It is Far too Early for a Requiem for Unstable Angina

Dr. Braunwald declared that high sensitivity troponins will make Unstable Angina a thing of the past.  That very well may be true, but in the United States we are not yet in the era of high sensitivity troponins.  And we do not know what their effect will be.

Here are many more cases of Unstable Angina.

Unstable Angina

A male in his 50's with no past history presented with new intermittent burning left chest pain, lasting 10 minutes at a time, radiating to the left arm, for 24 hours.  He had chest pain just prior to arrival in the ED, but it resolved prior to physician evaluation.  He did use cocaine a few days prior.  He had blood pressures in the 170/100 range.  Here is his initial ECG:

There is terminal T-wave inversion in V2-V5, highly suggestive of "Wellens' syndrome."
Patient had pain, is pain free, has intact R-waves, and terminal T-wave inversion
(Wellens' Pattern A)

There was no further pain, but a second ECG was recorded 1 hour later:

There is some evolution of T-wave inversion (V3 has a deeper negative deflection), increasing suspicion for Wellens' syndrome.

The ED was concerned about "Wellens' pattern," and gave aspirin, clopidogrel, and heparin.  He was not given anything for his blood pressure.  He was admitted to the hospital. The consultants were very worried as well, and discussed angiogram vs. stress test in the morning.

Comment: when a patient has cardiac ischemia and is hypertensive, the blood pressure should be controlled.  There are many choices. One is metoprolol.  There is an admonition not to use a beta blocker in patients who have cocaine in their system because if may produce "unopposd alpha" effects by blocking the vasodilating effects of beta-2. However 1) that admonition is based on faulty data from combined beta-1 and beta-2 blockade (namely propranolol -- metolprolol has almost no beta-2 blocking effects) and 2) the patient has not had cocaine for days.

The patient ruled out by 4 serial contemporary troponins over 9 hours.  

However, the first 2 were 0.020 ng/mL and the next 2 were ﹤ 0.010 ng/mL: limit of detection (LoD) is ﹤ 0.010 ng/mL and the URL is ﹤0.030 ng/mL.  Thus, 2 were measurable but not above the URL.

Wellens' syndrome can occur with trops below the URL, but they are rarely all below the LoD.

No further ECGs were recorded.

A cardiac echo was normal, showing no wall motion abnormality and EF of 65%.

No more ECGs were done (was there further evolution of T-wave inversion?  Was there resolution?)  In my experience, if troponins are all negative, the T-waves rarely evolve to Pattern B (deep symmetric inversion).  Instead, they often resolve.  Such resolution is NOT pseudonormalization (which is due to re-occlusion of the vessel), but rather due to resolution of ischemia.

The assessment in the light of a normal echo and normal troponins was that this was noncardiac chest pain or cocaine chest pain with nonspecific T-wave inversions.

There had been discussion of a stress test but the patient was discharged.  It seems he had been instructed to go to his primary MD and get a stress test.

Case progression.

Two days after discharge, the patient presented to another hospital ED with the same complaints of intermittent chest pain (3 episodes).  He had not seen his MD nor had a stress test yet.  His last episode of chest pain was just prior to ED arrival and was resolved upon arrival.  Here is the initial ECG:

Classic Evolution of Wellens' Waves

The physician had no access to previous ECGs.

The first troponin was negative.  The physician consulted the on-call cardiologist who thought it was very unlikely that this would be Wellens.'  He did not think it possible that the patient could have 4 days of intermittent chest pain with normal troponins throughout and without wall motion abnormality, and with a normal ejection fraction.

He thought the most likely cause was related to the patient's recent cocaine use and vasospasm. He did agree with the plan for stress test but felt like it could be done as an outpatient.

The patient was told to return for increased or longer lasting pain.

He did return the next day after another episode of pain, and was pain-free on arrival.

Here is the ECG:

More Wellens' Evolution, but with some loss of R-wave amplitude

This time the initial troponin I returned at 1.5 ng/mL.  The peak troponin is not available.

He had an angiogram which showed a 95% thrombotic LAD stenosis with preprocedure TIMI-3 flow.  It was stented.  There was also an 80% proximal LAD stenosis.

Here is the angiogram:

Here is the post cath ECG:

There is loss of R-wave in V2 and V3.  The T-waves have evolved as expected from Pattern A (biphasic) to deep and symmetric (Pattern B). 

A post cath echo showed anterior and apical WMA with EF of 55%.  Will this be permanent?  It is uncertain if there was irreversible loss of significant myocardium.  The loss of R-waves suggests that this is the case.


Learning Points:

1. Unstable Angina still exists.  Contemporary troponins are CERTAINLY not good enough to rule it out.

2.  Regional wall motion recovers rapidly after reperfusion of the infarct artery.  After chest pain is resolved, a normal echocardiogram should not reassure you!

3.  Pay attention to specific ECG findings!

4. Chest pain in a patient who uses cocaine is just as likely to be due to ACS as it is in a patient who does not use cocaine.  See this article and editorial.  

5. Chest pain that occurs more than one day after cocaine use should not be attributed to cocaine.