, and this was his reply: 
"This could be pericarditis but probably is normal variant."

The treating clinicians were worried about the ST elevations and called cardiology for emergent PCI consult. The cardiologists felt that the ECG did not represent ACS, and thought it was more likely pericarditis, so they did not take him to the cath lab.

His first troponin T then resulted elevated at 0.19 ng/mL.

A repeat ECG was performed and cardiology was re-consulted:
Roughly unchanged.

With the troponin elevated and ongoing pain, cardiology now decided to take him to the lab.

They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. No acute culprit.

He was admitted to cardiology.

Here is a quote from his initial cardiology admission note (after cath was done showing no acute culprit):

"...chest pain, non-radiating, pleuritic in nature, relieved by sitting forward"

"Plan: likely myocarditis"

Colchicine was ordered and the patient received the first dose in the afternoon.

Troponins gradually trended down from 0.19 ng/mL.

The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 cm with severe aortic insufficiency. The team was notified and they ordered a stat aortagram which showed type A aortic dissection from the aortic valve to the iliacs.

Aortic Root Dissection

The aorta was emergently repaired, and the patient had a complex course (including a saddle PE and subsequent GI bleed!) in the ICU but survived with excellent function.

Not surprisingly the cardiology HPI changed yet again in the next note following diagnosis of the aortic dissection:

"...chest pain that began acutely while was attempting to park his truck, described as dull pain which radiates to the back, without exacerbating or alleviating factors..."

Here is his ECG several days after diagnosis:
Again, normal variant STE
Pericarditis would have its own typical evolution, as would acute MI.

The patient returned one month later for an unrelated problem:

Learning Points:

It seems likely to me that the notion of "pericarditis" delayed or completely prevented diagnosis of aortic dissection in this young man. As we have described multiple times on this blog, false positive "pericarditis" kills by distracting the clinician from actual emergencies including OMI, dissection, PE, and others.

The vast majority of cases with chest pain diffuse ST Elevation are due to Normal Variant ST Elevation, NOT to pericarditis.

You diagnose pericarditis at your peril!  Acute MI is frequently misdiagnosed as pericarditis.  Patients with pulmonary embolism or aortic dissection who have normal variant ST elevation are at high risk of being diagnosed with pericarditis when what they have is far more serious!!  Pericarditis is a diagnosis of EXCLUSION.

On the ECG of pericarditis:
--There should be marked PR depression
--There should be flat ST elevation with low T-wave to ST segment ratio.
--There should be no reciprocal ST depression anywhere except aVR.
--And there should be confirmatory evidence, and evidence of EXCLUSION of other serious pathology.

See this case, also written by Pendell Meyers when he was a medical student:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!  (normal variant misdiagosed as pericarditis)

Other cases:

Palpitations and Chest Tightness: Should You Activate the Cath Lab (or Give Thrombolytics)? (normal variant, not pericarditis)

A Young Man with Sharp Chest pain
 (normal variant, not pericarditis)

You Diagnose Pericarditis at your Peril (at the Patient's Peril!)  --Acute MI misdiagnosed as pericarditis.

MY Comment by KEN GRAUER, MD (12/13/2019):
I LOVE this post — as it explores the important decision-making process associated with the ED diagnosis of Acute Pericarditis. I completely agree with many of the KEY findings conveyed by Dr. Meyers.
  • That said — I offer another perspective on some aspects of this case.
Before discussing my thoughts on interpretation of ECG in this case — it may be helpful to review some of the ECG criteria for acute pericarditis. I’ve excerpted in Figure-1, relevant paragraphs from a 2017 ESC (European Society of Cardiologyarticle on this subject by Xanthopoulos & Skoularigis (ESC: Vol. 15, No.15-9/6/2017).
Figure-1: Excerpt from ESC review on acute pericarditis (See text).

Among the KEY points regarding ECG diagnosis of acute pericarditis from Figure-1 (to which I’ve added some of my own points) — are the following:
  • Typical ECG findings of acute pericarditis are not always present! The ECG is far from a perfect diagnostic tool.
  • 4 STAGES are described in the ECG evolution of Acute Pericarditis findings. These can be summarized as: iStage I — in which there is generalized ST elevation in most leads (except perhaps in the “right-sided” leads = leads III, aVR and V1)iiStage II — in which this generalized ST elevation returns to baseline (ie, “pseudo-normalization” phase); iiiStage III — in which there is diffuse T wave inversionandivStage IV — in which the overall tracing normalizes.
  • Of these 4 stages — only Stage I is readily recognizable as potentially due to acute pericarditis. You would never guess “pericarditis” if given an isolated tracing from Stage II, III or IV.
  • The time course of these 4 ECG Stages (in those pericarditis cases in which they occur) — is highly variable. The ESC summary in Figure-1 states that Stage I may last “between hours to days” — before evolving into Stage II.
  • The shape of the ST elevation is typically concave-up (ie, a “smiley” configuration).
  • ECG signs usually associated with acute MI (ie, abnormally large or wide Q waves — reciprocal ST depression) are absent!
  • PEARL #1 — The appearance of the ST-T wave in lead II tends to resemble that in lead I with acute pericarditis. In contrast, with acute MI — ST-T wave appearance in lead II resembles lead III (and not lead I).
  • There may be PR depression in many leads — with “reciprocal” PR elevation in lead aVR.
  • The RATIO of the amount of ST elevation to T wave amplitude in lead V6 should be less than 0.25 (ie, height of the ST elevation, as measured from the end of the PR segment to the J-point — should be less than 1/4 of the height of the T wave in lead V6).
  • Editorial NOTE: Much attention has focused on this Ratio criterion in recent years. I have not been an advocate of this criterion — because I feel ( = my opinion) that it is often difficult attain consistency in measurements among practicing clinicians. All it takes is a very small error in how the amount of ST elevation is measured — to throw off your calculation of whether this ST segment height is over or under 25% of the height of the T wave in this lead. That said — I illustrate HOW this RATIO is arrived at in Figure-2, which I have adapted from the 3/16/2019 post in Life-In-The-Fast-Lane.

Figure-2: Illustration of how the ST segment to T wave ratio is calculated — adapted from Life-In-The-Fast-Lane (See text).

  • These words from Drs. Meyers and Smith should be at the forefront of every emergency provider, You diagnose acute pericarditis at YOUR peril! The reason for this is clear — Statistically (if you take all comers who present to the ED) — acute coronary syndromes are much more common than acute pericarditis as a cause of new-onset chest pain with ST elevation on ECG.
  • That said — this statistical prevalence in favor of acute coronary syndromes would be significantly reduced IF— the patient in question was a younger adult with a viral prodrome (ie, of fever, myalgias, pleuritic chest pain) — as a viral cause is the most common etiology of acute pericarditis.
  • IF, on the other hand — the patient with new chest pain is older and lacks predisposing viral symptoms — then acute pericarditis becomes a rare diagnosis in an ED setting.

Regarding the ECGs in THIS Case: For clarity — I put 3 of the 4 ECGs in this case together in Figure-3:

Figure-3: Three of the 4 ECGs in this case (See text).

My Impression of ECG #1: As per Dr. Meyers — there is diffuse ST elevation in ECG #1. There is no more than minimal PR segment depressionMDifferent Perspective on ECG #1: The above said — IF the history would have been that this patient was a young adult with a recent acute viral illness, who now presented with pleuritic and positional chest pain (exacerbated by lying supine, and reduced by sitting and leaning forward) — I would have interpreted ECG #1 as clearly consistent with acute Pericarditis. My reasoning is as follows:
  • ECG #1 — shows more than a little ST segment elevation of upward concavity shape in multiple leads (ie, leads I, II, III; aVF; and V2-thru-V6). I thought the diffuseness and amount of ST elevation in ECG #1 is clearly more than I’m used to seeing with repolarization variants. This is not to say that ECG #1 might not reflect a repolarization variant — but only to say that IF the clinical history and physical exam were consistent with what one might expect for acute pericarditis — that ECG #1 is clearly consistent with this diagnosis ( = my opinion).
  • Although with this amount of generalized ST elevation, I would have expected more PR depression than we see in ECG #1 — the lack of PR depression (in my opinion) does not rule out the possibility of acute pericarditis. In my experience — generalized ST elevation is a much more important ECG sign than PR depression (See My Comment at the bottom of the December 10, 2019 post in Dr. Smith’s ECG Blog).
  • The ST-T wave appearance of lead II in ECG #1 much more closely resembles the ST-T appearance in lead I than in lead III (See Pearl #1 above).
  • There is no reciprocal ST depression in ECG #1 (other than the expected ST depression in lead aVR). The q waves that are present are small and narrow, and consistent with normal “septal” q waves.
  • The ST segment to T wave amplitude RATIO in ECG #1 actually is consistent (to my measurement) with an ECG diagnosis of acute pericarditis (as per the insert to the right of ECG #1 — this ratio is >0.27, and therefore is positive!).
  • PEARL #3: In my experience of reviewing literally hundreds of internet cases in which the diagnosis of acute pericarditis was suspected — the overwhelming majority of clinicians FAIL to ever mention that they listened for a pericardial friction rub. If not mentioned as a positive or negative finding — this usually means that the clinician did not listen for a rub. Failure to listen for a rub is a critical oversight — because IF you hear a pericardial friction rub — then you have made the diagnosis of acute pericarditis! (Dr. Meyers emphasized that no rub was heard in this case). BOTTOM LINE — DONT FORGET to carefully listen for a RUB whenever considering acute pericarditis as a diagnostic possibility!

NOTE: In this particular case — errors were made in assessing the history. As per Dr. Meyers — inappropriate focus on the diagnosis of pericarditis appeared to delay (and almost prevented) the correct diagnosis of acute aortic dissection.
  • As per Dr. Meyers — Acute pericarditis must be a diagnosis of exclusion!
  • That said — acute pericarditis does occur on occasion ... so it is important to be saavy on the ECG signs of this diagnosis

Therefore, realizing that the patient in this case did not have acute pericarditis — I wanted to highlight some points about the 3rd and 4th ECGs that were done in this case.

QUESTION #1: Imagine the patient with ECG #1 did have acute pericarditis.
  • In this case — Would ECG #3, done several days later be consistent with the ECG evolution expected for true acute pericarditis?

ANSWER: There clearly is less ST elevation in ECG #3 in virtually all leads compared to ECG #1. As per Figure-1 — this is consistent with the evolution of Stage I-to-Stage II pericarditis, that is expected to be seen on serial ECGs over ensuing hours-to-days.
  • NOTE — I realize the patient in this case did not have acute pericarditis. I am merely HONING your ECG interpretation skills by highlighting that what we see in ECG #3 could be perfectly consistent with ongoing ECG evolution in a patient who did have pericarditis.

QUESTION #2: ECG #4 was obtained from the patient in this case about 1 month later, when he returned to the ED for an unrelated problem. Does ECG #4 serve to further our understanding? (HINT: Consider ECG #4 as the follow-up tracing to ECGs #1 and #3).

ANSWER: Unfortunately, ECG #4 does not further our understanding about this case. Compared to ECG #3 — there is additional ST-T wave flattening, and beginning T wave inversion in a number of leads, not unlike what might be seen as one evolved into Stage III pericarditis. That said — the heart rate is significantly faster than it was for the prior 2 tracings (ECGs #1 and #3) — so there is really no way to distinguish what might represent ST-T wave changes due to tachycardia vs evolution of the patient’s underlying disorder.

Our THANKS to Dr. Meyers for presenting this informative case!

Tuesday, December 10, 2019

Teenager with chest pain and slightly elevated troponin. What happens then?

This is a previously healthy male teenager who was awoken by chest pain.   He was seen at another hospital and found to have a slightly elevated troponin, then underwent a CT pulmonary angiogram (PE) protocol which revealed a right sided pneumonia.  He was treated with Ceftriaxone and azithromycin.

The pain is described as located in the midsternal area, radiating to the right arm, described as 8-9/10 and worse with deep inspirations.  He endorsed cough, fever, and body aches in the previous days.

Here is the initial ECG:

Time zero:
Sinus rhythm. 
There is PR depression: see especially leads II and V5.
The ST segment is not elevated relative to the TP segment, but it is elevated relative to the QRS onset.
QRS onset is the best location for ST segment comparison, and is the location recommended by Universal Definition of MI. Why?
PR depression is due to the negative atrial repolarization wave.  That wave is still resulting in J-point depression, so there should be J-point depression relative to the TP segment.
But here the J-point is NOT depressed, so there is actually ST elevation.
There is no reciprocal ST depression in aVL.
See here for explanation of the atrial repolarization wave.

This ECG is pretty typical of myopericarditis, and fits the clinical syndrome.
This ECG was read initially as normal, and cardiology was not concerned.

The first troponin I returned at 0.081 ng/mL (0.030 is URL).

He was admitted.

A second troponin I returned at 0.122 ng/mL.

Another ECG was recorded at 4 hours and was essentially the same.

In the evening, he became diaphoretic and complained of 9/10 continuous chest pain.  This ECG was recorded at 16 hours:
Computer reads ***Acute MI***
It's not clear to me why the computer read this as such.
What I find interesting here is the new Q-wave in lead III.

This interpretation triggered a rapid response. The pediatric team felt it might be ACS, but on review of his prior ECGs, it was thought to be really unchanged from the 2 prior and more consistent with myocarditis.

The troponin I returned at 9.3 ng/mL, then at 13.65 ng/mL.

The next AM, the patient had still more chest pain, and had this ECG recorded:

25 hours
Marked PR depression.
Inferior Q-waves remain.
Now there is marked ST Elevation in inferolateral leads.
T-waves are not much higher than STE, typical of myopericarditis.
The only STD is in aVR, also typical of myopericarditis.

The troponin returned at 9.45 ng/mL.

An emergent echo was done and showed a wall motion abnormality of the distal septum and anterior wall.

Echo does not necessarily differentiate acute MI from pericarditis: both may have wall motion abnormalities.

There was a CT chest image from the previous day.
This is not easy to read.  
The septum appears a bit darker than the rest, and you might be fooled into thinking there is ongoing ischemia here.  
But I showed it to our expert and chief of radiology, Gopal Punjabi, and he read it as normal. 

Dr. Punjabi has a fantastic radiology blog on Spectral CT:

A negative CT should not be relied upon to rule out ischemia.
However, had there been an area of decreased perfusion, the positive predictive value would be good.
See an examples of CT ischemia here.

Another troponin returned at 23.89 ng/mL.

Here is the troponin profile:

An MRI was done.  Thanks again to Dr. Punjabi for these images and explanations:

Since the is subendocardial sparing, this cannot be infarction, as the subendocardium is the most susceptible region in infarction.

Overall MRI impression:

This showed moderately depressed left ventricular systolic function with ejection fraction of 36-40% with regional wall motion abnormality involving the distal septum and part of the apex.  There was a small pericardial effusion.  On delayed enhancement imaging, there was evidence for patchy areas of delayed enhancement most marked in the distal anteroseptal and apical myocardium as well as the basal and mid segment of the anterolateral walls. The T2-weighted fat-suppressed images showed evidence of edema and areas of delayed enhancement.  There is also mild and diffuse pericardial enhancement all consistent with patchy myopericarditis.

30 hours
Near normalization of ST segments.
Q-waves in III remain.

CRP returned at 43.8 mg/L.
He tested positive for enterovirus.


Many EKGs in acute MI are highly suggestive of myo- and peri-carditis and are misdiagnosed as Myo- or Peri-carditis.

This is why I frequently write: "You diagnose pericarditis at your peril."

In someone over age 30, MI is far more likely.
Under 20, myocarditis is far more likely.

But young people do have MI, due to anomalous coronary arteries, coronary artery dissection, Kawasaki dz, even atherosclerotic plaque rupture, and other etiologies.

When it comes to coronary occlusion, you can't just say: "Well, myocarditis is more likely, therefore I will not investigate further.  You have to be CERTAIN.   Problem is, it is difficult to be certain wihtout an angiogram and/or MRI.  Echo can have WMA in both.  If there is NO WMA, then it is not coronary occlusion, but if there IS one, then you still don't have a diagnosis.

MRI takes too much time.

Angiogram is quick for diagnosis.

CT angiogram is rapid relative to MRI, and could make the diagnosis.

As above, regular contrast spectral CT, if positive, is fairly accurate for ischemia.  But it is not sensitive.

Here are some more ECG cases of myocarditis in young people:

8 yo with myocarditis:

16 yo with acute MI:

MY Comment by KEN GRAUER, MD (12/10/2019):
This have been a number of posts on Dr. Smith’s Blog, regarding the ECG diagnosis of what Acute Myocarditis is and is not (For example — My Comment on the 7/21/2019 post). Today’s case provides perhaps the best example of serial ECG evolution of this elusive entity. As a bonus — Dr. Smith adds labeled MRI images detailing the finding of “subendocardial sparing” that facilitates distinction between acute MI vs Myocarditis.

For clarity — I focus my attention on the serial ECGs shown in this case, which I put together in Figure-1.
  • For interest — I offer another perspective based on mslightly different interpretation of these serial tracings.
Figure-1: The 4 serial ECGs shown in this case (See text).

I begin with my Systematic Approach to interpretation of ECG #1:

Descriptive Analysis of ECG #1: There is a regular sinus rhythm at ~95/minute. All intervals (PR/QRS/QTc) are normal — and the frontal plane axis is normal at +65 degrees. There is no chamber enlargement.
  • Regarding Q-R-S-T Changes  Small and narrow Q waves are present in multiple leads (ie, leads I, II, III, aVF — and V5, V6). R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
  • The most remarkable finding on this tracing is that there is slight-to-modest ST elevation in each of the inferior leads (II, III, aVF) — and in lateral chest leads V5 and V6. The shape of this ST elevation is concave up ( = smiley-configuration)  and, there is J-point notching in lead V5, as well as the suggestion of slurring of the terminal part of the QRS complex in lead II.
  • NOTE: The finding of Psegment depression in at least several leads, with PR elevation in lead aVR is among the ECG findings listed as consistent with acute pericarditis/myocarditis. The problem I’ve experienced with this criterion (and I’ve looked for PR depression in virtually every tracing I’ve considered acute pericarditis in, for over the last 30+ years) — is that overall sensitivity and specificity of this finding (in my experience) is lacking. I’ve seen PR depression in both normal variants, and in patients with acute MI. I have therefore found this sign of limited usefulness in most instances when contemplating a diagnosis of acute pericarditis or myocarditis. I did not feel that the slight PR depression in leads II and V5 + PR elevation in lead aVR of ECG #1 contributed to the diagnosis ( = my opinion).
My Clinical Impression of ECG #1: I did not think ECG #1 taken by itself was especially typical of acute pericarditis or acute myocarditis.
  • PEARL #1: The KEY to clinical interpretation of this tracing in my opinion depends on the HISTORY. Our Descriptive Analysis remains the same = Sinus rhythm at ~95/minute + slight-to-modest ST elevation with an upward concavity in the infero-lateral chest leads, with some J-point notching/slurring.

Consider the following Clinical Scenarios:
  • Scenario #1  IF told that ECG #1 was obtained from an asymptomatic young adult being screened (ie, in a pre-sports-participation physical exam — or perhaps as part of the person’s job screening) — I would have interpreted ECG #1 as a normal repolarization variant. As the clinician tasked with reading all ambulatory ECGs for 35 medical providers over my 30-year career as family medicine Attending — I encountered numerous similar tracings in this clinical situation.
  • Scenario #2  IF told instead, that ECG #1 was obtained from an older adult with new-onset chest pain that sounded cardiac — I still would have thought this tracing unlikely to represent an acute cardiac event because: i) The Q waves are all small and narrow, and unlikely to represent infarction; ii) The ST elevation is in several anatomic areas — and the shape of these ST segments (upward concavity = “smiley” configuration), together with some J-point notching/slurring is much more suggestive of a repolarization variant; andiiiThere is no reciprocal ST depression. That said, IF this history of new chest pain was indeed worrisome — the fact that there is some ST elevation would be enough to merit additional evaluation (ie, repeat ECG; serial troponins; Echo during symptoms) until more certainty of the diagnosis could be obtained.
  • Scenario #3  IF told instead that ECG #1 was obtained from a previously healthy male teenager who was awoken by severe, pleuritic chest pain — that occurred in association with recent cough, fever, myalgias, and a CT scan diagnosis of pneumonia ( = which is the clinical history in THIS case) — then Acute Myocarditis needs primary consideration in your differential diagnosis even BEFORE you look at the ECG! In this case — even though I still do not think ( = my opinion) that ECG #1 is diagnostic of acute myocarditis — this tracing certainly could represent an early stage of acute myocarditis (or peri-myocarditis).

ECG #2 was obtained that evening ( = 16 hours after ECG #1). At this time — the patient had become diaphoretic, and he was complaining of 9/10 continuous chest pain. Serum troponins were clearly elevated ...

My thoughts on comparing ECG #2 with ECG #1 were the following:
  • Although the Q wave in lead III of ECG #2 is quite deep — a small-but-definitely-present Q wave was seen in lead III of ECG #1. Small and narrow Q waves are seen in virtually the same leads in both tracings. Although definitely deeper — the Q wave in lead III of ECG #2 remains narrow. In addition — there has been slight shift in the frontal plane axis (Note that the QRS in lead aVL of ECG #1 was more negative than positive — and in ECG #2, the QRS in aVL is clearly more positive). As a result — I did not think the deeper Q wave in lead III of ECG #2 was clinically significant.
  • Realizing that there is slight change in frontal lead QRS morphology (because of this axis shift) — I still thought there most probably was an increase in the amount of ST elevation in leads II, aVF, V5 and V6 of ECG #2. Given continuous ongoing symptoms (chest pain) — I interpreted ECG #2 as showing an increase in acute changes.
  • As per Dr. Smith — I felt the overall clinical picture was most consistent with acute myocarditis.

ECG #3 was obtained the next morning ( = 25 hours after ECG #1). Severe chest pain persisted ...
  • As per Dr. Smith — there has been a dramatic increase in the amount of infero-lateral ST elevation. In fact, the ST elevation has become generalized — and, is now present in all leads except leads aVR, aVL and V1 = a pattern typical of acute pericarditis and/or myopericarditis.
  • There is J-point ST depression in lead aVR — which, given the generalized ST elevation in almost all other leads — represents a typical “reciprocal change” for acute myopericarditis.
  • Q waves are unchanged since ECG #2.
  • As per Dr. Smith — Pdepression has become much more definite, and is now present in virtually all leads except leads aVR, aVL and V1. Marked Pelevation persists in aVR. Given this diffuse PR depression, in association with diffuse ST segment elevation — this tracing represents one of the few instances in which I’d agree that PR depression in ECG #3 clearly supports our diagnosis of acute myocarditis.

ECG #4 was obtained later that day ( = 30 hours after ECG #1).
  • Clearly there has been improvement in the ECG appearance of this final tracing. That said — J-point ST elevation remains in multiple leads (ie, leads I, II, aVF; V4, V5, V6). PR depression is clearly less. Q waves remain.

FINAL COMMENT: I thought this case remarkable for the insightful manner in which serial ECG changes unfolded as this case of acute myocarditis evolved.
  • It would have been interesting to see a true baseline ECG on this patient — so that we could know how much of the modest, concave-up ST elevation in ECG #1 represented this patient’s baseline vs an early acute change of his soon-to-evolve acute myocarditis.
  • PEARL #2: One of the BEST ways to HONE your ECG interpretation skills — is to GO BACK after you know the diagnosis — and take another look at serial tracings to see if you can now pick up subtle changes that were overlooked on your initial reading. Doing so — Don’t YOU now agree that ECG #2 shows a subtle but overall increase in the amount of ST elevation compared to ECG #1? (Figure-2).

Figure-2: Comparison of ECG #1 with ECG #2 (See text).

Our THANKS to Dr. Smith for presenting this illustrative case!

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