Saturday, May 18, 2024

Early repol or anterior OMI?

Chest Pain – Benign Early Repol or OMI?

Written by Destiny Folk, MD, Adam Engberg, MD, and Vitaliy Belyshev MD

A man in his early 60s with a past medical history of hypertension, type 2 diabetes, obesity, and hyperlipidemia presented to the emergency department for evaluation of chest pain. He reported substernal chest pressure with radiation to his left arm that started at work several hours prior to arrival and had somewhat improved since onset. He noted that his father died from a heart attack in his early 50s prompting his presentation to the emergency department.

Here is the initial ECG at 13:17 with no prior ECG in the patient’s chart for comparison:

What do you think?

This is another version of the same ECG, lower quality, and with an additional filter applied. See Ken Grauer's additional comments about this ECG at the end of the post!


The ECG shows sinus rhythm and relatively normal QRS morphology. There are findings concerning for anterolateral OMI including ST elevation and hyperacute T waves in the anterolateral leads most prominent in V2-V5, as well as hyperacute T waves in the inferior leads. There is also abnormal R wave progression with regression from lead V2 to V3 (assuming normal leads). This ECG is highly concerning for LAD occlusion despite it not showing a STEMI criteria.

If you look at this and aren’t sure if this is normal variant ST Segment Elevation in V2-V4 (Early Repolarization) or a subtle LAD Coronary Occlusion, you can use Dr. Smith’s Simplified 4 Variable Formula:
--This formula can be applied to ECGs with some STE in leads V2-V4 (there should be at least 1 mm of STE in at least one of these 3 leads) 
--This formula considers:
1) the QTc (computer measurement)
2) the R-wave amplitude, in mm, in lead V4
3) ST elevation as measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters in lead V3. 
4) Lastly, the QRS amplitude in V2 (both the R- and S- waves) are measured. 

Using these measurements, the formula calculates a value. If that value is greater than 18.2, it is quite sensitive and specific for LAD occlusion.

You can find the variables used to calculate the value on MD calc here:

Utilizing Dr. Smith’s Subtle Anterior STEMI Calculator (4-Variable), the value is greater than 18.2 which is concerning for LAD occlusion. 
We measured:
1) QTc = 386 msec
2) QRS amplitude V2 = 12mm QRS in V2
3) R-wave amplitude V4 = 5mm 
4) STE 60 V3 = 2.0 mm STE at 60msec after J point in V3 
Formula value = 19.0.

The Queen of Hearts read this ECG as OMI – Low Confidence

Click here to sign up for QoH Access

The providers taking care of this patient were concerned regarding his clinical history and initial ECG, so they next performed a bedside cardiac ultrasound. POCUS showed an anterolateral wall motion abnormality with hypokinesis most pronounced at the apex.

Speckle Tracking Echocardiography may provide another useful adjunct. On the TEX Mindray machines, global longitudinal strain is defined as less than or equal to -16%. The Apical 4 Chamber best captured the significant wall motion abnormality to the apical anterior wall. The apical anterior and septal wall segments were identified with significant strain pattern as showed below in the bullseye diagrams:

Essentially speckle echocardiography is measuring how far 'pixels' of the myocardium are moving during cardiac cycles. A positive strain means elongation whereas a negative strain is shortening. On our ultrasound machine, the TEX, normal strain is considered -18 % and higher (more negative). The closer the number is to 0 the less the myocardial fibers are moving. The computer uses the three cardiac axes: (longitudinal, circumferential and radial.

Unfortunately, I only obtained 2/3 of the complete bullseye, which essentially maps out the myometrium with corresponding blood flow (see below). Vitaliy went back to see if he could add in the missing anterior lateral and inferior septal movement, but could not.

For this patient segments (7 and 13; anterior) and (14 and 8; anterior septal) show significant longitudinal strain with negative (less shortening than normal, i.e. not moving).

The graphic below correlates blood flow with the bullseye segments. Note the purple LAD supplies all the strain segments (7,8,13,14) The strain pattern corroborates the mid and distal LAD occlusion!!

The red circles correspond with the areas identified with significant cardiac strain. 

Dr. Smith and other authors showed the utility of Speckle Tracking Strain Echo in this case report: 

Repeat ECG:
Slightly less hyperacute T waves, likely indicating improving flow compared to the first ECG.

Several hours later, angiogram showed:
Culprit lesion mid LAD, 75% stenosis, TIMI 3, thrombotic, likely the source of the distal LAD 100% embolic occlusion, with TIMI 0 flow. The culprit mid LAD lesion was stented. It is not clear in the report whether thrombectomy was performed on the distal LAD occlusion.

Below is the ECG obtained after cath lab intervention:

Arrows demonstrate the reperfusion T waves.

This ECG is consistent with reperfusion given the T wave inversions shown in V2-V6 as indicated by the red arrows.

The patient’s hs troponin I rose from 1,709 to 24,860 ng/L, and was not trended to peak. The patient was discharged approximately 24 hours after intervention.

The discharge diagnosis was that worthless and meaningless term "NSTEMI".

The discharge diagnosis should have been "OMI"

Learning Points

The T waves should always be viewed in proportion to the QRS and if the T waves looks too big for the QRS, you should be concerned for OMI. T wave inversions in the OMI territory are consistent with reperfusion as shown below. T wave inversions may persist for days prior to the patient’s ECG returning to baseline.

Use the Subtle Anterior STEMI Calculator (4-Variable) to differentiate normal variant ST elevation (benign early repolarization) from anterior STEMI. This formula can be found on MD calc at this link:

Wall motion abnormality and Speckle Tracking can be a useful adjunct in corroborating subtle ECG findings.

QOH could have improved recognition of OMI in this case. 


MY Comment, by KEN GRAUER, MD (5/18/2024):

The "good news" about today's case — is that the treating clinicians promptly recognized ECG abnormalities in the initial tracing — documented abnormal Echo findings in support of suspected LAD OMI — and facilitated timely cardiac catheterization in which successful PCI led to a positive outcome.
  • I'll add some thoughts about the first 2 tracings in today's case.

Taking another look at the initial ECG (that I've reproduced in Figure-1) — this tracing is simply not easy to interpret. (NOTE: The ECG that I show below in Figure-1 is the only tracing that I initially saw — which illustrates the challenges of interpreting suboptimal quality tracings. I never saw the improved quality version).
  • There is a large amount of baseline artifact that complicates assessment of ECG #1. The underlying rhythm is sinus. That said — it took me a while to weed through the ever-present baseline undulations in this initial ECG, until I finally could recognize that a low-amplitude upright deflection (sinus P wavedoes consistently appear before each of the 10 QRS complexes in the long lead II rhythm strip.

  • The distracting effect of this artifact is perhaps best appreciated by looking at the different ST-T wave appearance for the 2 QRS complexes that we see in leads V2 and V3. The principal diagnostic consideration, is whether this initial ECG is diagnostic of acute LAD OMI — for which these 2 anterior leads provide key input. But — Which ST-T wave is the "correct" one? (ie, the ST-T wave of beat #6 in leads V2,V3 — or — of beat #7 in these leads)?

  • That said, there does appear to be a "culprit" extremity responsible for much (most) of the artifact — which appears to be coming from the RA extremity, because baseline undulations are maximal in leads I, II and aVR — present but smaller in leads aVL and aVF — and absent in lead III  (See My Comment at the bottom of the page in the February 18, 2024 post in Dr. Smith's ECG Blog for review of how to quickly determine the "culprit" extremity)Therefore — It's worth a quick look at the patient to see if the RA electrode might be loose? — or — if there might be any other potentially "fixable" patient action that might account for the artifact.

  • NOTE: The filter setting for this initial ECG in today's case — was 0.05-to-40 Hz (lower right portion of Figure-1). This setting is consistent with monitor mode — which is the setting often used to help reduce artifact and baseline wander. However, monitor mode is less precise for assessment of ST-T wave morphology — than the 0.05-to-150 Hz filter setting recommended for diagnostic mode.
  • Although clearly there are times when excessive movement artifact prevents use of the 0.05-to-150 Hz setting — it's good to appreciate the potential effect that filter settings may have, and best to first try the optimal 0.05-to-150 Hz setting when the focus is on ST-T wave analysis in a patient with chest pain (See My Comment in the January 13, 2024 post for more on filter settings).

ECG Findings in the Initial Tracing:
As per Drs. Folk, Engberg, Belyshev and Meyers — Even despite the artifact, ECG #1 is remarkable for hyperacute T waves in a number of chest leads — abnormal R wave progression — and a disproportionately large T wave in lead aVF.
  • KEY Point: For however much technical issues may have complicated assessment of chest lead morphology — I thought the abnormal limb lead findings in ECG #1 were convincing enough to convey that an acute process was in progress because: i) There could be no doubt about the disproportionate hypervoluminous appearance of the T wave in lead aVF (compared to the tiny QRS complex in this lead)ii) Although not elevated — the ST segment coving in lead III was clearly abnormal, and further supported the hyperacuity seen in neighboring lead aVF; andiii) The ST segment straightening with slight-but-real ST depression in lead aVL, in the context of this patient with new chest pain — satisfied the "magic" reciprocal ST-T wave appearance between leads III and aVL that so strongly suggests an OMI-in-progress.

  • Additional Point: Given the amount of artifact in ECG #1 — requesting an immediate repeat ECG might have clarified the ECG presentation.

Figure-1: The first 2 ECGs in today's case.

The Repeat ECG:
The 2nd ECG was recorded 25 minutes later.
  • The artifact is gone! Although there is baseline wander — the clear and consistent QRST complexes now enable precise interpretation.
  • In this patient with new CP (Chest Pain) — lead V3 immediately draws attention (within the RED rectangle in ECG #2— because of its hyperacute T wave (clearly taller and "fatter"-at-its-peak and wider at its base than it should be — given small size of the QRS in this lead).
  • In view of the abnormal T wave in lead V3 — the T wave in neighboring lead V4 is also hyperacute (more voluminous than it should be — within the BLUE rectangle in this lead).
  • The 3rd definitely abnormal (disproportionate) T wave in ECG #2 — is in lead aVF (within the BLUE rectangle in this lead).

Realizing the technical difficulty inherent in assessing artifact-laden ECG #1 — there appears to be dynamic change compared to repeat ECG #2 done 25 minutes later.
  • The ST-T wave in lead V2 has normalized in ECG #2.
  • Although difficult to appreciate (because of the artifact in ECG #1) what may represent "real" change in leads V3,V4 between the 2 tracings — the T waves in leads V5,V6 clearly look less acute in the repeat tracing.
  • Subtle improvements are also noted in the limb leads of ECG #2. These include: i) Flattening of the ST segment in lead III in the repeat tracing; ii) Resolution of the slight ST depression in lead aVL; andiii) Reduced relative size of the hyperacute T wave in lead aVF.

  • BOTTOM Line: In this high-prevalence for OMI patient with new CP — these 2 serial ECGs are diagnostic of acute LAD OMI, with need for prompt cath confirmed by dynamic ST-T wave changes between the 2 tracings. IF symptoms were decreased at the time (25 minutes later) when ECG #2 was obtained — the improvement we see in ECG findings between these 2 tracings would suggest spontaneous reperfusion of the "culprit" artery was beginning.

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