Sunday, May 26, 2019

A man in his sixties with chest pain at midnight with undetectable troponin


Written by Pendell Meyers


A male in his 60s with no known past medical history presented at midnight with chest pain over the past 3 hours. The pain started just after eating, and at first he thought it was "reflux," however he decided to call 911 after a few hours when it did not improve.

Here is his presenting ECG:
What do you think?












Here are the relevant findings:
Slight STE in V1
2.5 mm STE in V2
Slight STD in V4-V6
Definite STD in II, III, and aVF
Hyperacute T-waves in V2, and likely also in aVL

These findings are highly specific for LAD occlusion. We have many cases of this pattern on this blog, involving STE and hyperacute T-waves in V1-V2, with STD in the lateral leads (see below for links). In this case there is also reciprocal STD in inferior leads and hyperacute T-waves in aVL. 


Side note: Sometimes this pattern includes morphology which some have described as "new tall T-wave in V1," or sometimes "T-wave in V1 greater than in V6" which is essentially just a description of a hyperacute T-wave in V1, with the exception that it would be better described as both tall and fat/large/wide/bulky T-waves, not just "tall". Dr. Smith noted "new tall T-wave in V1" in 14% of cases of early repolarization vs. 34% of subtle LAD occlusions in the derivation study of the anterior OMI formula. This initial ECG does not have this pattern, however lookout for this pattern in the serial ECGs.


Our team recognized that this ECG represents LAD occlusion. But it does not technically meet STEMI criteria. We immediately called the interventionalist to explain our concerns. They evaluated the patient and were also concerned, however they felt that immediate cath was not warranted because the STEMI criteria were not met.

We began maximal medical therapy, including nitroglycerin infusion. 

To make matters more difficult, the first troponin of course returned undetectable (our contemporary assay rarely budges until 4-6 hours after onset of OMI).

During this time, we incessantly performed serial ECGs, trying to find one that convinced cardiology. 

Here is the clearest one we could get:

By my measurement, there is at least 1 mm in V1, and at least 2 mm in V2. This meets formal STEMI criteria for a male over age 40. The T-wave in V1 is now relatively hyperacute compared to the first ECG. Lead aVL is definitely hyperacute now that we have a clear tracing of it. ST depression in V4-V6 is more evident.

Despite the fact that we believed this ECG meets STEMI criteria, cardiology colleagues disagreed. This is not uncommon, and not unexpected, as prior evidence (see the end of the post for literature review) shows that we have very poor inter- and even intra-reader reliability for measuring the ST segment.

The cardiologist stayed in the room personally to see if the patients symptoms and ECG findings would be persistent despite medical therapy.

Sure enough, the ECG findings and ischemic pain indeed persisted over the course of 20-25 minutes, and the cardiologists correctly decided to proceed with emergent cath rather than further medical management, as is recommended by multi-national guidelines regardless of the ECG findings or interpretation.

We got one last ECG before the patient went to cath:
Now there is ST depression in V3, almost as if a de Winter's T-wave is developing.


 The time between presentation and cath was just under 2 hours.

100% mid LAD thrombotic occlusion was found and stented with excellent angiographic result.

Here is an ECG the next day confirming downstream reperfusion:
Of note, there is lack of pathologic Q-waves and expected reperfusion findings, suggesting relatively favorable infarct size compared to the at-risk territory.

Echo showed wall motion abnormalities of the anterior, septal, lateral, and apical areas. 

Peak troponin T was 1.87 ng/mL.



Learning Points:

We must be expert at subtle ECG findings of Occlusion MI, because our current paradigm is insufficient.

Serial ECGs can often help to make a difficult decision easier.

Persistent ischemia despite maximal medical management is highly likely to be due to Occlusion MI and is an indication for emergent catheterization regardless of ECG findings.

Contemporary troponin assays are frequently undetectable within the first 4-6 hours of Occlusion MI, when the benefit of emergent reperfusion is maximal.

See these other cases of LAD occlusion with similar subtle patterns of STE and hyperacute T-waves in V1-V2, with STD in V5-V6:

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.











McCabe et al, Journal of the American Heart Association. Physician accuracy in interpreting potential ST-segment elevation myocardial infarction electrocardiograms. Journal of the American Heart Association 2013;2:e000268.
A cross-sectional survey was performed by having emergency medicine physicians, cardiologists, and interventional cardiologists review 36 ECGs from the Activate-SF database of prospective STEMI activations. 12 (33%) of the 36 cases had no culprit lesion (defined as no STEMI), whereas the other 24 (66%) were true positives with total acute occlusion (defined as STEMI). This corresponded well with the actual overall rate of false positive STEMI activations in the entire registry of 36% which was recorded from prospective practice. For each ECG clinicians were asked, “based on the ECG above, is there a blocked coronary artery present causing a STEMI?” 124 physicians interpreted a total of 4392 ECGs. Overall kappa value of interreader agreement was only 0.33, reflecting poor agreement. Overall sensitivity and specificity for true positive STEMI (occlusion) was only 65% (95%CI 63-67%) and 79% (95%CI 77-81%). There was a 6% increase in the odds of successful interpretation with every 5 years of experience since medical school graduation. After adjusting for experience there was no difference in the odds of overall accurate interpretation between specialties. However, interventional cardiologists had the highest group specificity at 89%, while emergency medicine attendings had the highest group sensitivity at 74%. This excellent study is supported by many others showing poor inter-rater reliability (35-37).
Carley et al. What’s the point of ST elevation? Emergency Medicine Journal 2002;19:126-128.
Cross sectional study in which 63 clinicians who commonly prescribe thrombolytics for acute MI were asked to identify and quantify the degree of STE present in 3 sample ECG complexes. They were also asked to mark the ECG where they identified the J-point. Overall, STE was not identified in 23 (12%) cases. For figures 1-3 below, the percentage of doctors who correctly identified the J-point correctly was 29%, 61%, and 13%.

Tandberg et al. Observer variation in measured ST-segment elevation. Annals of Emergency Medicine 1999 Oct;34;448-52.
A blinded, paired-sample survey was administered to 52 subjects including emergency physicians, emergency medicine residents, and senior medical students. They were given a packet of 40 ECGs, blinded to the fact that it actually consisted of a random order of identical pairs of only 20 ECGs from patients with “enzymatically proven myocardial infarction.” They were asked to measure all ECGs, then the difference between the each reader’s two measurement of the same ECG was studied. The average difference in segment height among all groups was 0.28 mm. Overall statistical agreement between paired ST-segment measurements was very good (K=0.85). However, “one fifth of the time, intraobserver measurements of paired ST-segment elevations differed by more than half a millimeter.” When specifically asked whether the ST-segment elevation was greater than or equal to 2.0 mm, readers disagreed with themselves in 14% of cases.


Friday, May 24, 2019

LBBB. Is there Occlusion MI (OMI)? Is so, which artery is it?

This was sent to me by Mohammed Shogaa:

Case:

A previously healthy patient presented in acute pulmonary edema, and had this ECG recorded:
Sinus tachycardia
What do you think?













Mohammed was impressed by the concordant ST depression in inferior leads.  This is indeed a good sign of OMI in LBBB, and in this case it is indeed helpful to make the diagnosis.

Inferior ST depression in normal conduction, as I have always written, is RECIPROCAL to ST elevation in lead aVL, and is often more visible than the STE in aVL (see example images at end of post).  Here, there is indeed STE in aVL, but it is less than 1 mm.  Our data would suggest that concordant STE in aVL that is less than 1 mm is not as specific as one might like for OMI, although it is indeed abnormal and should really heighten your suspicion.

When it is accompanied by inferior reciprocal concordant STD, that should make you even more suspicious.

Here the inferior reciprocal STD is indeed more than 1 mm.   So I would call this diagnostic of OMI in LBBB, even though, technically, it does not meet the Smith Modified Sgarbossa criteria.

There is also excessively discordant ST depression (ST/S greater than 30%) in lead V6.  This is very specific for occlusion!

Which artery is it?

Just as in normal conduction, the measurements of ST Elevation in many OMI do not meet the STEMI "criteria," the measurements in LBBB frequently do not meet the Smith Modified Sgarbossa criteria.

Criteria are simply cutoffs with imperfect sensitivity and specificity.

Of leads V1-V4, V2 has the most proportionally discordant STE, with STE at 2.5-3 mm and an S-wave of 13 mm.  If we assume STE is 3 mm, then the ratio is 3/13 = 0.23.  Remember that 25% is 80% sensitive and 99% specific.  But 20% is 84% sensitive and 98% specific.  So really, 20% is a very useful cutpoint.

The cath lab was activated.

A 100% LAD occlusion, proximal to the first diagonal, was found and opened.

Here are the subsequent ECGs:
Much more normal LBBB


Later still:
More normalized



Later still:
The LBBB is resolved and there are (Wellens'-like) inverted reperfusion T-waves in V1-V3.


Learning Point:

Criteria are guidelines only.

This first ECG had 2 different findings that ALMOST met the Smith modified Sgarbossa criteria.  Plus excessively discordant ST depression, which is the 2nd of 2 Smith modified rules (ratio of STD greater than 30% of preceding R-wave).

Both strongly suggested a proximal LAD occlusion.




References

Meyers HP et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study


Smith SW et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presenceof Left Bundle Branch Block With the ST-Elevation to S-WaveRatio in a Modified Sgarbossa Rule.  Full text.


Here are 3 cases of high lateral OMI in which the STD in inferior leads is more apparent than the STE in I and aVL:







===================================
Comment by KEN GRAUER, MD (5/24/2019):
===================================
Objective assessment of acute patients with LBBB has been greatly facilitated by Smith-Modified-Sgarbossa Criteria (SMS Criteria). As discussed in detail by Dr. Smith above — application of these criteria to the case at hand predicted acute OMI for this patient who presented to the ED in acute pulmonary edema.
  • The “beauty” of SMS Criteria — is that they provide a method with user-friendly calculations that clinicians can readily learn to apply.
  • In addition to the use of SMS Criteria — I have always favored a qualitative approach, in which recognition of ST-T wave Shaping that just should not bthere reliably clues me into accurate diagnosis. The more leads on a 12-lead tracing that show abnormal ST-T wave morphology — the more comfortable I am that there is acute pathology. And when there are multiple leads showing ST-T wave changes that “shouldn’t be there” in addition to objective SMS Criteria — I become even more confident in my diagnosis.
  • NOTE — It may take a while to become comfortable with qualitative assessment when there is LBBB. Herein lies the “art” of electrocardiography. In the hope of illustrating this concept — I’ve put together the initial ECG obtained in the ED on this patient ( = ECG #1 in Figure-1) — together with the 3rd ECG in this case, that was obtained some time after reperfusion ( = ECG #3).
Figure-1: The 1st and 3rd tracings obtained from the patient in this case (See text).
=================
The problem in diagnosis that arises — is that LBBB may: iMask infarction Q waves; iiProduce poor R wave progression, if not frank anterior QS complexes; iiiManifest ST-T wave depression in lateral and also inferior leads as an expected repolarization change from LBBB without ischemia; and/or, ivResult in at least some degree of anterior ST elevation (and/or anterior T wave peaking).
  • Taking these expected physiologic changes of LBBB into account — I look first for ST-T wave changes that simply do not reflect a physiologic response.
  • In my experience, when there is an acute event in a patient with LBBB — only 1 or a few leads may show ST-T wave Shaping that just should not bthere. In such cases, once I identify even 1 or a few leads that are definitely abnormal — it often becomes easier to appreciate more subtle morphologic abnormalities in the remaining leads.
  • The more leads showing definitely abnormal ST-T wave morphology — the greater the likelihood of an acute cardiac event. This is especially true when SMS Criteria are also positive.
MThoughts on ECG #1:  In this case — I thought there were no less than 7 leads showing definitely abnormal findings in the initial ECG ( = ECG #1 in Figure-1).
  • My attention was immediately captured by the shape of the slight-but-definite ST elevation in lead aVL (RED arrow in this lead). The rounded shape of this ST segment with downward coving is not a normally expected response.
  • Each of the inferior leads in ECG #1 show reciprocal ST depression. The most markedly abnormal shape is the abrupt angulation (GREEN arrowat the point where the end of the QRS complex joins the beginning of the ST segment. The horizontal “ledge-like” ST depression seen in these inferior leads (BLUE arrows) is distinctly abnormal.
  • Similar, clearly abnormal horizontal “ledge-like” ST depression is also noted in lead V5 (BLUE arrow in this lead). This shape of ST depression should not be seen with non-ischemic LBBB.
  • Finally — the acute angulation where the elevated J-point merges with the ST segment especially in lead V1, but also in lead V2 is clearly abnormal in shape (RED arrows in these leads).
  • In contrast — I thought the ST-T wave shape in other leads was far less decisive. The shape of the downsloping ST segments in leads I and V6 is not unlike the shape of lateral ST-T wave depression expected in non-ischemic LBBB. I found the shape of the ST segment in lead V3 the most difficult to assess. This ST segment in lead V3 lacks the angulation highlighted by the RED arrows in leads V1 and V2 — so by itself, I would not have been convinced of abnormality. However, in the context of clear abnormality of the ST segment in neighboring leads V1 and V2 — I suspected abnormal ST elevation extended at least to lead V3. I thought the ST segment in lead V4 was indecisive.
BOTTOM Line: Although there is no mention of chest pain in this case — acute pulmonary edema is clearly a clinical setting that is commonly associated with acute MI. In this clinical context — the presence of LBBB (not known to be new or old) + at least 7 (if not 8) leads with clearly abnormal ST-T wave deviation in the distribution we see in Figure-1 strongly suggests acute LAD occlusion until proven otherwise.

MThoughts on ECG #3:
  • The best way to improve on recognition of clearly abnormal ST-T wave findings in the setting of LBBB — is to routinely go back and compare the initial ECG of each case you encounter, with follow-up tracings obtained after acute reperfusion. NOTE the dramatic improvement in ST-T wave appearance in ECG #3 — compared to the clearly abnormal ST-T wave findings in each of the 7 highlighted leads in ECG #1 (Figure-1).

Sunday, May 19, 2019

LVH with expected repolarization abnormalities, or acute OMI?

A patient with DM presented with acute chest pain.

Here was his ED ECG:
There is LVH in limb leads, with a 17 mm R-wave in aVL, and deep S-wave in inferior leads.
With this much voltage, one expects some repolarization abnormalities.
Indeed, there is a bit of ST depression in aVL (discordant to the tall R-wave) that does not appear to be out of proportion.
There is inferior ST Elevation, but the S-waves are also of high voltage.
Is this an inferior STEMI?  Or is the LVH with expected repolarization abnormalities? 

There is also some ST depression in V2.  Possible posterior involvement?









Comment

To me, the inferior ST Elevation is out of proportion to the S-wave.  This is however a subjective opinion, as I do not have any data-based rule.  If you measure it, the STE is 2.5-3.0 mm at the J-point, relative to the PQ junction.  With an S-wave amplitude of 17 mm, this is a ratio of 14.6 - 17.6 %.   Without any formal research data to support my opinion, I have advocated that, in LVH, a ratio greater than 15% is abnormal and highly suspicious for STEMI.  (The article by Armstrong  that advocates 25% in V1-V3 for anterior MI is severely flawed and should not be used -- see my comments at the bottom of the page and the associated post).

Here is a great example of limb lead LVH with inferior PseudoSTEMI.  (Thanks to Life in the Fast Lane for this one).
Notice the high voltage.  Notice that there is STE in III with reciprocal STD in aVL
The ratio in III is 1 mm divided by 17 mm. = 6%.  This is normal.


It is important to remember that these entities can have STE in III with reciprocal STD in aVL in the absence of acute MI:

LVH
LV Aneurysm
LBBB
WPW

For this reason, we excluded all these kinds of ECGs in our study showing the very high sensitivity and specificity for inferior MI of STE in III with reciprocal STD in aVL:  ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

Case continued:

In this case, there was an ECG that had been recorded the previous day when the patient had presented with hyperglycemia.
The baseline had zero STE in inferior leads.
This proves that the STE seen on the first ECG is indeed new and ischemic.



2nd ED ECG:
There appears to be less STE now.



The Cath lab was activated.

First troponin returned at 0.048 ng/mL (0.030 is URL), suggesting that this is a true positive.  previous troponins were less than 0.010 ng/mL (undetectable)

Cr was 3.0, with GFR quite low.  Because of this, the interventionalist was tempted to use medical therapy alone, in order not to further damage the kidneys.  Although the contrast used for CT scans probably causes little or no damage to kidneys with low GFR, angiography, especially with PCI, uses far more contrast and can indeed damage kidneys.

Results

Angiogram showed a narrowing of the RCA with TIMI III flow and probable ruptured plaque, but not certain.  The RCA has some posterolateral branches.  The best management strategy was far from clear.   There was a desire to not give too much contrast for fear of renal failure.  Medical management was considered.

Ultimately, intervention was undertaken and there was a complication: either dissection or thrombus formation at the stent, with a decrease to TIMI-1 flow.  Further intervention and use of eptifibatide (a GP IIb-IIIa inhibitor) was undertaken to fix this.

Here was the post stent ECG:
The inferior ST Segments really look ischemic here, with upward convexity (coving).  There is terminal T-wave inversion consistent with reperfusion.
The T-waves in V2 and V3 are far larger, indicating reperfusion of the posterior wall.

The Cr rose to 4.1 mg/dL.

Here is another ECG a bit later
Reperfusion T-waves (inverted) in II, III, aVF, with a reciprocally upright T-wave in aVL
There are now large T-waves in V2 and V3 -- these are clearly reperfusion T-waves of the posterior wall.

If you recorded the posterior wall, there would be negative posterior reperfusion T-waves.
But since it is recorded on the anterior wall, and ADDED to the upright anterior wall T-waves, the result is an extra large T-wave in anterior precordial leads.

Read this article on Posterior Reperfusion T-waves.

Troponin Profile



Echocardiogram:
The wall motion abnormality involves the inferior wall and some of the inferoseptal region, c/w with an infarct in the PDA territory of the RCA.  One view suggests some inferolateral hypokinesis as well but this is less convincing.


Here is another very interesting case of inferior MI in LVH, in which the interventionalist blamed the ST elevation on LVH

ST changes due to limb lead LVH?



Here is a very detailed post on the topic of LVH pseudoSTEMI vs. STEMI, with a great case.

LVH with anterior ST Elevation. When is it anterior STEMI?


Here is part of the discussion in this post:

Is there a “Smith-modified-Sgarbossa” rule for ST elevation in LVH?
Similar to the anterior STE seen with LBBB, the degree of STE in leads V1-V3 of patients with LVH is generally proportional to the depth of the proceeding S wave. In the case of LBBB, it has been shown that STE that exceeds 25% of the proceeding S-wave depth is disproportionately high, and identifies ACO with excellent specificity.9 Could this also work in LVH?

One retrospective analysis by Armstrong et al. suggested that, with LVH, STE in V1-V3 that exceeds 25% of the preceding QRS complex could be an accurate means for ruling out ACO, and fairly sensitive for identifying ACO. 

Smith comment: The Armstrong paper did not have appropriate methods to study this.  The appropriate methods would be to take consecutive ECGs with high voltage and ST elevation in the leads with ST elevation, separate them into those with and without LAD occlusion, and see what are the differences in ST/S ratio.  I have inserted at the bottom of this post some examples from Armstrong's paper.  You will see that they are not cases that you would have difficulty with.  I have tried to study this topic twice and failed because there are very few cases of high voltage in V1-V4 and LAD occlusion.   In fact, even this case does not fit, as the voltage in the affected leads does not meet LVH criteria!


Most importantly, since STE in LVH rarely exceeds 4 mm in height, the 25% criterion is likely far too insensitive. For example, in a patient with an S-wave 30 mm in depth, the STE would have to exceed almost 7 mm.  


===================================
Comment by KEN GRAUER, MD (5/19/2019):
===================================
I found this a difficult case — that to me illustrates how challenging it may be to try to assess serial tracings for subtle signs of acute ischemia in patients with both LVH and slight variability from tracing-to-tracing in QRST morphology.
  • I limit My Comments to the first 3 tracings shown for this patient — which for clarity, I have put together in Figure-1.
  • The KEY to comparison of serial tracings — is to appreciate any differences that might exist in QRS and ST-T wave morphology between one tracing and the next — and then to try to determine whether or not such differences are due to an acute change — or, whether they might be due to other factors (ie, frontal plane axis shift; lead position variation; or other non-ischemic hard-to-define-and-quantify differences). As per Dr. Smith — some of this assessment is admittedly subjective without firm reference to data-based rule.
  • My Preference when assessing serial tracings on a patient — is to begin by complete, systematic interpretation of any one of the tracings in the group. I then make a lead-by-lead comparison with each of the remaining tracings in the group.
Figure-1: The first 3 tracings that are shown for the patient in this case (See text).
=================
MThoughts on ECG #1:
  • I think it most logical in this case to begin with the initial ECG done in the Eon this diabetic patient with new-onset chest pain. There is a fairly regular sinus rhythm at ~80-85/minute. All intervals (PR, QRS, QTc) appear to be of normal duration.
  • Axis  The frontal plane axis in ECG #1 is significantly leftward (about -40 degrees) — consistent with LAHB.
  • Chamber Enlargement  There is a deep negative component to the P wave in lead V1 This may be consistent with LAA (Left Atrial Abnormality)QRS amplitude is dramatically increased in ECG #1 — satisfying voltage criteria for LVH by: ilead aVL findings (R ≥12mm in aVL)ii) by Cornell Criteria (Sum of R in aVL + S in V3 ≥20mm [female] or ≥28mm [male] — andiiiby Peguero Criteria (deepest S in any chest lead + S in V4 ≥23mm [female] or 28mm [male] ). ST-T wave appearance in lead aVL is consistent with at-the-least strain equivalent” pattern. (For details on “My Take” for assessing LVH by ECG — CLICK HERE and HERE).
Q-R-S-T Changes in ECG #1:
  • Waves  A small and narrow septal q wave is seen in lead aVL.
  • Wave Progression  Lead aVL looks “out-of-place”. It’s very unusual for an all-negative complex in lead V1 — to be immediately followed by an almost-all-positive complex by lead V2 — only to return to a predominantly negative QRS complex by lead V3. I suspect some technical misadventure (perhaps lead misplacementto account for this unusual sequence of R wave progression.
  • ST-Waves  There clearly is ~2mm of J-point ST elevation in each of the 3 inferior leads — albeit this is associated with an upward-concavity ( = “smiley”-configuration) to the ST segment. Elsewhere, the ST-T wave appears flat in leads aVL and V2. The T wave inversion in lead V1 is not necessarily abnormal — and ST-T waves in leads V3-thru-V6 do not appear abnormal given the increased QRS amplitude.
COMMENT — As a single initial tracing in this patient with new-onset chest pain — I was not at all certain about the clinical significance of the ECG findings I have justed noted for ECG #1
  • I thought there was a technical problem with the tracing (ie, Lead V2 looks out-of-place) — and this could clearly affect assessment of chest lead appearance. 
  • There is a dramatic increase in QRS amplitude (~30 mm S wave in V3 + lots of overlap with the S in V4 and the R in V5) — and, ST-T wave appearance in lead aVL is consistent with a “strain-equivalent” pattern — so this patient has marked LVH
  • did see the 2mm of J-point ST elevation in each of the inferior leads — but I thought ( = my opinion) that the shape of inferior ST-T waves was not necessarily abnormal given the marked LVH — and, the lack of clear evidence for acute posterior involvement (or for that matter, clear evidence for involvement in any of the other 9 leads) made me uncertain as to whether ECG #1 reflected anything more than marked LVH + LAHB. I didn’t feel able to make a call ...
=================
MThoughts on ECG #2:
  • I found ECG #2 (recorded the previous day when the patient had presented with hyperglycemia) — to be confusing rather than illuminating ( = my opinion).
  • QRS morphology in the limb leads is virtually identical (ie, marked left axis with LAHB). However, there are some changes in chest lead appearance: iTransition is delayed in ECG #2 (doesn’t occur until between leads V5-to-V6 — whereas the R wave became predominantly positive between leads V4-to-V5 in ECG #1); andiiQRS amplitude still satisfies voltage criteria for LVH in ECG #2 — but not as dramatically as it did in ECG #1. Attention to potential differences in QRS morphology between tracings being compared is important — because significant shift in frontal plane axis and/or alteration in chest lead positioning can sometimes make it very difficult to know whether ST-T wave differences reflect acute change vs positional change. I did not think QRS morphology differences between ECG #1 and ECG #2 were enough to alter my assessment of ST-T wave changes.
  • ST-Wave Differences between ECG #vs ECG #— The inferior lead ST elevation seen in ECG #1 is clearly new compared to ECG #2 done a day earlier. That said — ST segments are clearly coved in lead II of ECG #2; coved and slightly elevated in lead V2 — and present a straight ST segment takeoff in leads V3-thru-V6 in ECG #2 that to me looks more acute than the more benignly-shaped upward concavity seen in these same leads in ECG #1. So in some ways — ST-T wave appearance in ECG #2 (done a day earlier) looked more worrisome to me than did ECG #1 ( = my opinion).
=================
MThoughts on ECG #3:
  • Comparison of QRS morphology in ECG #1 compared to ECG #3 looked quite similar (no more than minimal chest lead differences). Looking at all 12 leads in both tracings — I was not convinced that there were significant acute ST-T wave changes between the 2 tracings ( = my opinion).
=================
FINAL Comment: The 4th and 5th tracings on this patient (shown above) — clearly confirm evolution of an acute event. The purpose of my discussion was merely to highlight how challenging assessment of serial tracings can be — especially when there is LVH and other slight variations from one tracing to the next. Our THANKS to Dr. Smith for presenting this challenging case!
  • P.S.It turns out that all 3 of the tracings in Figure-1 showed a highly unusual appearance for the QRS complex in lead V2. Of note — R wave progression across the chest leads looked very different (and normal!) in the 4th ECG on this patient ( = the post-stent ECG) — and different still in the 5th (final) ECG. Therefore — I wonder what the true R wave progression would look like in this patient IF an ECG was to be done with validated chest lead electrode placement ...

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