Wednesday, November 22, 2017

A 30-something with 8 hours of chest pain and an elevated troponin

I received this email:

"Hi Steve,

"I'm curious what you thought of these ECGs.  They were on a 34 y/o with constant CP x 8 hours-- 1st at presentation, and 2nd 90 min later after Trop returns positive at 1.5 ng/mL.  

"He had diaphoresis initially at 3 am when it started.  

"Pain is non pleuritic and there is no radiation.  Now improving to 3/10.  

"He also reported having chest pain with exertion x 2 weeks.  Resolved with several min of rest.  No identified cardiac risk factors."

Here is the initial ECG:
Sinus tachycardia.
T-wave inversion in V3; also in III.

Incomplete RBBB.
One other finding.

Here is the 90 minute ECG after troponin returned positive:
Still sinus tach
T-wave inversions in V1-V3
T-wave inversion in III

Here is my response:

--With the tachycardia and T-wave inversions V1-V3 and in lead III, with ongoing CP, I would be worried about Pulmonary embolism.
--Bedside echo:  RV?  Look at legs: DVT?
--Do CTPA (or at least d dimer, then CT if positive).
--If negative, then needs emergent coronary angiogram.
--Tell me outcome!

(The other finding is an S1Q3T3; see below for its significance)

Here is the answer:

You’re right.  

The CP with exertion made me think it was ACS/Wellens.  I performed a bedside echo and thought the septum wasn’t moving well.  However, in retrospect it was likely RV dilatation.  Cards took to the Cath lab and no CAD (afternoon).  CTA showed saddle PE.  IR performed catheter directed thrombolysis.

He never reported SOB.  I also thought the Troponin was too high for PE.

Does the TWI in III make LAD ischemia unlikely?

And my answer to his question:

3 giveaways to the diagnosis:

First, the positive troponin confirms that there is myocardial injury, which helps to narrow an otherwise broad differential diagnosis.  (The ECG findings are quite nonspecific until you have definite evidence of myocardial injury, at which point ACS and PE go to the top of the list).

1. Chest pain persists with T-wave inversion. 

Wellens' is a pain free state.  That is to say that T-wave inversion in ACS is significant when it is a post-ischemic state, after reperfusion. That is why Wellens' is a pain free state.  When there is persistent pain with T-wave inversion, think of other etiologies.  Furthermore, the T-wave inversions just don't look like Wellens' waves (see below).

2. T-Wave inversion in lead III differentiates ACS from PE.  If the differential is ACS vs. PE and there are precordial T-wave inversions, then T-wave inversion in lead III is very specific for PE.  See Kosuge study below.

3. Most important, tachycardia.  Sinus tach is unusual in type I MI.

Classic Wellens' T-waves, evolving over 26 hours (7 successive ECGs)

The ECG in Pulmonary Embolism:  

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, or sinus tachycardia, then they have a (+) likelihood ratio. S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

When there is a positive troponin, then the findings are related to myocardial injury, and then PE and MI are at the top of the differential, and Kosuge's article (see below) applies.

This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  

Just to be clear: these are all patients being evaluated for PE, whereas Kosuge studied those with only ACS and PE left on the differential.  We should apply Kosuge's data to our case here because of the positive troponin.  

They found the following positive likelihood ratios for PE:
1. S1Q3T3  3.7
2. Inverted T-waves in V1 and V2, 1.8
3. Inverted T-waves in V1-V3, 2.6
4. Inverted T-waves in V1-V4, 3.7
5. Incomplete RBBB 1.7
6. Tachycardia, 1.8. 

Finally, they found these independent predictors of PE:
Note that tachycardia only has an Odds ratio of 1.8.  Remember that is the odds ratio comparing all patients without PE to those with PE.

If you did an OR for all patients with ACS vs. those without ACS, it would be far higher.

Tachycardia is unusual in ACS unless there is cardiogenic shock or a second simultaneous pathology.

In our case here, there is S1Q3T3, precordial T-wave inversions, incomplete RBBB, and tachycardia.  All together, that makes for a very high odds ratio.

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  

This does not contradict the conclusions of Kosuge et al., who studied a select population of patients who were known to have either PE or ACS.  Of those select patients, the ones who also had T-wave inversions in the right precordial leads were studied.  Of these, T-wave inversion in lead III was very specific for PE.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 

Finally, Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be lower because we diagnose more of the submassive PEs that have minimal symptoms.

Sunday, November 19, 2017

It is not a STEMI; it is an opportunity to save myocardium!

I was teaching about subtle coronary occlusion at EKG conference to our residents a couple days ago.  About coronary occlusion that does not meet STEMI criteria and that many physicians would miss.

They were asking me about whether, if they missed one of these, would they have missed a STEMI?

I responded: 

"No, you would not have missed a STEMI, and you would not be blamed for anything, but you would have missed an opportunity to save the patient's heart."

Just as I was explaining this, a text message came through from a former resident, with this ECG and the question: "Diagnostic ECG?"
What do you think?
Notice the computer only sees the inverted P-waves.

I responded:

"Those are hyperacute T-waves."

The residents all chimed in: "Do not miss this opportunity!"

So I texted back: "Do not miss this opportunity to save the patient's heart.  It is definitely diagnostic."

As it turns out, this was a prehospital ECG:

The medics transmitted this to the Emergency physician, asking whether cath lab activation was indicated or not.

The emergency physician diagnosed coronary occlusion (based on the STE in I and aVL, with reciprocal STD in lead III and the hyperacute T-waves in V3-V5). 

A cardiologist somehow got involved.  He disagreed and said not to activate, and "instead of listening to me," commenced to "educate me as to why the EKG is normal."

Comment on ECG:
The pair of leads III and aVL are diagnostic of occlusion.
The hyperacute T-waves in V3 and V4 are diagnostic of occlusion.
The combination is diagnostic of proximal LAD occlusion.

So I asked what the history was, and here it is:

A 60-something man, previously healthy, has sudden CP and diaphoresis.   He presented to a clinic where the ECG (not available) was normal and there was a negative single troponin.  He was discharged to home from the clinic.

He called 911 for recurrence of pain.

My response was:

"Given the history, you could almost activate the cath lab without an ECG!"

But instead, the emergency physician persisted, and recorded this ED ECG shortly afterwards:
Now there is an obvious anterolateral STEMI

At angiogram, the proximal LAD was occluded.

Wednesday, November 15, 2017

A male in his 50s with chest pain. What is your interpretation?

Written by Pendell Meyers, edits by Smith:

A male in his 50s with no significant past medical history complained of several episodes of chest pain over the course of the past 24-48 hours, which became acutely worse and persistent approximately 1 hour prior to arrival.

Here is his presentation ECG:
What is your interpretation?

Sinus rhythm. Normal QRS morphology with the exception of possibly high voltage. There is minimal elevation of the J point in III and aVF, with significant reciprocal ST-T depression in aVL and I, as well as ST-T depression in V2 with minimal J-point depression in V3. The large, symmetric, bulky T-waves in the inferior leads are highly suspicious for hyperacute T-waves, and this suspicion is confirmed in aVL by the massive area between the baseline and the ST-T depression/inversion compared to the QRS complex, making this definitively consistent with a reciprocal hyperacute T-wave. This ECG even without knowing the appropriate clinical history has extremely high probability of acute coronary occlusion in the inferior and posterior distributions. Additionally, there is ST elevation in V1, indicating RV involvement. The ST depression of posterior MI sometimes attenuates the ST elevation of concomitant RV MI, but in this case there is clear ST elevation in V1 even in spite of the fact that there is ST depression in V2.

The physicians were able to look up a baseline ECG:
All findings on the presentation ECG are new compared to this baseline ECG. Specifically, notice the negative T-waves in the inferior leads with positive T-wave in aVL at baseline, which are "pseudonormalized" in the presentation ECG above. These differences again confirm acute coronary occlusion. 

The physicians were highly suspicious of the findings on the presentation ECG. They did not immediately activate the cath lab but instead called the interventionist on call who was also worried and together they decided to activate the cath lab. He was moved to the critical care area of the Emergency Department and a repeat ECG was performed:
Findings in the inferior leads are not much changed, however there is even more ST elevation in V1, confirming concomitant right ventricular MI. The ST depression is somewhat attenuated, likely because it is being caught between the anterior/rightward vector of the RV MI and the posterior vector of the posterior MI.

Smith comment: We have a manuscript under consideration in which we found that ST elevation in V1 in an inferior MI is very specific for RV MI, especially when there is ST depression in V2.  However, STE in V1, in inferor MI, is not sensitive enough (about 85%) to rule out RV MI.  Therefore, I recommend a right sided ECG for every patient with inferior MI, unless it will delay coronary intervention.  No right side ECG was recorded.

Initial troponin T was undetectable.

The patient was taken for angiography:
Before intervention: there is a proximal to mid RCA occlusion. The angiogram report states it was a total thrombotic occlusion with TIMI-0 flow.
The tortuous vessel appears to be a right ventricular marginal branch.
This is surprising because it indicates that there may not be a right ventricular infarct.
On the other hand, sometimes there is a second branch to the RV.

After PCI of the RCA: TIMI-3 flow through the entire RCA.
Here you see a more distal branch that appears to supply the RV.

Without right sided ECG, and without typical RV physiology of hypotension, and without an echo showing RV dysfunction, it is impossible to tell from the information we have whether, in fact, an RV MI was present.
Repeat ECGs ordered after cath:
J-points all nearly back to baseline. There is terminal T-wave inversion in leads III and aVF, with reciprocal terminal upright T-waves in aVL and V2. This confirms reperfusion in the inferior and posterior distributions. 

Further T-wave changes indicating progression of reperfusion findings.

Peak troponin T was 2.68 ng/mL (large MI) at approximately 12 hours from presentation. Echo showed an inferior and posterior wall motion abnormality.

Learning points:

Lead aVL often has the most definitive and most easily noticeable evidence of inferior acute coronary occlusion.

Serial ECGs make difficult decisions easier.

Comparison with old ECG can make the diagnosis.

Initial contemporary troponin within the first few hours of onset of acute coronary occlusion will usually be negative.

ST elevation in V1 in the right context is indicative of acute coronary occlusion of the right ventricle, especially in the context of ST depression in lead V2.

Record a right sided ECG in cases of inferior MI.

Here is an interesting case with ST elevation in V1:

RV MI diagnosed by ST elevation in V1

Tuesday, November 14, 2017

Is this acute coronary occlusion? Simple ACS? Where is the culprit lesion?

This was sent by Brandon Stein.

This patient presented with chest pain:
What do you think?

There is "inferior" ST depression.  When you see this, especially with down-up T-waves, as in III and aVF, it is reciprocal to barely visible ST elevation in aVL.  Then look at V2 and V3.  Both have hyperacute T-waves, which suggests the LAD.  The combination of STE in aVL and V2 is typical of a first diagonal occlusion (the first lateral branch off the LAD).

It was described in the below article.  They called it a "mid-anterior" or "mid-anterolateral" infarction without involvement of the septum or apex.

Brandon was very astute and recognized the acute coronary occlusion.  The cath lab was activated and there was a first diagonal 100% occlusion.

Here is the post cath ECG:

Compare to the presentation ECG:
The post cath ECG has significantly small T-waves in V2-V5
All of the STE in I and aVL is resolved.
All of the inferior ST-T ischemia is resolved

Peak troponin I was only 1.36 ng/mL, thanks to immediate recognition and rapid reperfusion!!

Learning Points:

1. Coronary occlusion need not have "diagnostic" levels of ST elevation.
2. NonSTEMI frequently needs the cath lab NOW.
3. First diagonal occlusions have their own footprint that is recognizable.  Its sensitivity and specificity are really unknown, however.  But every time I see it, I recognize it and have not been wrong yet.


Friday, November 10, 2017

A middle-aged woman with chest pain and a "normal" ECG in triage

This was sent to me by a former resident from a community hospital:

A middle-aged woman complained of chest pain and was seen in triage.

She had a ECG recorded.

The computer interpreted the ECG (GE Marquette 12 SL) as:

"Sinus Bradycardia.  Normal ECG."

It was not seen by a physician.

Here it is:
Computer interpretation: 
"Sinus bradycardia. Normal ECG"

--This ECG does, at first glance, appear normal

--It is sinus rhythm.
--The QRS is normal

--There is possibly an abnormal Q-wave in lead III, and non-specific T-wave in aVL, but the computer did not see it.

--All the intervals are normal, including the PR, QRS, and QTc at 455 ms
--There is ST elevation in V2-V4, but it is within normal limits.

That is, it appears to be normal ST Elevation and the computer thinks it is normal STE.

There is one thing that is clearly abnormal, but computers are not programmed to detect it:

When there is ST Elevation in V2-V4, it is only normal when there is:
1) high R-wave voltage and 
2) a short QTc
3) relatively high QRS voltage in V2

This ECG has a relatively long QTc, low R-wave amplitude, and low QRS amplitude

That is why the formulas work.

STE60V3 = 2.5 mm, QTc = 455 ms, RAV4 = 6 mm, QRSV2 = 11
3-Variable formula = 27.9 (very high, diagnostic of LAD occlusion)
4-Variable formula = 23.05 (very high) 

To my knowledge, no computer algorithm has yet been programmed with the formulas

The ECG was not shown to a physician.

Later, the patient collapsed in triage and became unresponsive.  She was in full arrest with ventricular fibrillation.

Fortunately, she was resuscitated.

She had a 100% LAD occlusion.

She survived neurologicially intact.   I don't know what her subsequent cardiac function was, but that is not the point of this post.

But it could have been a disaster.


This paper has received some press recently:

Safety of Computer Interpretation of Normal Triage Electrocardiograms

The algorithm used was also the GE Marquette 12 SL.

It purports to show that you don't need to read the ECG if the computer says "normal".   That it saves you from pesky interruptions.   Many on Twitter seem to agree.

222 of 855 (26%) were interpreted as normal.  The confidence intervals were 97-100%.  Would you like to be 97% sure you're not missing an emergency?

Neural Networks are coming:

We compared a new deep neural network (DNN) machine learning artificial intelligence algorithm from Cardiologs technologies(DNN) to Veritas conventional algorithm in the interpretation of 1473 ED ECGs:

Veritas: Of 364 ECGs (24% of total) that it interpreted as "normal," is missed 5 emergencies.
DNN: Of 493 ECGs (33% of total) that it interpreted as "normal," it missed 2 emergencies.

As you can see, it had both fewer false positives and fewer false negatives. That is powerful, and it will only get better as it learns from more and more ECGs.
So things will get better as technology advances.

By the way, this deep neural network algorithm does calculate the 3-variable "Smith score" and displays it for the physician.  It did not use machine learning for this task; it was programmed.

Learning Points:

1. It is hazardous to trust the computer, even when it interprets "Normal"
2. I never trust a computer interpretation.  I only look at it after I have read the ECG, and only in order to see if it found something that I overlooked.
3. If the computer says "normal", it takes very little time to confirm this with visualization (at least for me, and anyone can get good at it with practice)
4. Learn to recognize LAD occlusion.  It is not always obvious.  And the computer will not help you.

Here are some previous posts in which the computer interpreted the ECG as "normal."

Chest Pain Diagnosed as Gastroesophageal Reflux

Another case of arrest:

Another case of arrest:

It is easy to be led astray by the computer....

Wednesday, November 8, 2017

Anterior ST Elevation with Elevated Troponin, but with low T/ST ratio, 2 Cases

Case 1

This case was sent by Michael Masias (EMCurious, Twitter handle: @EMedCurious), an ultrasound fellow in the Department of Emergency Medicine at UC San Diego.

He sent this ECG with the following inquiry:  

"What do you think about this? 21 year old with chest pain. I am getting a result of "STEMI" by using the 3-variable formula, and "no STEMI" with the 4-variable."
Computerized QTc = 418

Here was my immediate answer:
"Tough one! There is a very low T/ST ratio. That is to say, the J-point is very elevated in V3 and V4 but without a tall T-wave. That is unusual for both early repol and LAD occlusion, and suggests myo- pericarditis. But I do think it is early repol.  I don't think it is STEMI. Tell me more."

I should also have added that tachycardia does not fit with anterior MI unless there is cardiogenic shock.

More Analysis:
There is ST Elevation in V2-V5 that meets "criteria" for anterior STEMI.
There is over 3 mm of STE (at J-point, relative to PQ jct.) in V3 and V4.
In a 21 year-old, only 2.5 mm in V2 and V3 is required, and only 1 mm in V4.
So there are 2 consecutive leads with STE that exceeds "critieria."

3-variable formula = 24.56 (above 23.4, indicating LAD occlusion)
4-variable formula = 12.96 (very low due to high QRS voltage in V2)
This formula is meant to help differentiate early repol from LAD occlusion.
It does not differentiate other etiologies of STE elevation!

The 4-variable formula is more accurate, but this is not validated.

More information:
"21 year old with 3 days of sharp left sided chest pain. He had a pharyngitis 1.5 weeks prior. He was transferred to me for STEMI but when he arrived he was very comfortable and the tachycardia didn’t fit, in my opinion. So I did a bedside echo and he was hyperdynamic with no signs of heart failure, and all walls looked good to me. I did speak with the interventionalist on call and they thought it was early repol."

Smith comment: this was a very astute evaluation. Anterior MI will not have hyperdynamic cardiac function with excellent ejection fraction!

We recorded another ECG 45 minutes later:
There is less ST elevation now.

"The first troponin I returned at 4 ng/mL. The patient remainded comfortable in the ED and cardiology just recommended observation so I admitted him for formal echo and serial troponins."

"The patient never underwent angiogram, but echo did not show a wall motion abnormality and this rules out STEMI."

Case 2

Medics came into the ED and showed me this prehospital ECG on a 40-something patient with chest pain:
My opinion was that this was normal ST Elevation, not LAD occlusion.

There is ST Elevation in V2-V5.  The STE meets STEMI criteria.
There are prominent J-waves in V4-V6
There is a saddleback in V2
Saddleback STE in V2 is rarely due to MI in my experience.
Computerized QTc was 414 ms.
I did the formulas and came up with values that were quite high, indicating LAD occlusion.

Why do I think it is not STEMI?
Because the ST elevation is more pronounced than the T-wave is hyperacute (low T/ST ratio).  The ST segment is either downsloping (saddleback) or almost flat.  This ST segment shape is a result of the relatively low T-wave voltage.  When a T-wave is tall and large (not this case), the ST segment by necessity slopes steeply upward to the tall T-wave.  When a T-wave has comparatively low voltage, as do these T-waves, the ST segment is relatively flat.

I went to talk with the patient.  He had been having a cough and fever for about a week, and had gone to a clinic for dyspnea 3 days prior.  The pain had been intermittent for the previous 3 days and there seemed to be some positional component to it, but he really could not describe it well and was holding his chest.

We recorded this ED ECG:
Approximately the same.

I was not convinced, even by my formulas.  We sent a troponin I, which returned quite elevated, at 4.80 ng/mL, within an hour of arrival.

That caught my attention, but I thought, due to the symptoms and the ECG, that this was probably myocarditis.

I repeated the ECG:
Not much different

I did a bedside echo and was worried for an anterior wall motion abnormality (WMA).

Unfortunately, this is common in myocarditis.  Absence of WMA would confirm myocarditis. Presence of WMA does not differentiate.

However, I was not willing to bet the patient's life on it.  I talked with the interventionalist and we arranged for the patient to go to the cath lab, but did not actually "activate" the cath lab as one would with a STEMI.

A repeat troponin was 4.9 ng/mL

The coronaries were clean.

Next day formal contrast echo was normal.

Diagnosis: myocarditis.

Next day, a friend at another hospital found a previous ECG on this patient:
The same kind of ST elevation was not present previously.
This shows that the findings were NOT due to early repol, but a consequence of myocarditis.

Monday, November 6, 2017

How can you persuade your cardiologist to take a Non-STEMI patient to the cath lab emergently?

This case was sent by Joseph Ryan (@DocJoseph08), chief resident from Corpus Christi's EM residency program.  

This middle-aged patient complained of acute chest pain and called 911.

He had the following 12-lead ECG in the ED at time zero:
There is ST depression diffusely.
This is diagnostic of ischemia.
There is a Q-wave in V2 and a possible hyperacute T-wave.
It is now clear the patient has acute coronary syndrome.
It is not clear that there is, or is not, a complete coronary occlusion.

The patient was treated with aspirin and sublingual NTG on arrival, which did not relieve his pain.

Cardiology was called but they were not interested in taking the patient to the cath lab.

First troponin I returned at 0.65 ng/mL.  This confirms myocardial infarction.

After that, another ECG was recorded one hour after the first one:
The ST depression appears a bit worse.
There is a touch of ST elevation in V2.

The patient had unrelieved pain, so again cardiology was called, but they stated that the case did not warrant emergent angiography, as it "did not meet STEMI criteria."  The resident pleaded with them to take him, but they would not.

He was given Plavix 600 mg, heparin with infusion, and a nitroglycerine infusion.  His pain continued.

2 hours later (3 hours after onset)
Now there is ST elevation in aVL, aVR, and more in V2 (but the T-wave is less hyperacute). 
The ST depression in more profound.
This is very concerning for proximal LAD occlusion.

17 minutes later
About the same

2 minutes later
About the same

6th ECG, only 4 minutes later
Increasing ST elevation in V1, V2, aVL and aVR, with worsening ST depression.

2nd Troponin I returns at 3.34 ng/mL.

At this point, the cardiologist was convinced and the patient went for PCI and had a 100% proximal LAD occlusion opened and stented, with an approximate 4 hour door to balloon time.

Here is the post PCI ECG:
Beginnings of Reperfusion T-waves in V2 and aVL.
These are identical to Wellens' waves, except that there is no R-wave in V2.

And one day later:
Evolution of T-wave inversion

Echo was performed right after cath lab and showed:
1.  Left ventricular systolic function is impaired.  Left ventricular ejection fraction is 40-45% with anteroapical akinesis. 
2.  Concentric left ventricular hypertrophy.
3.  Mild mitral insufficiency.

Peak Troponin I was over 50 (they do not quantify above that.)

Peak Troponin T was 4.50 (this correlates with a very large myocardial infarction)

Smith commentary:

Learning Points

1. The purported dichotomy between STEMI and Non STEMI is a false one.
2. Patients without ST elevation, or with ST elevation that does not meet diagnostic "criteria,"  may have total coronary occlusion and may have a lot of myocardium at risk, which may infarct without immediate treatment.  This patient had a very large anterior infarction but never, even after 3.5 hours, was there ST elevation that met diagnostic "criteria."
3. Both the American Heart Association/American College of Cardiology guidelines (1) and the European Society of Cardiology Guidelines (2) recommend less than 2 hour intervention on patients with refractory angina from ACS.  I have quoted those documents below.

Also: if you think that this represents Left Main occlusion, you are incorrect.  Read this post, which explains all: STE in aVR, with diffuse ST depression, does not represent left main occlusion 

Anecdotally, by my conversations and emails with people all over the world, this recommendation appears to be ignored by many cardiologists/interventionalists.  Why is it ignored?  One reason, I believe, is a misunderstanding of the results of randomized trials of emergent vs. delayed, angiography and PCI for NonSTEMI.  It is erroneously believed that these trials were negative.  However, patients with refractory pain were excluded from these trials.  In the largest such study, the TIMACS trial in NEJM (3), they found no difference between "immediate" and "delayed" angiography and PCI except for in patients with a high GRACE score of 140 or more.  But "immediate" was a mean of 16 hours, which is not immediate!  Furthermore, they excluded patients with ongoing chest pain; this exclusion was not stated in the methods.  But I know they excluded these patients because I emailed the first author, Dr. Mehta, and he replied that "I doubt investigators would have enrolled pts with ongoing CP in this NSTEACS trial."

Many readers of this blog, and providers who attend my ECG talks, ask me:

"How can I get my interventionalist to take these patients to the cath lab?"

My answer:

Tell them "Your own guidelines state that these patients with refractory pain should go within 2 hours."

The only caveat is that you must be certain that the symptoms, ECG findings, and elevated troponin are due to acute coronary syndrome, and not another etiology of type II MI, such as hypotension, tachy- or bradycardia, anemia, aortic stenosis, hypoxia, etc.

Guideline quotes


4.4.4. Early Invasive and Ischemia-Guided Strategies: Recommendations
Class I
1. An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures) (42, 44, 138, 338). (Level of Evidence: A)

European Society of Cardiology:
5.6.3 Timing of invasive strategy Immediate invasive strategy (less than 2 hours):
Very-high-risk NSTE-ACS patients (i.e. with at least one very-high-risk criterion: hemodynamic instability, Recurrent or ongoing chest pain refractory to medical treatment, life threatening arrhythmias or cardiac arrest, mechanical complications of MI, acute heart failure, recurrent dynamic ST-T wave changes, particularly with intermittent ST elevation) according to Table b) have been generally excluded from RCTs.  Owing to a poor short- and long-term prognosis if left untreated, an immediate (i.e. less than 2 h from hospital admission, analogous to STEMI management) invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings.


1.  Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). European heart journal 2016;37:267-315.

2. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:e344-426.

3. Mehta SR, Granger CB, Boden WE, et al. Early versus delayed invasive intervention in acute coronary syndromes. The New England journal of medicine 2009;360:2165-75.

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