Chest pain and Convex ST Elevation in Precordial Leads

A 30-something y.o. male with PMH significant for anxiety, asthma, and alcohol use disorder presented with chest pain x 1 week.  Patient thinks he has an asthma flare, with wheezing. He subsequently developed fevers and chills, and then left-sided chest pain associated with a cough. His breathing and infectious sx then improved. Today, however, he developed constant chest pain radiating into left arm around 1345. He states the pain is improving now. He had associated “swimmy, head rush,” which is no longer present. He denies associated shortness of breath, sweating, numbness, tingling. Onset of pain was while sweeping at work. He was able to ride bike on the day of presentation without difficulty.

No cardiac history. Non-smoker, no EtOH, no h/o DVT. No leg swelling. No risk factors for CAD.

Here is his ECG:

There is ST elevation, up to 2.5 mm in V2, with convexity.
Generally, STE with convexity in any of leads V2-V6 is abnormal and highly suggestive of ischemia (anterior MI, LAD occlusion).

As always, pre-test probability is critical.  And this patient’s pretest probability was extremely low.

One is not supposed to use the formula that differentiates Normal Variant ST Elevation (often referred to as early repolarization) when there is convexity.  However, if one did, here is the result:

QTc = 428 ms
ST Elevation at 60 ms after the J-point in lead V3 (STE60V3) = 2.5 mm
R-wave amplitude in V4 (RAV4) = 12 mm
Total QRS amplitude in lead V2 (QRSV2) = 25 mm

4-variable formula value = 17.92.  This is below the cutoff for LAD occlusion (18.2), but not by a lot, so one must be careful.

There was a previous available.  I did not see it until writing this post:

The new one is changed.  Is that significant?

Although looking for change from an old ECG can be very helpful, it is not foolproof.

See this post and references below:
Kambara (see below) showed that early repolarization is dynamic; see this case and discussion: 

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

So we did a bedside echo:

Parasternal short axis shows excellent anterior wall contractility

A subsequent ECG approximately one hour later with continued chest pain:

Now there is an RSR’, but the P-wave is inverted, so the RSR’ is due to lead placement too high.
No evolution, no evidence of OMI/STEMI

QTc = 419
STE60V3 = 4.5
RAV4 = 19
QRSV2 = 17.5

Formula value = 18.83 (this is now consistent with LAD occlusion)

At this time, the first troponin I returned undetectable, below 0.010 ng/mL, which if the chest pain was acute, might be expected in OMI.  However, this patient had very prolonged chest pain.

So we waited for another, and a troponin drawn 2 hours later was still less than 0.010 ng/mL.

1.  The 1st ECG has false positive convexity.
2.  The 2nd ECG has a false positive 4-variable formula

I discharged the patient after excluding other serious causes of chest pain.

Learning points:
1.  Be skeptical of an apparently positive ECG when the pretest probability is extremely low.  (Do not be skeptical if the ECG is unequivocally positive!)
2.  Although the reperfusion decision does not depend on troponin in acute chest pain, an undetectable troponin in prolonged chest pain is strong evidence that the ST elevation is not ischemic.
3. Use Echo
4.  The formula does have false positives.
5.  Convexity rarely has false positives.

References on stability of early repolarization over time.

1. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

2. Mehta MC. Jain AC.  Early Repolarization on the Scalar Electrocardiogram.  The American Journal of the Medical Sciences 309(6):305-11; June 1995.

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.


Comment by KEN GRAUER, MD (2/18/2019):


Excellent example by Dr. Smith of how use of other parameters (ie, pre-test probability; Echo at the bedside & serial troponins) may prove invaluable for ruling out acute cardiac disease. 

  • Although a previous ECG was found on this patient — this apparently was not available in the ED at the time acute decisions was done. I therefore focus my comments on the 2 ECGs that were done in the ED (Figure-1).

Figure-1: The 2 ECGs in this case that were done in the ED. Not included in Figure-1 is the previous ECG on this patient — as this tracing was not available at the time acute decisions were made (See text).
In my experience — there is a tendency (even among experienced interpreters) to jump at specific ECG findings, without first using a systematic approach to interpret the initial tracing — and then, failure to apply lead-to-lead comparison of this tracing with other ECGs in the case. I generally start with full evaluation of the initial tracing ( ECG #1which is the TOP tracing in Figure-1):

  • Rate & Rhythm: There is a fairly regular sinus rhythm at ~65-70/minute.
  • Intervals: The PR, QRS & QT intervals are all normal.
  • Axis: There is a rightward axis of ~100 degrees (ie, predominant negative deflection in lead I ).
  • Chamber Enlargement: None.
  • QRST Changes waves – wave progression – ST-wave changes)A small Q wave is seen in lead III — there is an rSR’ complex in lead V1, consistent with incomplete RBBB (narrow QRS; s waves present in both leads I and V6— Transition (ie, the place where the R wave becomes taller than the S wave is deep in the chest leadsdoes not occur until lead V6 (if then, as depth of the S in V6 looks to be equal to height of the R in V6 …). Perhaps the most remarkable finding in ECG #1 is the coved (and worrisome) ST elevation that is seen in leads V2-thru-V6.

IMPRESSION of ECG #1Sinus rhythm — right axis — incomplete RBBB — delayed transition — coved ST elevation in leads V2-thru-V6, albeit without reciprocal changes. Pre-test probability is low for acute cardiac disease (ie,younger age of this patient and a history more suggestive of an acute febrile illness rather than cardiac chest pain) — but, further evaluation is clearly indicated given ST elevation to rule out a worrisome cause (ie, MI, myocarditis).

  • There may be malposition of lead V3 in ECG #1. That’s because appearance of not only the QRS complex, but also the ST-T wave in lead V3 looks very different than in neighboring leads V2 and V4. In fact, the shape and amount of ST elevation looks quite similar in leads V2, V4 V5 — so the appearance of lead V3 just doesn’t “make sense”. That said, the overall “theme” of ECG #1 is clear regardless of whether lead V3 is or is not accurately placed.


What is Different in ECG #2?

In ECG #2 — there once again is sinus rhythm — right axis deviation — and an incomplete RBBB pattern. That said — ST elevation is clearly less compared to what had been seen in ECG #1. What Else is different between these 2 tracingsWhat might account for some of these differences?



It is much more likely that leads V1 and V2 were placed inappropriately high on the chest in ECG #2. This is because: ithe initial component of the P wave in both V1 and V2 in ECG #2 is negative (the initial component of the biphasic P wave in ECG #1 was positive; and the P was all positive in V2 in ECG #1); andiithere is now an rSr’ pattern alsoin lead V2 in ECG #2.

  • The zone of Transition is very different in ECG #2 !!! Note that there is already a substantial R wave by lead V4 — and the R wave clearly becomes predominant between V4-to-V5. In contrast, the R wave never became predominant in ECG #1.

IMPRESSION of ECG #2The shape and amount of ST-T wave elevation in lead V3 of ECG #2 looks to be similar to what it was in leads V2, V4 and V5 in ECG #1. It is possible that the reason the amount of ST elevation is less and the ST segment shape took on a more benign-looking appearance (ie, concave up) in leads V4-thru-V6 of ECG #2 may simply be a result of the fact that these 3 leads now all manifest a predominant R wave. There is probably no meaningful change in ST-T wave appearance between ECG #1 and #2.

  • The BEST evidence supporting the absence of any serious heart disease in this patient was forthcoming from the combination of — low pretest probability — completely normal Echo — negative troponin values. As a result, the patient was safely discharged from the ED.
  • It is likely that there was lead misplacement in both tracings — and probably a difference in the way in which chest leads were misplaced. Failure to recognize this might result in wrongly attributing the “change” in ST-T wave appearance between ECGs #1 and 2 as due to a dynamic change.
  • It would be extremely helpful to obtain another 12-lead on this patient after meticulously verifying lead placement. If this true “baseline” ECG (with verified lead placement) still results in a worrisome-looking convex ST elevation repolarization pattern — it would be good to have this on the chart in the event this patient returns to the ED with another episode of chest pain.
  • A useful PEARL to consider in patients with worrisome-looking baseline tracings — is to GIVE THE PATIENT miniaturized copy of their ECG to carry on their person, so that they can then show this to medical providers in the event of a subsequent trip to the ED.

Our THANKS to Dr. Smith for presenting this case.



  • For “My Take” on use of the Systematic Approach to ECG Interepretation — CLICK HERE.
  • For more on recognizing Lead V1, VMalposition — CLICK HERE.

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