Wednesday, January 16, 2013

Male in his 40's with chest pain.

A male in his 40's was in his usual state of health until 3 hours prior when he developed L-sided chest pressure, radiating to the neck, while walking.  He called 911.   His prehospital ECG is identical to the first ED ECG shown below.  Based on this, the paramedics activated the cath lab, administered nitroglycerin, and the pain resolved. 

This ECG was then recorded in the ED:
There is at least 2 mm STE at the J-point in leads V2 and V3, but the morphology of the T-wave is typical of early repolarization (slow upstroke, fast downstroke).  There is minimal ST elevation in I, aVL, V5 and V6.  There are not exclusions to using the formula: no inferior ST depression, no upward convexity, no precordial T-wave inversion, no Q-waves, and no terminal QRS distortion.  Thus, the Early Repolarization vs. LAD occlusion equation can be applied (see sidebar for Excel applet that can be use to make this calculation): STE60V3 is 4 mm, QTc was 416ms, and RA-V4 is 15mm.  Thus, the equation value is [1.196 x STE60V3]+[0.059 x QTc]–[0.326 x RA-V4] = 23.753, which is greater than 23.4 and would indicate STEMI.   The specificity of the rule is not perfect, but a value above 23.4 should at least prompt you to aggressively evaluate the patient.


--STE60V3 = ST elevation at 60 ms after the J-point, relative to the PR segment, in lead V3
--QTc is Bazett corrected QT interval
--RA-V4 is the R-wave amplitude in lead V4

This was not recognized, and the ECG was interpreted as early repolarization.  A bedside echocardiogram reportedly showed no wall motion abnormality. 
A repeat ECG was recorded:
Here, V2-V5 have less ST elevation and the T-waves are smaller.  It appears normal, and different from the presenting ECG.  An application of the equation has equivocal results depending on whether the STE60V3 is measured at 1.5 or 2.0 mm.

Nevertheless, the change shows that the previous ECG was indeed due to acute coronary syndrome (ACS).  

This was not seen and the cath lab was de-activated.  The patient was admitted and ruled out for Acute MI with serial troponin I less than 0.04 ng/ml (using a sensitive troponin assay).  

Not all ACS has a positive troponin.  When negative, it is of course called “unstable angina.”  Unstable angina (see more such cases here) usually presents with a normal or nonspecific ECG, or with ST depression or T-wave inversion, but it may present with transient ST-segment elevation.  And, surprisingly, transient ST elevation does not always result in a positive troponin.  The ischemia may resolve so quickly that there is both no wall motion abnormality and the troponin is negative!

With the advent of high sensitivity troponin in the future, perhaps such cases will become more rare.  But this increased sensitivity may come at the expense of worse specificity, or more false positive troponins. 

The patient was discharged, and 13 days later presented with identical chest pain, which again resolved, and had the following ECG after resolution of pain:
There is new T-wave inversion in I, aVL, V4-V6.  There is terminal T-wave inversion (biphasic) in V2 and V3, but complicated by the U-waves seen in these leads.  This T-wave inversion represents a form of Wellens’ syndrome, indicating spontaneous reperfusion of a brief left anterior descending coronary occlusion.


Outcome: This time, the troponin was positive [which one would expect when there is not just resolution of STE, but also T-wave inversion (Wellens')].   The patient underwent coronary angiography, which showed severe subtotal LAD disease and 70% left main disease.  He underwent coronary artery bypass surgery. 

This case illustrates the importance of paying close attention to the ECG and its evolution.  Using the formula may help.

1.  Coronary occlusion may be brief, with spontaneous reperfusion.
2.  Serial troponins may be negative even in ACS with transient ST elevation (unstable angina may have transient ST elevation)
3. Though early repolarization may change over months, if it changes from one ECG to the next on the same day, it is probably not early repol.
4.  Use the equation to help you differentiate early repol from LAD occlusion.


  1. If this formula was accepted widely, what would be done differently?

    1. I'm not sure it is either widely known or accepted. It was only recently published.

  2. Dear Dr Smith,
    What made you immediately exclude (or at least omit from the discussion) the diagnosis of pericarditis? Diffuse concave st elevations, no reciprocal changes (aside from avr), STE II>III, and perhaps even subtle PR depressions .
    thank you for this invaluable resource!

    1. Pericarditis usually has an ST axis of around 60 degrees, resulting in STE in II (as you say) and V5 mostly. Though it happens, maximal STE in V2 and V3 is unusual. Most unusual though is even a hint of ST depression anywhere, and one might imagine that there is reciprocal ST depression in lead III (reciprocal to aVL). Could a patient with pericarditis have an ECG like this? Probably. But there would not be resolution of symptoms (and ECG findings!) so quickly. This is only typical of reperfusing MI.

      Finally, pericarditis is far less common than MI, and even less common than previously thought. A recent study using CT coronary angiography showed that half of patients with transient ST elevation and normal coronaries (who might have been diagnosed with pericarditis) have extraluminal plaque in the territory with ST elevation that accounts for the findings.

      Steve Smith

  3. Congrats..great case..8 wonder if those Inferior leads q waves are pathological ones

    1. They look pathological. Probably old inferior MI.

  4. Hi Dr.Smith.. I tried to apply the equation on 24year old male who came with atypical chest pain for two days. Troponin 33.9 CK 3300 with CKMB 300 . trop peaked 39 then dropped to 16 on third day.. ECHO was normal. have a look on ECG file PDF


    1. Mateeq, I looked at the ECG and it does not look like an LAD occlusion. Was it? And was it occluded at the time of the ECG? That is hard to determine, but if the patient had chest pain at the time of the ECG and the angiographic culprit was a thrombotic LAD lesion (whether open or closed), then likely yes. But this one would fool me or the equation if that is so. I very much doubt that the LAD was occluded at the time this ECG was recorded.

      Steve Smith

    2. Thanks. . In fact pci was not available at that time.. treated medically as ACS.. i will follow if he is going to do pci later

    3. Hi Dr. Smith,
      In relation to the first EKG and negative troponins, how do you differentiate who can benefit from cath in negative troponin patients as there can be some harm chasing ekgs without evidence of acute MI? In other words, if this was not stemi but instead some mild depressions or mild ischemic t wave inversions and they ruled out for MI (negative trops, maybe normal echo), do you in your practice still push for cath? Thanks, always appreciate your take.

    4. Joe,
      It requires recognizing that the EKG is ischemic. It is unequivocally ischemic if you have the expertise to interpret it: first, it meets the formula criteria, then it resolves. This change can only happen if the findings really are ischemic findings.
      Steve Smith


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