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:
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 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)
17 minutes later
2 minutes later
6th ECG, only 4 minutes later
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:
And one day later:
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
Comment
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
References
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
Comment
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
ACC/AHA
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
5.6.3.1 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.
References
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.
Hello.
ReplyDeleteGreat post thanks
A question... Can we say that the leads v3 v4 v5 have de wellens waves suggesting LAD occlusion?
Thanks.
You mean de Winters, not de Wellens! de Winters waves look very similar to this and one could say they are an atypical version. Wellens waves are post-ischemic T-wave inversions, totally different!
DeleteI am an interventional cardiologist. Not documented, but I presume this was an off hour event. Any moron would look at the data and the ecg and know failure to cath would result in an adverse outcome. The only way to get the recalcitrant cardiologist out of bed, should she resist the call to do her duty, would be for the ER doc to tell her that he was going to document in the chart that she (the cardiologist)was practicing below the standard of care and would be held liable for any adverse event. This is a sleep deprived cardiologist case, not a difficult ECG/clinical case.
ReplyDeleteBruce, This is not an isolated case. Of course, off hours is no excuse I'm sure you would agree. 121 of 168 hours in the week are off hours. I communicate every week with at least one emergency physician who can't get his cardiologist to take a patient like this to the cath lab and the cardiologist believes that it is not indicated. That is one reason that 25% of acute total coronary occlusions do not get immediate cath and indeed do not get one until 24 hours. See this meta-analysis published a couple months ago: https://academic.oup.com/eurheartj/article/38/41/3082/4075374
DeleteWhat seems obvious to us is not obvious to everyone. Unfortunately.
Steve Smith
Dr. Smith:
ReplyDeleteDiffuse subendocardial ischemia often presents as diffuse STD most obvious at lateral leads (I, aVL, V5, V6). Could isoelectric J point at the lead aVL in the first ECG imply that it is about to elevate (since there should be STD at aVL during typical presentation of diffuse subendocardial ischemia)?
Allen Hsiao
Allen, the typical ST depression vector in diffuse subendocardial ischemia is towards the apex (II, V5). This makes for slight ST depression, or isoelectric ST segment, in aVL. That aVL is elevating shows that the ischemia in the high lateral wall is becoming transmural.
DeleteSteve Smith
Thank you for the clarification!
ReplyDeleteDr. Smith
ReplyDeleteOn EKG's 2 and 3, is there significant enough ST elevation (regardless of the de Winter's) to activate the cath lab for a 1st diagonal or LAD lesion?
ie
http://rebelem.com/five-ecg-patterns-you-must-know/
Jackson,
Deletewhat I'm trying to say is that, yes, activate the cath lab! But none of these meet "criteria."
Steve
Highly illustrative case by Dr. Smith. I believe the answer to the question, “How to persuade the Cardiologist to take this patient to cath?” — is that the ED physician has to INSIST that the cardiologist come in and evaluate the patient. Bruce Auerbach’s comment is on right on target. As per Bruce, the chart should document that the cardiology consultant REFUSED to see the patient … It should be obvious from the 1st ECG that a patient with new-onset severe chest pain is having an acute cardiac event — even though this 1st ECG is not yet diagnostic of acute coronary occlusion. The ECG 1 hour later shows dynamic ST-T wave change. This confirms acute evolution in a patient with unrelieved acute chest pain. A call in the middle of the night to the Chief-of-Staff might help “nudge” the on call cardiologist out of bed. This is not an easy situation for the ED physician — but patient care comes first. THANKS to Dr. Smith for his superb ongoing work in this area. By continuing to publish insightful cases such as this — the hope is that eventually this lesson will be learned by those who still refuse to see the light …
ReplyDeleteI'm an ED medical officer working in a hospital where cath lab is not available around the clock. In this center in such instance (this patient, presenting off hours), he would've received IV thrombolytic therapy. Moreover he presented within 3 hours of onset. Would IV thrombolytics be an acceptable standard of care when facing recalcitrant cardiologist? (no question if cath lab is not available)
ReplyDeleteYes, especially now the the ACC/AHA guidelines give the go ahead for STE in aVR. See 2013 guidelines.
DeleteBased in these serial ECGs, (prior to cath)would it be reasonable to say that this patient has diffuse subendocardial ischaemia that is probably secondary to left mainstem insuffiency ?
ReplyDeleteDiffuse subendocardial ischemia due to LAD occlusion! Not Left Main.
DeleteGreat information
ReplyDeleteWow, great post.
ReplyDelete