Saturday, August 17, 2019

Acute Chest pain in a 50-something, and a "Normal" ECG

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent this case

A 50-something man presented with acute chest pain.

Here is his ECG:
As you can see, the computer called it completely normal
What do you think?


















The computer did not even mention the ST elevation.  It could at least say: "ST Elevation, consistent with normal variant," or "consistent with ischemia or normal variant," or "consistent with early repolarization."  But it simply says "normal."

An interpretation of "normal" could, of course, deceive many providers.

Analysis

This could be normal variant ST Elevation in V2 and V3.  There is 1.5 mm STE in at the J-point in lead V2 (relative to QRS onset, otherwise known as PQ junction).  There is 1.0 mm in V3.

So this is a normal amount of STE in V2 and V3, defined by Universal Definition of MI as up to 2.0 mm in men over age 40.  So there is definitely no STEMI, and the STE is normal.  So the computer is correct in calling it normal.

But after reading this blog, you all know that most OMI do NOT meet STEMI criteria.  Some patient's baseline ECG has zero STE.  Some patient's baseline has normal variant STE.  You don't know which kind of patient this is.

Some normal STE is actually due to OMI.  Some normal STE is not due to ischemia at all.

It is your responsibility to determine if STE is ischemic or not.

How do we do so?

Use the formula.

QTc = 385
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18

Formula value = 19.94 (very high, indicating LAD occlusion).

Any value greater than 18.2 is likely to be LAD occlusion.

For graphs of sensitivity, specificity, and accuracy at various cutoffs, see this post:

More precise interpretation of the results of the 4-variable formula.


12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


Chris Mondie's note:

"My read: Acute proximal LAD occlusion. Hyperacute T waves which tower above the preceding R waves, poor precordial R wave progression. Large T in V1.  Smith subtle LAD equation indicative of acute LAD occlusion. 

"Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI. 

"Cardiology agreed to take the pt to the lab but thought it would likely be negative. 

"100% proximal LAD successfully stented. 
Defibrillated out of v fib in the cath lab. 
Initial TnI was negative. 

"I thank you for constantly updating your blog and allowing free open access education on EKG interpretation. I recognized this as a STEMI immediately and I was only able to do so solely because of your blog."


===================================
Comment by KEN GRAUER, MD (8/18/2019):
===================================
Our thanks to Dr. Chris Mondie for providing this case. Credit to him for performing stat Echo in the ED — which, with the finding of anteroseptal wall motion abnormality immediately confirmed the need for prompt cath, even before a 2nd tracing was done.
  • For clarity — I’ve labeled a number of KEY findings in the initial ECG performed in the ED ( = ECG #1 in Figure-1).
Figure-1: The initial ECG done in the ED (See text).



MTHOUGHTS on ECG #1: This is not a normal tracing. The remarkable ECG findings are multiple:
  • There are small-but-definite Q waves in each of the inferior leads (RED arrows). These Q waves in leads III and aVF are surprisingly wide — and to me are suggestive of inferior infarction at some point in time (possibly acute).
  • It is difficult to assess ST-T waves in the inferior leads — because we only have 2 QRST complexes in each lead — and, there is baseline wander in lead aVF obvious artifact with a different appearance of the ST-T wave for each of the 2 beats in leads II, III and aVF. IF clarification of these findings was important (as to whether something acute was ongoing in the inferior leads) — I would immediately repeat this ECG. That’s because despite lack of reciprocal ST-T wave changes in lead aVL — it looks like there may be slight-but-real ST elevation with slightly fatter-than-they-should-be T waves (probably hyperacute) in each of the 3 inferior leads (Compare the elevated J-point to the horizontal RED baseline in each of these leads).
That said, there is NO urgency for clarifying what is going on in the inferior leads — because clear indication for immediate cath is already forthcoming solely from the appearance of the chest leads in this patient with new-onset worrisome chest pain. Among the remarkable chest lead ECG findings include:
  • As per Dr. Mondie — the T waves in leads Vand especially in V“tower over” the respective R waves in these leads. These are hyperacute waves.
  • Whereas the base of these T waves in leads V2 and V3 does not seem all that wide — the base of the overly tall T wave (compared to its respective R wave) in lead Vis wide. So, until proven otherwise — we need to assume hyperacute waves in at least leads V2-thru-V4.
  • There are Q waves in leads V4, V5 and V6 (RED arrows in these leads). Although these lateral chest lead Q waves are not that deep — the do appear to be wider-than-expected for “septal Q waves”.
  • Two other reasons to suspect that these are not “normal septal Q waves” in leads V4-thru-V6 are: iAlthough normal septal Q waves may occasionally be seen in lead V4 — they are generally not as large in lead V4 as the septal Q waves in leads V5 and V6. However, the Q wave that we see in lead V4 of ECG #1 IS equally large and wide as the Q waves in V5 and V6. This most probably is not normal; andiiInstead of the usual progressive increase in R wave amplitude as we move from lead V2-to-V3 — there is slight decrease in R wave amplitude. While I can’t rule out lead placement as the reason for this slight decrease in lead V3 R wave amplitude — the finding of a larger-than-expected Q wave in neighboring lead V4 makes me suspect that this is a real phenomenon related to ongoing anterior OMI.
  • There appears to be slight-but-real ST elevation in leads V4 and V5 (I’m uncertain about V6). The amount of ST elevation in lead V4 (even if it doesn’t satisfy stemi criteria) looks more than what I’d normally expect in this lead (Compare the elevated J-point to the horizontal RED baseline in these 2 leads).
  • Of the 2 QRST complexes that we see in lead V1 — the T wave of the 1st complex is taller-than-normally-expected for an upright T wave in lead V1 (V1 usually does not have tall T waves). Once again, due to technical issues — we do not know which of the 2 QRST complexes that we see in lead V1 is accurate ...
BOTTOM LINE: Some of the above abnormalities I mention are subtle. Individually — they probably would not mean much. BUT:
  • In a patient with new-onset worrisome chest pain — the potentially hyperacute T waves in leads V2V3 and V4 should be more-than-enough to merit prompt cath.
  • Once determined that stat Echo shows an anterior wall motion abnormality — the diagnosis of acute ongoing OMI is confirmed!
  • The possibility of something acute ongoing in the inferior leads is real. Support for the likelihood of acute ECG changes is then strengthened by identifying the additional subtle ECG abnormalities that I describe above in other leads on this tracing.

Once again — our THANKS to Dr. Chris Mondie for presenting this case!



Thursday, August 15, 2019

5 Cardiologists said this is not a STEMI. But was it an OMI?

Written by Pendell Meyers

A male in his early 50s presented with waxing and waning chest pain starting at rest. He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS.

Here is his initial ECG:
What do you think?














Sinus rhythm
-STE in V1-V5, possibly a tiny amount in V6, and small amount in I and aVL, and II
-Reciprocal STD (although perhaps isoelectric at J point, immediate STD after the J point) with very ischemic appearance in lead III (down-up T-wave is strongtly suggestive)
-Large T-waves in V2-V4, which may be either a normal variant or hyperacute
-Very tiny Q wave in lead V2, as well as V6, I, and aVL, which is not seen in normal variant
-STEMI criteria are not formally met; although V2 has sufficient STE (greater than 2.0 mm), neither of it's neighbors have enough STE to meet criteria (V1 is close at 0.5 mm of the "required" 1.0 mm)


This is all highly diagnostic of acute anterior MI, with the most likely etiology being OMI of the proximal-mid LAD.

The formulas would be formally contraindicated because of the Q-wave in V2, but if we use them anyway the results are (using QTc 397 ms):


4 Variable formula: 20.32
3 Variable formula: 24.08

Both formulas predict LAD occlusion.





The physician called the on-call cardiologist immediately to discuss this ECG, but the cardiologist reportedly said not to activate the cath lab because he/she was not convinced by the ECG. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI."


The first troponin I returned elevated at 0.11 ng/mL.

Serial ECGs were obtained, including this one several hours later:
Slightly more STE and longer QT than prior.



Although I do not see much difference between the ECGs, for some reason (perhaps ongoing pain or rising troponins) the case was reevaluated at this time and the decision was made to perform cath.

They found 100% acute mid-LAD Occlusion MI, stented with excellent angiographic result.


Peak troponin I was greater than 75 ng/mL (the assay does not measure higher than this apparently).





Learning Points:

STEMI criteria misses 25-40% of OMI, like this case for example.

Due to our paradigm which lags far behind the current achievable skill level, cases like this will continue to be missed or delayed until we solve the problem by replacing the paradigm.

This is another case demonstrating OMI with all ST segments concave.

Pay attention to even the tiniest Q-waves in the right context and assume they are new until proven otherwise. New Q-waves during MI are NOT wide ("greater than 40 ms") until later.

Any Q-wave in V2 in the presence of an otherwise normal QRS complex is abnormal.

Repeat ECGs are almost always helpful.

Use of the formulas would have improved recognition of this OMI.

Ongoing ischemia (by symptoms, ECG, or troponin) despite maximal medical management is an indication for emergent cath lab activation.


===================================
Comment by KEN GRAUER, MD (8/15/2019):
===================================
Once again, the wrong question was asked in this case. That's because it should not matter IF the initial ECG in this case ( = ECG #1 in Figure-1) represents an acute STEMI or an acute OMI — since initial management should be the SAME:
  • Considering that this patient had multiple cardiac risk factors good story for ongoing new ischemic-sounding chest pain and, the ECG abnormalities seen in ECG #1 — prompt cath to define the anatomy, with goal of acute reperfusion if acute OMI is confirmed is the treatment of choice.
  • Unless a prior ECG on this patient can be found that shows identical findings as we see in ECG #1 — there is NO way to rule out acute OMI. As a result — it’s hard to justify not doing acute cath ...
Figure-1: The 2 ECGs in this case (See text).



MTHOUGHTS on ECG #1: Dr. Meyers has skillfully detailed the abnormal ECG findings. To facilitate visualization — I’ve put both tracings together and labeled the following key points:
  • There is loss of the initial r wave in lead V1 — with development of a small-but-real Q wave in lead Vof ECG #1. Overall QRS morphology in lead V2 is strange, with this qRS complex being “sandwiched in” between an rS complex in lead V1, and an rS complex in lead V3 — so there may be some lead misplacement of lead V2. That said — the small q in V2 is almost certainly a real finding, and clearly abnormal.
  • There is more than 2 mm of ST elevation in lead Vof ECG #1 (Compare the RED horizontal baseline with the RED arrow in this lead). The very wide T wave base, with T wave peak clearly exceeding R wave amplitude in this lead clearly defines the T waves in V2 as being hyperacute.
  • Disproportionate T wave amplitude (compared to R wave height) in leads V3 and V4 define those T waves as also being hyperacute.
  • Note that there is more ST elevation in lead V4 of ECG #1, than there is in lead V3 (Compare the RED horizontal baseline with the RED arrow in these leads). There shouldn’t be more ST elevation in V4 than in V3.
  • Finally (as per Dr. Meyers) — the ST-T wave in lead III is clearly abnormal (curved RED line) — with the scooped ST segment ending in a biphasic (negative-then-positive) T wave.
BOTTOM LINE: Without an identical-looking prior tracing — there is NO way to rule out the possibility (if not probability) of acute ST-T wave findings in at least leads V2-thru-V4 Q in V2 reciprocal change in lead III, in this patient with new chest pain. A millimeter definition of acute STEMI should not be needed to justify the need for prompt cardiac catheterization.
  • NOTE: With proximal LAD OMI — one typically sees: isignificant ST elevation beginning in leads V1,V2; iireciprocal ST depression in each of the 3 inferior leads (II,III,aVF); andiiisignificant ST elevation in lead aVL. Because we only partially see these features in ECG #1 — I would interpret this tracing exactly as Dr. Meyers did = probable “proximal-mid acute LAD occlusion”.

MTHOUGHTS on ECG #2: Several hours later — ECG #2 was obtained. As per Dr. Meyers — for the most part, there has been little change between the 2 tracings. That said:
  • I think there is now more ST elevation in lead Vof ECG #2 than there was in ECG #1 (Compare the BLUE horizontal baseline with the BLUE arrow in this lead).
  • Note that there is once again more ST elevation in lead V4 than in lead V3 of ECG #2. This is not a normal finding.
BOTTOM LINE: Given the clinical history — ECG #2 should not have been needed for making the decision to take this patient to the cath lab ...

Our THANKS to Dr. Meyers for this insightful case!




Tuesday, August 13, 2019

The ECG was correct. The angiogram was not.

This was sent by Cam Mosley and Michael Truax, LSU-Baton Rouge Residency.


74 yo male with previous MI years ago presented with chest pain and nausea.

An ECG was recorded:
Sinus rhythm with PVCs.
What else?
















My interpretation (and theirs: they activated the cath lab): 

It is clearly a subtle proximal LAD occlusion (OMI).  

Why?
-- Subtle STE in I, aVL, V2
-- Hyperacute T-waves in aVL, V2, V3
-- Q-wave in V2, which is always abnormal
-- reciprocal ST depression in III, aVF.  Thus, the STE in V2 cannot be normal.

Here is the outcome he sent:

Cath negative other than 40% LAD stenosis.
They looked at aorta too and it was ok.
Initial troponin = 0.02 ng/mL (ref up to 0.030).

Here is my response:

"What did subsequent ECGs show?  Same?  Or resolution?  That is the key.  LAD can be briefly occluded with negative trops and no thrombus seen (the thrombus lyses).  But if this is the case, then the ECG will resolve. If the ECG is the same, then it is truly a false positive.  If the ECG resolves, then it was indeed what it looks like: LAD occlusion, though brief (transient)."

So he sent the post cath ECG:
Indeed, the ECG confirms reperfusion, with resolution of ST in I, aVL and V2, terminal T-wave inversion in aVL, full inversion in V2, and resolution of hyperacute T-waves.
























As you can see, the angiogram is not the final arbiter of acute coronary syndrome.  Angiograms sometimes show no evidence of ACS.  The thrombus lyses and may not leave behind any visible culprit lesion.  Although unusual, it is not rare.

In this study, approximately 10% of Transient STEMI had no culprit found:

Early or late intervention in patients with transient ST‐segment elevation acute coronary syndrome: Subgroup analysis of the ELISA‐3 trial


One must use all available data, including the ECG, to determine what happened.

Final Diagnosis?

If the troponin remained under the 99% reference, then it would be unstable angina.  If it rose above that level before falling, it would be acute myocardial injury due to ischemia, which is, by definition, acute MI.  If that is a result of plaque rupture, then it is a type I MI.  The clinical presentation would be one of either unstable angina or type I MI, even if no culprit was found on angiography.


See this post for another case of OMI with a negative angiogram, and here are more references:


Inferior hyperacute T-waves and ST elevation. Angiogram is normal. What happened?



Bibliography, with edited abstracts


There were 821 cath lab activations and 86% were treated by mechanical revascularization. In 76 patients (8.5%), no coronary artery stenosis was documented. Observations documented angiographically included coronary spasms (6.6%) and muscle bridges (5.3%). During a mean follow-up of 11.2±6.4 months, one patient developed an acute myocardial infarction requiring coronary intervention. All other patients were free of any cardiac event.


Article 2, full text


Of 898 patients who had cath lab activations for primary PCI, normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken.   None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain.



Characteristics of 690 consecutive patients with presumed STEMI referred for primary PCI.  87 (13%) had angiographically normal coronary arteries and were compared with patients with angiographically shown culprit lesions (control group; n = 594). Nine patients with significant coronary disease, but no identifiable culprit lesion, were excluded. Electrocardiograms (ECGs) from both groups were reviewed by 2 cardiologists blinded to angiographic findings.  On expert review of ECGs, 55% of patients in the normal coronaries group had ST-elevation criteria for STEMI (vs 93% in the control group, but the ECG was considered consistent with a diagnosis of STEMI by both observers in only 33% (vs 92% in the control group)   Left branch bundle block independently correlated with normal coronary arteries on multivariate analysis (odds ratio for STEMI 0.016).   The discharge diagnosis in the normal coronaries group was predominantly pericarditis (n = 72; 83%), but these were not adjudicated by the authors.  Other diagnoses were myocarditis in 3 patients (3%), Takotsubo cardiomyopathy in 2 patients (2%), presumed coronary spasm secondary to intravenous drug abuse in 2 patients (2%), cryptogenic AMI in 1 patient (1%), dilated cardiomyopathy in 1 patient (1%), massive pulmonary embolus in 1 patient (1%), cholelithiasis in 1 patient (1%), and pneumonia in 1 patient (1%).

The most likely alternative diagnosis suggested by both observers for the non-AMI ECGs in the normal coronaries group was normal variant ST changes (25% observer 1 and 26% observer 2) and early repolarization abnormality (25% observer 1 and 14% observer 2). 




The medical records of 941 patients undergoing coronary arteriography for presumed ACS within 48 h of onset were critically reviewed. In 70 patients (7.4%, 35 males) no CAD was documented. Alternative substrates of acute myocardial ischemia included coronary artery anomalies (7 patients, 10%), coronary spasm (10 patients, 14.3%), spontaneous coronary dissection (2 patients, 2.8%), paradoxical embolism through a patent foramen ovale (4 patients, 5.7%), embolism from left atrium or calcified aortic valve (4 patients, 5.7%), imbalance between oxygen demand and supply (20 patients, 28.5%), mitral valve prolapse (11 patients, 15.7%). No alternative substrates were found in 12 patients (17.1%). Absence of CAD is an uncommon finding in patients undergoing coronary artery angiography for ACS.


===================================
Comment by KEN GRAUER, MD (8/13/2019):
===================================
Superb case by Dr. Smith — for which the title tells all: “The ECG was correct; the angiogram was not”. As per Dr. Smith, there should be little doubt that in the setting of new-onset chest pain for this 74yo man with prior history of coronary disease — that the initial ECG ( = ECG #1 in Figure-1) represents acute OMI due to proximal LAD occlusion.
  • For clarity — I’ve taken out the long lead II rhythm strips, and have placed the initial ECG and post-cath tracing next to each other in Figure-1. I have done this because lead-to-lead comparison of these 2 tracings CONFIRMS each of my statements below.
  • I would add the following to the excellent discussion by Dr. Smith ...
Figure-1: The 2 ECGs in this case (See text).



MTHOUGHTS: Dr. Smith has noted abnormalities in 6 leads in the initial ECG ( = ECG #1). In my opinion — there are 11 (out of 12) leads in ECG #1 that are definitely abnormal the abnormal rhythm — which taken together, are diagnostic until proven otherwise of acute OMI.
  • There are 3 late-cycle (end-diastolicPVCs in ECG #1 (in simultaneously-recorded leads I,II,III; aVR,aVL,aVF; and V1,V2,V3).
  • Clinically, the finding of late-cycle PVCs (ie, PVCs that occur relatively later in the R-R interval— is of comparable diagnostic significance as the onset of AIVR, which is so commonly seen when there is reperfusion of the “culprit artery”. Retrospectively — we see that this is exactly what happened! That is, the acute abnormalities in ECG #1 have in large part resolved in ECG #2 due to spontaneous reperfusion of the “culprit artery” — which was heralded by development of these late-cycle PVCs!
  • As per Dr. Smith — Lead Vin ECG #1 is clearly abnormal because of: ithe Q wave that should not be present in lead V2, especially since there appears to be a tiny-but-present initial r wave in lead V1; iislight ST elevation of abnormal shape in lead V2; andiiithe hyperacute T wave in lead V2. That said — I suspect there is slight misplacement of the lead V2 electrode in ECG #1 — because it just doesn’t make physiologic sense to “sneak in” a qRs complex in V2, that falls in between the rS complex in V1 and the rS complex in lead V3. That said, regardless of slight lead misplacement of V2 in ECG #1 — the above-stated abnormalities are almost certainly still valid! NOTE: A much more logical sequence of R wave progression is seen in leads V1,V2,V3 in ECG #2 — which I believe supports my suspicion that there was some lead misplacement of lead V2 in ECG #1.
  • Considering the slight ST elevation and/or hyperacute T waves noted by Dr. Smith in leads I, aVL; V2, V3 — I thought that hyperacute waves were also present in leads V1 and V4-thru-V6. Normally, one should not see the 0.5 mm of ST elevation with frank upright T wave in lead V1. And — Aren’t the T wave peaks in leads V4, V5 and V6 broader (fatter) than they should be? NOTE: Confirmation that leads V1 and V4-thru-V6 clearly show acute changes in ECG #1 is forthcoming from lead-to-lead comparison with ST-T wave appearance of these same leads in ECG #2!
  • Finally — not only leads III and aVF — but also the 3rd inferior lead ( = lead II) show acute reciprocal changes in ECG #1. While the ST segment is not depressed in lead II of ECG #1 — the straightening of this ST segment in lead II, with abrupt angling to mark onset of T wave upslope in this lead is clearly abnormal, and consistent with acute change. NOTE:  Confirmation that ST-T wave appearance in lead II of ECG #1 clearly indicates acute change is evident from near normalization of the ST segment in this lead in ECG #2.
BOTTOM LINE: Dr. Smith makes the superb point in this case that, “The ECG was correct; the angiogram was not”.  As per Dr. Smith — skillful assessment of the post-cath ECG in context with the clinical history in this case tells us there almost certainly was transient proximal LAD occlusion despite the finding of no more than 40% narrowing of the LAD on cath. The main points embedded in my discussion above are:
  • The finding of late-cycle PVCs that then resolve as chest pain and hyperacute ECG changes resolve is further evidence supporting spontaneous reperfusion of a coronary artery that was transiently occluded.
  • The more leads you can identify that show abnormal acute changes — the more confirmation you have that an acute cardiac event is ongoing. Not all leads in ECG #1 show the same degree of acute abnormality. But when 11 out of 12 leads show what looks to be acute ECG changes in an older adult with new-onset chest pain — the inescapable conclusion is of an acutely evolving cardiac event.
  • The BEST way to hone your ECG interpretation skills is to BE SURE to look at follow-up tracings! While it might be easy to overlook the acute abnormalities in leads II; V1; and V4-thru-V6 — it is much easier to appreciate that these leads were abnormal in ECG #1, when you compare how different the ST-T wave appearance of these same leads is in ECG #2.
Our THANKS to Dr. Smith for this interesting case!



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