Friday, April 11, 2014

Unstable Angina: Dr. Braunwald asks if it is time for a Requiem

In a recent commentary, Dr. Eugene Braunwald asked if it is time for a Requiem for Unstable Angina (ACS without a positive troponin, as defined by a rise and/or fall with at least one level above the 99% reference value).

http://circ.ahajournals.org.ezp2.lib.umn.edu/content/127/24/2452.full.pdf+html

Here is a quote:

"Indeed, in its 2008–2009 report, the World Health Organization revision of the definition of MI stated: 'Many patients who in the past would have been diagnosed as having unstable angina will now be diagnosed as having had an MI.'  In the next few years, there will likely be much wider use of higher-sensitivity assays for cTn and acceptance of the universal definition of MI.  As a consequence, UA is likely to be further marginalized, its definition will become highly dependent on the particular assay for cTn used, and the term will become ever more ambiguous and cause confusion because it will mean different things to different people. Indeed, it is not clear that ACS events can occur without some increase in circulating cTn when measured by a high sensitivity assay."

This article prompted some recent Tweets about whether Unstable Angina (UA) still exists in the age of sensitive biomarkers. Don't all ACS rule in by serial trops now?

UA certainly does still exist, at least for now, because in the U.S. we do not yet have FDA approval for high sensitivity troponin (hscTnI).  And we do not yet know for certain whether hscTnI will abolish UA, or just diminish the number of patients with troponin (-) ACS.

Perhaps when we get hs troponin in the U.S. (not yet), it will be exceedingly uncommon, but with the use of contemporary troponin assays, it is an important phenomenon still.

Below are some old examples, and one new one:

Here are several previously posted cases.  

Here is another that was just posted on April 4.

Now I have yet another to post:

A patient with DM and, it seems, heavy alcohol use had also been recently admitted for chest pain: she ruled out for MI (sorry, I do not have the ECGs from that presentation), then had a positive stress test, which led to an LAD stent (thus, she had unstable angina, but that is only the first of two episodes for her).

She presented to the ED some time after the stent, complaining of fatigue and chest pain.  She had stopped taking her Clopidogrel.  She had also stopped her propranolol.  She was dehydrated and ketotic.  BP was normal and she was tachycardic.  There was a systolic murmur.

Here is her ED ECG:
There is sinus tach, perhaps due to both dehydration and possibly also to some propranolol withdrawal.  It is abnormal, but there is nothing specific for ischemia.  It certainly could represent ischemia, but no definite active ongoing ischemia.  The QT appears to be about 380 ms and thus QTc = 570ms (see leads II and III).  This QT is very long and suggests that the "T" waves in II, and III are really U-waves.  I strongly suspect hypokalemia, but (oddly) no K was measured until over 24 hours later.  


She had a stat formal echo which showed hyperdynamic heart and anterior wall motion abnormality but with EF of 85%.  There was no serious valvular disorder.

Her pain resolved.  She ruled out for MI with contemporary high sensitivity troponins.

The next morning she had a VT arrest and was resuscitated.  Here is her post resus ECG:
Large ST elevation.  It has a very odd morphology, even mimicking Brugada and Hyperkalemia, but it must be assumed to be LAD occlusion

She was taken for cath and had a 100% LAD occlusion that was stented.

She did well.

Lesson:

Unstable Angina still exists.  It is dangerous.  It may be missed by both ECG and (by definition) troponin.  It happened twice in this patient.  It is too early for a Requiem.

5 comments:

  1. Pseudo-hyperK+ mimicing pseudo-Brugada mimicing an actual AWMI? That's an awesome "cold read" ECG.

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  2. The first EKG is worrisome. V2-V3 have lost their normal concave ST-T segment. I have seen the same pattern on a patient sent to the waiting room with a "normal" EKG who later coded in the waiting room. This is also where the ST elevation showed up in your second EKG...

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    1. Yes, but this is a common nonspecific finding in ECGs with deep S-waves.

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  3. In first ecg there is t wave inversion, is it Wellen's t wave
    Or if during pain if this ecg recorded than what is importance of t wave inversion in this case?

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    1. The T-wave inversion is very nonspecific. It does not look like Wellens'. Also, Wellens' is a syndrome, not an ECG finding: Typical Chest pain (crescendo angina) in someone at risk for CAD, lasts up to one hour, resolves.)

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