Monday, September 5, 2022

Unstable Angina still exists. It can be missed especially high sensitivity troponin is not used. Sometimes you can catch it on the ECG.

A 50-something woman with H/o HTN, ESRD, CAD S/p complex PCI to ostial LAD and ramus (10/2020) and CABG x3 (LIMA to LAD, SVG to OM, SVG to ramus)

She complained of intermittent episodes of substernal chest pain, radiating to left shoulder, lasting 2-3 minutes.

This had been worked up before at another ED on 3 occasions for the same chest discomfort.

--The 1st time, she was "ruled out" with a point of care (POC) troponin<0.03 ng/mL.

--The 2nd time, she was "ruled out" again with a POC troponin <0.03 ng/mL.

--The 3rd time, she "ruled out" with a laboratory-based 4th generation troponin at 0.018 ng/mL (Abbott Architect, LoD = 0.010 ng/mL, URL = 0.030 ng/mL)


Do NOT use the point of care troponins that are on the market now. (Excellent high sensitivity point-of-care troponins are are coming soon).

Advice #2:

Use high sensitivity troponin (NOT 4th generation troponin).  Any troponin using units of ng/mL or mcg/L is a 4th generation (NOT a high sensitivity 5th generation).  

Aside: "High sensitivity" mostly means "high precision".  The value obtained is very accurate even at VERY low levels.  This is represented by the "coefficient of variation" (a measure of the reproducibility of results obtained from measuring the same sample many times); a CV of 10% at a very low level is good.  For high sensitivity, the CV should be 10% at a level substantially lower than the 99% URL.

Initial ECG, without pain, with K = 5.9 (K level unknown at that point in time)

K returns at 5.9 mEq/L.

The initial troponin returned at 6 ng/L.

Hyperkalemia was treated with D50 and insulin about 2.5 hours after this EKG.

15 minutes after administration of D50 and insulin, the patient had an episode of chest pain 3 hours later that lasted only 2-3 minutes, but they were able to record an ECG during that short time interval.

Significant ischemic ST depression in II, III, aVF and V5-6.

Pain resolved rapidly with NTG

1 hour later, without pain

The repeat K returned at 5.9 again.

The repeat troponin returned at 22 ng/L (URL for a woman is 16 ng/L, so this qualifies as a myocardial infarction.

Another 1 hour later, again pain free:

Some evidence of ischemia/reperfusion is seen in V5,6, with some slight ST depression and T-wave inversion.

No further troponins were measured.

The patient was given aspirin and heparin.

Next day echo showed:

--The estimated left ventricular ejection fraction is 71 %.

--There is no left ventricular wall motion abnormality identified.

--The estimated pulmonary artery systolic pressure is 34 mmHg + RA pressure.

--Mild aortic stenosis (Vmax 2.5 m/s, mean gradient 13 mmHg, dimensionless

index 0.42 , estimated valve area 1.5 cm2).

--Mitral valve insufficiency 1+

--Normal left ventricular cavity size.

--Normal estimated left ventricular ejection fraction .

--No wall motion abnormality .

Angiogram showed:

Culprit Lesion (s): Suspect ostial LAD in-stent restenosis and proximal LAD stenosis

2 more posts on unstable angina in the era of high sensitivity troponin:

Unstable Angina Still Exists in Era of high sensitivity troponin, with a short lesson on troponin interpretation

Learning points:

1. Unstable Angina still exists, even in the era of high senstivity troponin; it is dangerous.
2. Do not use POC troponins to rule out MI until the high sensitivity assays are on the market.
3.. Always use serial high sensitivity troponins if the first result is measurable, UNLESS there has been chest pain that began AT LEAST 3 hours prior to blood draw AND the pain was of sufficient duration to result in myocardial necrosis.  Such duration is not exactly known, but certainly pain of less than 5 minutes is not sufficient to rule out ACS with troponins.
4.. Repeat ECGs with recurrent pain and try to record during the episode of pain.   

Comment by KEN GRAUER, MD (9/5/2022):
Important post by Dr. Smith — in which he provides a number of Pearls regarding the use of specific troponin products currently available, in association with subtle serial ECG changes.

Complicating today's case — was the presence of hyperkalemia, which is the focus of my comments. Although the serum K+ level recorded in today's case was only 5.9 mEq/L — it's difficult from the information available to know how much of an effect (if any) this elevated serum K+ level may have had on serial ECG findings (especially since the repeat serum K+ level despite treatment with D50 and insulin once again came back at the identical 5.9 mEq/L value).
  • We have discussed numerous cases of hyperkalemia in Dr. Smith's ECG Blog — including the "textbook" sequence of ECG findings that are taught to occur with progressive degrees of hyperkalemia (See My Comment at the bottom of the page in January 26, 2020 post of Dr. Smith's Blog). While I find awareness of the generalizations for these progressive ECG signs is helpful — it's important to emphasize that "not all patients read the textbook" — and there may be marked variations in both the sequence and occurrence of QRS widening, T wave peaking, P wave shrinking, etc. For example — progression from sinus rhythm to VFib as the 1st ECG sign of hyperkalemia has been documented (emDocs, 2017 — Management of Hyperkalemia)

PEARL: When a patient has hyperkalemia — it is impossible to know how much the elevated serum K+ may be influencing QRS width and ST-T wave morphology until you normalize serum K+ — and then REPEAT the ECG!

  • For example — IF there was significant ST depression on the baseline tracing — then the "net effect" of such ST depression might sufficiently attentuate the T wave peaking of hyperkalemia in a way that produces "pseudo-normalization" of ST segments and T waves.
  • Hyperkalemia may mask the ST-T wave changes of acute infarction. Alternatively — hyperkalemia may produce a "pseudo-STEMI" pattern that simulates acute infarction.
  • With severe hyperkalemia — You can get an idea of the extent that excess serum K+ may be altering the ECG by the improvement seen within minutes of giving IV Calcium. However, because the duration of action of IV Calcium is limited (ie, to ~30-60 minutes) — improvement of hyperkalemia-induced ECG changes following a dose of IV Calcium will be transient (until other measures produce a longer-lasting effect).

  • CAVEATS: Assessing the effect hyperkalemia may have on ECG findings becomes especially challenging: i) When your patient is also having ischemic chest pain; ii) When details about the timing of serial ECGs, patient symptoms, and the timing serum K+ lab draws is not precise; andiii) When you consider that some patients do not develop any ECG signs of hyperkalemia at all before they develop their lethal arrhythmia.

Clinical Example:
I thought the best way to illustrate how hyperkalemia may complicate the assessment of ECG ischemic changes — would be to draw on a case from one of our previous Blog posts. In Figure-1 — I show the initial ECG obtained in the ED from this December 11, 2018 post. This patient presented to the ED with DKA in a comatose state.
  • Although T waves are peaked and pointed with a narrow base — We do not usually see biphasic T waves in hyperkalemia, as are present in leads V1-thru-V6. What might this indicate?

Figure-1: The initial ECG from the December 11, 2018 post in Dr. Smith's ECG Blog. This patient presented comatose in DKA.

As emphasized earlier — the effect of hyperkalemia on the ECG is additive to (superimposed on) however the baseline ECG looked!
  • IF the baseline ECG is abnormal, with preexisting ST-T wave depression — then the degree of T wave peaking from hyperkalemia may be significantly attenuated. OR — You may get a "mixed" picture, with ST segment coving and an initial negative component to the T wave before terminal T wave peaking (as seen in Figure-1).

CASE Follow-Up:
The patient in this 2018 post was acidotic with severe dehydration and a glucose of 1400 mg/dL at the time the initial ECG in Figure-1 was recorded. Serum K+ = 9.0 mEq/L.
  • The patient was intensively treated with 4 liters of fluid, repetitive doses of IV calcium, albuterol and insulin.

  • The ECG was repeated (Figure-2). What do you see?

Figure-2: Comparison of the initial ECG from the December 11, 2018 post — with the repeat ECG after treatment (See text).

Comparison of Pre- and Post-Treatment ECGs:
It should be emphasized that serum K+ was not yet normal at the time ECG #2 in Figure-2 was recorded (serum K+ = 5.8 mEq/L). As a result — we still do not know what this patient's baseline tracing truly looks like. That said — it should be clear from ECG #2 that there has been significant improvement in the severity of this patient's hyperkalemia.
  • A low atrial rhythm is present in ECG #2 (ie, negative P wave in lead II — but positive P wave in lead I). There is a PAC. The rhythm was sinus in ECG #1.

  • There has been a significant axis shift since ECG #1 (ie, The frontal plane axis in ECG #2 is +70 degrees — whereas there was marked left axis in ECG #1). Given the adverse effect hyperkalemia has on conduction — the presence of an unusual frontal plane axis and/or marked axis shift from the patient's baseline tracing are additional indicators from ECG #1 suggesting the degree of hyperkalemia was severe!

  • The QRS has become narrow in ECG #2. The QRS complex was definitely wide (ie, at least 0.12 second) in ECG #1.

  • The peaked and pointed T waves from ECG #1 are no longer present. Instead — fairly deep, symmetric T wave inversion is now seen in leads V3, V4 and V5, with at least suggestion of abnormal ST segment coving in these leads. Whether these ST-T wave abnormalities in ECG #2 are new and indicative of ischemia? (and whether they might be even more pronounced if the ECG was repeated after complete resolution of hyperkalemia) is uncertain. 

BOTTOM LINE: Seeing ECG #2 explains the highly unusual picture of ST segment coving with biphasic T waves that was seen in ECG #1 when serum K+ = 9.0 mEq/L.
  • The Message is Clear — IF the patient presenting with hyperkalemia is also acutely ischemic — these ischemic ECG changes may not be recognizable until serum K+ is normalized and the ECG is repeated.

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