Thursday, April 30, 2015

A Case of Clinical Unstable Angina in the ED

A woman in late middle age with a history of a mild stenosis of the RCA seen on CT coronary angiogram 4 years prior presented 2 hours after the onset of nondescript substernal chest discomfort that radiated to both axillae.

Her daughter was worried and brought her to the ED.  This is her initial ECG:
There is a suggestion of inferior MI: the T-waves in II, III, and aVF are slightly large.  There is T-wave inversion in aVL, which is a soft sign of inferior MI.

She received nitroglycerin, and the discomfort was relieved, but she attributed the relief to the removal of a tight-fitting garment.

A repeat ECG was unchanged after pain relief.

I was worried about her, but with pain resolution and a non-diagnostic ECG, there was no indication for cath lab activation at night.

The first troponin was undetectable.

Nevertheless, I was still worried about her and gave her aspirin, ticagrelor, and heparin, and admitted her to the hospital.

After admission, serial troponin I later climbed, peaking at 1.6 ng/mL.

A formal Echo the next AM showed an inferior wall motion abnormality.  A repeat ECG in the morning was recorded:
This shows resolution of the enlarged T-waves, confirming that there had been inferior ischemia.

I was sure there would be a tight RCA lesion that would need stenting.

However, the angiogram showed a chronic total occlusion of the RCA, with the inferior wall supplied by collaterals.  No stent was deployed.

The angiographer explained it this way: "she could have had some small left to right collateral channels that closed off, and then she recruited more collaterals to reperfuse."  Perhaps as a result of nitroglycerin.

Nevertheless, until angiography was done, this was presumed ACS of the RCA (or possibly circumflex) until proven otherwise.

Learning Point

1.   Inferior hyperacute T-waves can be extremely subtle

2.   Even if they do not lead you to cath lab activation, such T-waves, along with lead aVL and the convincing history, may persuade you in spite of an undetectable troponin, to give maximal medical therapy (aspirin, ticagrelor, and heparin) for ACS.

3.  The territory of a chronic total occlusion which is supplied by collaterals is particularly vulnerable.


  1. Interesting case. I looked after a similar case with transient inferior STE on his ECG. I thought that he would have a tight RCA lesion also. His RCA was found to be chronically occluded and he had a tight lesion in his LCX which supplied the right by collaterals.

  2. Hello Dr. Smith,
    it seems when speaking about "large T waves" of occlusion, it seems to me that the width of the T wave (perhaps considered the "bulk") is as important as the height, and that the T wave can seem widen more than the increase in amplitude.

    I have not seen this referenced directly, but can you comment please?


    1. Dave,
      This is certainly true and I have always tried to make that point.
      I always use the term "large" or "bulky" when talking of hyperacute T-waves, not "tall" or "high amplitude".
      Perhaps I have not been specific enough when stating this.


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