Saturday, May 11, 2019

A 50-something male with acute chest pain

A 50 y.o. male was sitting at a work conference when he began having substernal chest pain with diaphoresis.  He had a history of hypertension, but no history of heart problems.  The pain was 7 out of 10 when this ECG was recorded:

The QTc = 375
What do you think?
Computer interpretation:


The overreading cardiologist confirmed the computer interpretation (did not diagnose OMI or STEMI).

To me, it is clearly a STEMI.  But many do not recognize ECGs like this! 

The ECG in the last post is much more obvious, but not recognized: 

What happens when you don't recognize an OMI? 

By my visual measurement, STE at the J-point relative to the PQ junction in V2 = 1.5, V3 = 2.0, V4 = 1.5.  Since the threshold for "STEMI" is 2.0 in V2 and V3 for men over age 40, and the threshold in V4 is 1.0 mm, this ECG actually meets STEMI criteria.   (Of course not all ECGs that meet STEMI criteria are STEMI; there are many false positives, but they do NOT look like this one.) 

Usually, the computer algorithm is accurate in measuring ST elevation at the J-point, so I defer to it for this.  But such measurement simply does not matter!

When there is ST elevation in these leads, and all else is normal (normal QRS, upward concavity, no ST depression or T-wave inversion, no Q-waves), then the differential diagnosis is normal variant STE vs. LAD occlusion.

Normal variant STE always has good R-wave progression.

That is why the 4-variable formula is so accurate at making the diagnosis of LAD occlusion when there is no STEMI diagnosed.

If we calculate the formula in this case, the value is 20.75 which is far above the cutpoint of 18.2, confirming that this is an LAD occlusion and NOT normal ST elevation.

Hyperacute T-waves: there are those who would say that these large T-wave are what make the ECG diagnostic of LAD occlusion.  This is NOT correct.  However, one could accurately say that the T to R ratio makes the diagnosis.  In our very large study comparing normal variant to LAD occlusion, the T-wave size was the same in both groups, but the T-wave amplitude to R-wave amplitude in V2-V4 was much larger because of small R-waves in the MI group and large R-waves in the Normal group.  I often say, "When the T-wave towers over the R-wave, beware!"

In our study, small R-wave amplitude was by far the best single variable predictor of MI vs normal!!  The AUC was 0.86 for this one variable.  Thus the formula uses the R-wave amplitude in V4 (RAV4).  Other significant variable were ST Elevation at ms after the J-point in lead V3 (STE60V3), QTc, and total QRS amplitude in V2 (QRSV2)

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

Case continued

The cath lab was activated immediately.

At angiogram with a rapid door to balloon time:

Culprit is 100% occlusion of the LAD Mid segment.

Here is the post stent ECG:
This is probably the amount of ST elevation (zero) that this patient has at baseline.
Note the beginning of Wellens' (reperfusion T-waves) in V3-V6. Even V2 has a steep downslope of the T-wave, suggesting early Wellens wave there.

This was the next AM:
Obvious Reperfusion (Wellens') T-waves V2-V6.

Peak troponin I was 28.1 ng/mL

Echo next day showed:

Normal left ventricular cavity size.
Left ventricular hypertrophy concentric .
Regional wall motion abnormality-anterior and apex, hypokinetic.
The estimated left ventricular ejection fraction is 46 %. Visually it is 50-55%.

Learning Points:

1. Minimal STE and large T-waves is only normal variant when there is large R-wave amplitude and progression.
2. Use the formula before you assume ST elevation is normal
3. Beware reclassifying what you think is LAD occlusion to normal variant.  There are false negatives with the formula, and it is much worse to under-diagnose LAD occlusion than to overdiagnose it!
4.  Learn to recognize subtle LAD occlusion!!

Read this post:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

Better: Watch this 1-hour video lecture:  One hour lecture on Subtle ECG Findings of Coronary Occlusion

UPDATED: "Subtle Findings of LAD Occlusion".  This was recorded at the Controversies and Consensus Lecture I gave in Northampton MA in September 2017.  It is not as professionally produced as the above "One Hour lecture on Subtle ECG Findings of LAD Occlusion," but is more up to date.

Comment by KEN GRAUER, MD (5/11/2019):
This ECG provides yet one more example of acute OMI that all-too-easily could be missed — and, in this case was not recognized by the cardiologist overreading this patient’s initial ECG.
  • For clarity — I’ve reproduced the initial ECG obtained in the ED for this patient in Figure-1.
  • Dr. Smith has detailed use of his 4-variable formula for this case — in which the calculated value = 20.75 is definitely positive (well above the cutpoint = 18.2). I like knowing the score from Dr. Smith’s formula — because when it is so decisively positive (as in this case) — this provides instant support for your suspicion of acute OMI.
  • I assessed this initial ECG before I knew the formula score. In the interest of providing an alternative approach — my sequential thoughts while evaluating this case were those that I detail below.
  • COMMENT: In an ideal world — the computer would automatically calculate the value of Dr. Smith’s 4-variable formula — and, incorporate this as part of the computerized interpretation. Instantly knowing the formula score as the clinician is looking at the ECG would optimize decision-making — since knowing that a formula score is high would clearly alert the interpreter of the need for extra careful scrutiny!
Figure-1: The initial ECG in this case, obtained in the ED on this patient with new-onset chest pain (See text).
MSequential Thoughts in Evaluating this Case:
  • The history we are given is worrisome = severe new-onset chest pain in a 50-year old man. Knowing that severe chest pain is ongoing at the time the initial ECG in Figure-1 was recorded is helpful — because it maximizes the chance of seeing ECG abnormalities if there is acute OMI.
  • COMMENT — When I know that the ECG I am interpreting was obtained from a patient with new-onset cardiac-sounding chest pain — my level of scrutiny is heightened. My threshold for suspecting that ST-T wave changes may be acute is immediately lowered — and, my mindset” is transformed in needing to convince myself that any subtle abnormalities I might see are not acute, rather than the other way around. I suspect this “mindset transformation” did not occur in the cardiologist who overread this tracing as “nondiagnostic”.
Regarding Figure-1: After noting sinus rhythm — normal intervals — slight leftward axis (not enough to qualify as LAHB) — and no chamber enlargement — I focused my attention on Q-R-S-T Changes:
  • Q Waves  There is an extremely tiny Q wave in lead aVL. This clearly is not significant. Although there are no Q waves per se in the inferior leads — the QRS complex is fragmented in leads III and aVF. This is of unknown significance.
  • R Wave Progression  Transition is delayed in Figure-1. That is, the R wave does not become taller than the S wave is deep until between lead V4-to-V5 (Transition should normally occur no later than between V3-to-V4). Of note — an initial r wave is present in each of these first 4 chest leads — but this r wave does not become progressively taller as is normally expected. As per Dr. Smith — assessment of R wave progression is critically important when considering possible acute anterior OMI. COMMENT — Unless you are using a Systematic Approach to ECG interpretation — it is all-to-easy to forget to assess R wave progression ...
  • ST-T Wave Changes  ST-T waves are flat in lead III, and the T wave is flatter-than-expected in lead aVF. These are nonspecific findings. As I looked at the chest leads — my attention was immediately drawn to lead V3 (within the dotted BLUE rectangle in this lead). The visual picture” of the wave in lead V3 should immediately be recognized as being disproportionately tall in the context of QRS amplitude in this lead (We can measure T wave height in V3 = 8mm; and compare this to the height of the r + s wave in this lead = 9mm — but it is the disproportionality in the visual picture between the QRS and the ST-T wave that we should instantly recognize!). In a patient with worrisome, new-onset chest pain — there is NO way that the T wave in lead V3 is normal.
  • Although the T wave in neighboring lead Vis not quite as tall as the T wave in V3 — in the context of the disproportionality that we just saw in lead V3 — there is also NO way that T wave in lead V4 is normal.
  • Neighboring Leads  I was not initially impressed by the ST-T wave in lead V2. Clearly, there is some ST elevation in V2 — but there is an upward concavity, and the amount of ST elevation in lead Vby itself would not necessarily be excessive. BUT — in the context of a patient with worrisome, new-onset chest pain and the ST-T waves we just commented on in leads V3 and V4 — the ST-T wave in lead V2 is most probably also abnormal. Similarly, the T wave in lead Vin context with what we see in neighboring leads V3,V4 has-to-be interpreted as part of the process! (I suspect the subtle ST elevation in leads V1 and V6 is also part of the process — though this could be debatable, and does not in any way influence our overall interpretation).
BOTTOM Line: Even before knowing the score of Dr. Smith’s formula — in a patient with new-onset severe chest pain, the ECG in Figure-1 has-to-be interpreted as an acute OMI until proven otherwise.
  • NOTE: I’ve intentionally expanded the above step-by-step thought process in slow motion. In “real time” — I arrived at my conclusion of acute OMI in need of prompt cath in less than 5 seconds. Speed (and increased accuracy in pattern recognition) comes with practice.

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