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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