Thursday, August 1, 2013

Man in his 60's with very subtle ECG and pain not controlled with medical therapy

A male in his 60's presented 30 minutes after the onset of crushing substernal chest pain.  Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG.  The patient had never had pain like this before.  The pain improved from 9/10 to 3/10 after NTG.  Here is the initial ED ECG:
QRS axis = 11, T-wave axis = 13.  There are very subtle signs of ischemia here: minimal ST elevation in I and aVL with minimal reciprocal ST depression in lead III.  Most specific is the abnormal ST segment and T-wave in aVF: it is downsloping with a subtly biphasic (down-up) T-wave.   There is also poor R-wave progression in anterior leads, but no ST elevation to suggest acute anterior MI.  This could be, however, evidence of old anterior MI.  Also, the T-waves in V4-V6 are taller than they should be relative to the R-wave amplitude.

This ECG, especially along with the very typical history, was very worrisome, but not absolutely diagnostic of, ischemia.  Several serial ECGs showed no change, even after the pain finally resolved to 0/10 after NTG.

He was given aspirin, clopidogrel, IV nitroglycerine, and heparin, the general cardiologist was called and notified that this patient was very high risk and needed close attention.  He readily agreed, and the plan was to admit for close observation, serial ECGs and troponins, and to scrutinize for any recurrence of pain or change in the ECG.

The first troponin I then returned at 0.063 ng/ml (upper limit of normal = 0.025 ng/ml).  Repeat ECG remained unchanged.

He remained pain free and the plan remained to admit with a diagnosis of Non-STEMI on medical therapy with plan for angiogram in the morning.

Just before admission to the hospital, the patient admitted to recurrent pain and appeared uncomfortable.  Therefore, the cath lab was activated urgently.

The suspicion was for a circumflex (or obtuse marginal branch) or diagonal artery occlusion or subtotal occlusion.

At cath, there was a 95% proximal LAD stenosis, proximal to a large diagonal.  A stent was placed and the patient became pain free.

The ECG the next AM is here:
QRS axis = 50, T-wave axis = 42.  The T-wave inversion in III is resolved, but this may be only due to a change in QRS axis.  In any case, there is minimal T-wave inversion in aVL and the ST elevation is resolved.  The ST depression in III is resolved.  The abnormal ST-T complex in aVF is resolved.

The troponon I peaked at only 1.117 ng/ml.  Echo the next AM showed a new Regional Wall Motion Abnormality of the distal septum, apex, and anterolateral wall with an estimated EF of 55%.  This anterior WMA is probably stunned myocardium that will recover (although the poor R-wave progression is consistent with previous completed infarction of the anterior wall).  This patient was at risk of a very large anterolateral STEMI and loss of large amount of myocardium.

Learning Points

1. Subtle ECG findings led to very rapid evaluation and treatment of this high risk ACS
2. The ECG alone is not an indication for urgent cath.
3. The entire clinical picture was then made more clear by an elevated troponin
4. The indication for urgent cath was uncontrolled ischemia in spite of maximal medical therapy in a patient with objective evidence of ACS as the etiology of the symptoms.

When there is not a STEMI, what are the indications for emergent cath?

The indications are uncontrolled ischemia, with objective evidence of ongoing ischemia.

I.   Objective evidence of ischemia
     1. Ischemic ST elevation; ST elevation known to be due to ischemia though not diagnostic of STEMI.
            a. Not ST elevation due to a normal variant or to LVH or LBBB etc. OR
            b. Dynamic ST elevation
     2. Ischemic ST depression (see the 5 primary patterns of ischemic ST depression)
            a. Not ST depression due to hypokalemia or LVH or LBBB
            b. Dynamic ST depression
     3. Positive troponin (this is a late finding!)
     4. New wall motion abnormality on ultrasound

Ischemic T-wave inversion is not necessarily evidence of ongoing ischemia!  Rather it is often a sign of reperfusion, even if evolving on serial ECGs!

II. Inability to control the ischemia with medical therapy alone (Ongoing ischemia)
     1.  Continued, refractory ischemia on the ECG or
     2.  Continued, refractory symptoms of ischemia (espeically chest pain) or
     3.  Shock, venticular dysrhythmias, pulmonary edema

In cases in which the ECG shows active ischemia, resolution of pain may be very deceptive.  Ischemia can be symptom free.  Studies of patients with known ischemia proven by dynamic ST segments on 12-lead ST segment monitoring show frequent periods of ischemia, including ST elevation and depression, not associated with symptoms.  Thus, if there is known ischemia manifesting on the ECG, these ECG findings of ischemia must resolve along with the symptoms.


  1. An electrocardiogram as the first might have been overlooked by any ED physician. What are the subtle changes you found in this ECG?

    1. The subtle findings are best seen in III and aVF: especially aVF, with an ST segment that goes down then up

  2. Do you think the regional wall abnormality found in the distal septum is responsible for the early injury pattern(minor STE + increased T wave amp)in lead II?

    1. I don't think that is related, and I'm not certain there are significant findings in lead II, although I grant that the T-wave is a bit large.

  3. in wellen's syndrome the resolution of pain should not be lead us to say that " theres nothing or it's gastric reflux".
    i think a key point is that whenever the pain goes off the ekg manifesations should do the same.
    i noticed that in V1 there's inverted T wave and it's associatedd with an inverted T wave in III, should some one put on top of differential diagnostic the possibility of Pulmonary Embolism ?

    Dr lotfi bensekrane.

    1. Both symptoms and EKG need to resolve. There are studies showing dynamic ST segments (on 12 lead monitor) that are asymptomatic. So if only symptoms go away, but EKG does not resolved, ischemia is persistent.

  4. Dr. Smith,

    I find myself a little confused by this case. I have reread the post called the 5 primary patterns of ischemic depression. My question is why does this ECG not show a isolated high lateral STEMI? Is it because of the tiny amount of ST-D in the inferior leads?

    1. I think it does show isolated high lateral MI, plus evidence of old anterior MI. It turned out to be BOTH acute high lateral AND anterior MI. Proximal LAD disease affects the anterior AND lateral walls.

  5. In retrospect, do you see the ST changes in leads I and aVL as 1mm and indicative of STEMI?

    1. They are, in retrospect, real. However, if you routinely based the diagnosis on this, you would have a lot of false positives.



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