UA vs NSTEMI

Hunter

Hunter

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I had a patient recently who had all the presentations of an AMI; chest pain, felt like pressure, 7/10 relieved by nitro, clammy skin, SOB, O2 Sat 89% on room air, p in the higher 90's, BP was 118/??(can't remember) after the nursing home had given him one of nitro. Both 4 and 12 leads all showed NSR however, but it was obvious he was in distress, and he said it felt just like the last time he had a heart attack.

So me and my partner where talking about it after we dropped him off. We came to the question, what's the difference between a NSTEMI vs Unstable angina? As far as pre-hospital is concerned, how do we tell the difference between the two, and does it really matter as they're both going to be treated almost the same once you arrive at the hospital.
 
In the prehospital setting you will not be able to tell a difference and they are managed the same. UA turns into a NSTEMI when myocardial damage occurs as evidenced by increased cardiac enzymes. UA is sub critical and causes symptoms but not actual damage to cardiac tissue. NSTEMI is a retrospective diagnosis after serial enzymes are collected hours later.
 
NSTEMI implies there's been myocardial necrosis/damage with presence of positive cardiac enzymes, Troponin, CK-MB, etc... With UA there may not be positive enzymes.
 
I remember trying to understand how to recognize a "non-Q-wave MI" on the ECG, and being frustrated at trying to make an impossible clinical diagnosis. After all, how can I diagnose something that hasn't had a chance to develop yet?

Similarly, the UA/NSTEMI distinction has its problems, not least of which is they can look the same in terms of symptoms and the ECG. Making the distinction based on biomarkers (CK-MB or troponin) is the common practice, but it has turned out to be a moving target as cardiac enzyme tests have gotten more sensitive.

Since the underlying pathophys is the same, many people have just started calling the whole mess Acute Coronary Syndrome (ACS), and avoiding the fine distinctions that the UA/NSTEMI definitions forced us into.

So, in this view, if the symptoms and ECG suggest cardiac ischemia, it's ACS. And ACS can have positive troponin levels, or negative levels. (Actually, with the new high-sensitivity troponin assays, some people argue that a negative troponin = not ACS, but I'm not so sure...).

So you can just say "Seemed like ACS to me," and you will be right whether or not the labs are positive!
 
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KellyBracket said:
I remember trying to understand how to recognize a "non-Q-wave MI" on the ECG, and being frustrated at trying to make an impossible clinical diagnosis. After all, how can I diagnose something that hasn't had a chance to develop yet?

Similarly, the UA/NSTEMI distinction has its problems, not least of which is they can look the same in terms of symptoms and the ECG. Making the distinction based on biomarkers (CK-MB or troponin) is the common practice, but it has turned out to be a moving target as cardiac enzyme tests have gotten more sensitive.

Since the underlying pathophys is the same, many people have just started calling the whole mess Acute Coronary Syndrome (ACS), and avoiding the fine distinctions that the UA/NSTEMI definitions forced us into.

So, in this view, if the symptoms and ECG suggest cardiac ischemia, it's ACS. And ACS can have positive troponin levels, or negative levels. (Actually, with the new high-sensitivity troponin assays, some people argue that a negative troponin = not ACS, but I'm not so sure...).

So you can just say "Seemed like ACS to me," and you will be right whether or not the labs are positive!
Click to expand...





FLdoc2011 said:
NSTEMI implies there's been myocardial necrosis/damage with presence of positive cardiac enzymes, Troponin, CK-MB, etc... With UA there may not be positive enzymes.
Click to expand...







Aprz said:
http://hqmeded-ecg.blogspot.com/2012/11/watch-recorded-version-of-ecg-blog-live_30.html

Skip to exactly 20:00.
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Chase said:
In the prehospital setting you will not be able to tell a difference and they are managed the same. UA turns into a NSTEMI when myocardial damage occurs as evidenced by increased cardiac enzymes. UA is sub critical and causes symptoms but not actual damage to cardiac tissue. NSTEMI is a retrospective diagnosis after serial enzymes are collected hours later.
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So what I basically gather is that nstemi is undiagnosable in the field. As the only way to prove nstemi is by proving myocardial tissue necrosis through test that aren't available to majority of prehospital providers.

So the only thing we would be able to say is unstable angina.
 
Hunter said:
So the only thing we would be able to say is unstable angina.
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Like I say, UA may be passé.

(Bad link replaced)

Unstable angina died last week, at the European Society of Cardiology’s annual Congress in Munich.

The term "unstable angina" was 41 years old, and is survived by its close sibling, non–ST-segment elevation myocardial infarction (NSTEMI). The cause of death was increasing reliance on high-sensitivity (hs) cardiac troponin assays and the Third Universal Definition of MI that was released last week, and was in part designed to address the shifting acute coronary syndrome landscape created by hs cardiac troponin assays.

Cardiologists first coined unstable angina in 1971 and, in the years following, applied it to hundreds of thousands of patients annually, patients with chest pain caused by acute, ischemic cardiac episodes that failed to produce the electrocardiogram change – an ST-segment elevation – that is the hallmark of a full-blown myocardial infarction.

Over time, increased sophistication in the ability of cardiologists to discern cardiac pathology led to the term NSTEMI; as recently as last year, official cardiology diagnostic guidelines considered unstable angina and NSTEMI virtual twins. The distinction was that NSTEMI produced a measurable, pathognomonic rise in serum levels of cardiac troponin or other serum markers of cardiac damage, with no such rise discernable in unstable angina patients.

The Third Universal Definition changed that. As explained by Professor Freek Verheugt, a Dutch cardiologist who commented on the implications of the new definition last week at the ESC meeting, the new definition’s official adoption of hs cardiac troponin levels as the gold standard for myocardial infarction diagnosis left unstable angina in limbo. It had "disappeared," he said.

"If hs troponins are completely neutral in a patient with chest pain, it’s impossible that the patient has significant coronary disease," he explained to me in an interview. "They therefore have some other condition causing the chest pain. Troponin tests are so sensitive now that they exclude a cardiac cause" when no rise occurs.

In other words, patients with acute chest pain, no ST-segment elevation, and a discernable rise in hs cardiac troponin have NSTEMI. Patients with acute chest pain, no ST-segment elevation, and no rise in their hs cardiac troponin level must have a noncardiac cause for their pain.

Unstable angina, R.I.P.

–Mitchel Zoler (on Twitter @mitchelzoler)
 
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I definitely agree that ACS can have positive or negative enzymes.

And further, not all positive troponins mean it's an NSTEMI. For you guys it's not really an issue, but it is in an inpatient setting where ultimately I'm responsible for the coding/billing and what diagnosis code something goes under and whether or not "core measures" get followed or implemented.

We see "troponinemia" all the time that is NOT an MI or ACS.... definitely changes how things are coded and billed.

And we see plenty of Type 2 MIs/NSTEMIs due to something like sepsis/CHF/arrhythmia that end up not having full "ACS treatment" started.
 
KellyBracket said:
Like I say, UA may be passé.

(Bad link replaced)

Unstable angina died last week, at the European Society of Cardiology’s annual Congress in Munich.

The term "unstable angina" was 41 years old, and is survived by its close sibling, non–ST-segment elevation myocardial infarction (NSTEMI). The cause of death was increasing reliance on high-sensitivity (hs) cardiac troponin assays and the Third Universal Definition of MI that was released last week, and was in part designed to address the shifting acute coronary syndrome landscape created by hs cardiac troponin assays.

Cardiologists first coined unstable angina in 1971 and, in the years following, applied it to hundreds of thousands of patients annually, patients with chest pain caused by acute, ischemic cardiac episodes that failed to produce the electrocardiogram change – an ST-segment elevation – that is the hallmark of a full-blown myocardial infarction.

Over time, increased sophistication in the ability of cardiologists to discern cardiac pathology led to the term NSTEMI; as recently as last year, official cardiology diagnostic guidelines considered unstable angina and NSTEMI virtual twins. The distinction was that NSTEMI produced a measurable, pathognomonic rise in serum levels of cardiac troponin or other serum markers of cardiac damage, with no such rise discernable in unstable angina patients.

The Third Universal Definition changed that. As explained by Professor Freek Verheugt, a Dutch cardiologist who commented on the implications of the new definition last week at the ESC meeting, the new definition’s official adoption of hs cardiac troponin levels as the gold standard for myocardial infarction diagnosis left unstable angina in limbo. It had "disappeared," he said.

"If hs troponins are completely neutral in a patient with chest pain, it’s impossible that the patient has significant coronary disease," he explained to me in an interview. "They therefore have some other condition causing the chest pain. Troponin tests are so sensitive now that they exclude a cardiac cause" when no rise occurs.

In other words, patients with acute chest pain, no ST-segment elevation, and a discernable rise in hs cardiac troponin have NSTEMI. Patients with acute chest pain, no ST-segment elevation, and no rise in their hs cardiac troponin level must have a noncardiac cause for their pain.

Unstable angina, R.I.P.

–Mitchel Zoler (on Twitter @mitchelzoler)
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But this doesn't explain inflammation without lasting damage?
 
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Veneficus said:
But this doesn't explain inflammation without lasting damage?
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Inflammation, as in oxidative, long-term stuff? Or something else?

If this discussion gets too basic/bench/mechanistic, I think I'll have to bow out!
 
KellyBracket said:
Inflammation, as in oxidative, long-term stuff? Or something else?

If this discussion gets too basic/bench/mechanistic, I think I'll have to bow out!
Click to expand...

sorry, mechanistic question.
 
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