Thursday, June 28, 2018

If you had recorded an ECG during chest pain, what would it have shown?


A 40-something male presented to triage.  He had suffered a couple bouts of typical chest pain in the last 24 hours.   This ECG (ECG #3) was recorded immediately after the last episode of pain spontaneously resolved.  The pain had lasted about one hour.
There are classic Wellens' waves in V2-V5.
This is "terminal" T-wave inversion: the latter part of the T-wave turns down (inverts).
There are preserved R-waves in the involved leads (necessary to be called Wellens' waves)

There is no LVH in the involved leads.  This is important, as LVH can cause PseudoWellens' waves.

This Wellens' pattern with terminal T-wave inversion (in contrast to deep symmetric T-wave inversion) was called "Pattern A" by Wellens hinself in the original papers.
Wellens' original Papers:

(Some later authors ignored Wellens own classification of "Pattern A" and called this "Type" B!! -- let's go back to Wellens' own classification)
Here is an example of the misclassification:

This is Wellens' syndrome: Since the patient had anginal chest pain that is now resolved, it meets the criteria for Wellens' syndrome (criteria: resolved anginal chest pain, typical Wellens' waves in LAD distribution with preserved R-waves, absence of LVH which can cause pseudoWellens' waves).

See these posts for Wellens' mimics:

Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)

Anterior STEMI?

Is it Wellens' Syndrome?

Wellens' waves are NOT equivalent to Wellens' syndrome: Pseudo-Wellens' due to LVH and HTN

Case continued

Unlike many cases of Wellens' syndrome, this patient actually presented with active pain.  So you are going to get to see what the ECG would have shown had you recorded one during pain!

This was the first ECG (ECG #1) recorded during pain:
This shows ST elevation and hyperacute T-waves in the LAD distribution.
This is highly suspicious for acute LAD occlusion.
It even meets STEMI criteria: 

2.5 mm STE in V3, 2 mm STE in V4 (at the J-point, relative to the PQ junction)
If you calculate the 3- and 4-variable formulas, you can use these numbers:

STE60V3 (ST Elevation at 60 ms after the J-point in lead V3) = 3.5
QTc (computerized) =                                                                    418
QRSV2 (total QRS amplitude in V2) =                                            5
RAV4 (R-wave amplitude in V4) =                                                24

See subtleSTEMI app for iPhone for the formulas:

3-variable = 21.024 (this is low because of the very high R-wave amplitude in V4)

4-variable = 18.266 (We now know that this is a more accurate formula, and a value above 18.2 is very specific for LAD occlusion.)

This is the actual 4-variable formula:
0.052*QTc-B - 0.151*QRSV2 - 0.268*RV4 + 1.062*STE60V3.

Just today, an external validation of 3- and 4-variable formulas to Differentiate subtle LAD occlusion from normal Variant ST Elevation was just published online in the Annals of Noninvasive Electrocardiology:

This is a validation of these 2 papers by Smith:

This validation confirms that the 4-variable formula is very accurate and is better than the 3-variable formula!

Case continued

The patients pain resolved and another ECG (ECG #2) was recorded 18 minutes after the first:
All STE is resolved.

Then this ECG (ECG #3, again) was recorded another 17 minutes later when the patient was completely pain free (this is the Wellens ECG you saw at the top of the post):
This demonstrates how Wellens' waves manifest the aftermath of a reperfused STEMI

The cath lab was activated and a 95% hazy LAD lesion with thrombus and TIMI 3 flow (good flow) was found and stented.

Here is the first post-cath ECG (ECG #4).
Similar to the previous

This was recorded the next AM (ECG #5):
Now the Wellens' waves have evolved, as they always do (if it really is Wellens').
They are now deeper and almost symmetric.
These are "Pattern B" T-waves.

What Wellens did not describe, but what I have found to be true, is that Wellens' Pattern A are found soon after reperfusion, and that they always evolved into Pattern B waves.
Wellens did not have many serial ECGs to scrutinize.  He wouldn't have noticed this.
I have found it to be universally true.  

Evidence for Wellens as a reperfusion syndrome

To my knowledge, there is no research paper demonstrating this.  From my experience, I am confident that if it were formally studied, it would be born out.  

I believe that I was the first to represent Wellens as a reperfusion syndrome, in my book, The ECG in Acute MI, pages 22-23 and 51, and in chapter 27 on Reperfusion and Reocclusion.

My recognition of this was based papers by Wehrens and Doevendans on terminal T-wave inversion as a sign of reperfusion after use of thrombolytics.  Notice that both papers have Wellens as senior author, and it is very curious that he did not make the connection between his own syndrome and the identical ECG he described in these studies!

Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J. 2000 Mar;139(3):430-6. PubMed PMID: 10689257.

Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bär FW, Wellens HJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol. 1995 Jun 15;75(17):1206-10. PubMed PMID: 7778540.

More outcome 

Peak troponin I was 0.58 ng/mL

Echo the next day showed:
Regional wall motion abnormality-distal septum anterior and apex large.
Regional wall motion abnormality-anterior probable.

Ed Burns has a very nice complete summary of Wellens' syndrome here:

Comment by KEN GRAUER, MD (6/28/2018):
Highly insightful post with superb explanation by Dr. Smith, illustrating by sequential evolution over 5 serial tracings what Wellens’ Syndrome is, and what it is not. I found comparison of the first ECG in this blog post (TOP nn Figure-1  recorded immediately after the last episode of chest pain had spontaneously resolved) — with the initial ECG that was recorded duringchest pain (BOTTOM) to be especially interesting.

  • Is there a difference in frontal plane axis between the 2 tracings?
  • Is there a difference in QRS amplitude in the various leads between the 2 tracings?
  • Is there voltage for LVH in either (or both) tracings?
  • What might account for these differences? Why should we care?
Figure-1: TOP ECG — recorded immediately after CP resolved. BOTTOM ECG — recorded during initial episode of CP (See text for details).
  • The frontal plane axis has clearly shifted. In the TOP tracing — the axis is about -15 degrees (note the predominantly negative complex in aVF). In the BOTTOM tracing — the axis is about +40 degrees (clearly positive in aVF).
  • Voltage criteria for LVH is satisfied in the TOP tracing in lead aVL (ie, an R in aVL ≥12mm). However, this criterion is no longer satisfied in the limb leads for the BOTTOM tracing, in which the frontal plane axis is no longer negative. NOTE: As per Dr. Smith — diagnosis of Wellens Syndrome is not impeded in the TOP ECG, because LVH criteria are clearly not present in the chest leads where the Wellens ST-T wave changes are noted!
  • The zone of transition in the chest leads has also shifted. The R wave becomes predominantly positive only between leads V3-to-V4 in the TOP tracing — whereas transition occurs earlier (ie, already by lead V2) in the BOTTOM tracing. Along with this change in transition — QRS amplitude is markedly increased in the BOTTOM tracing. In fact, voltage criteria for LVH are satisfied in lead V6 (ie, R≥18mm in this lead).
Comment: The importance of attention to frontal plane axis, the area of transition, and relative QRS amplitude in various leads is often overlooked when comparing serial tracings. In this particular case — the astute conclusions highlighted by Dr. Smith (ie, Wellens Syndrome in the TOP tracing after CP resolved; Acute ST elevation in the BOTTOM tracing during CP) are not altered — but there are times when determining if there are or are not acute ST-T wave changes between serial tracings may be especially challenging IF differences in axis, transition zone and QRS amplitude are not noted.
  • Ensuring consistent chest lead electrode placement is essential for serial comparison of findings in leads V1-thru-V6. Large body habitus, chest wall abnormalities, varied electrode place (over vs under the breast) in women, are among some of the reasons why differences may be seen in transition zone and chest lead QRS amplitudes over serial tracings if attention is not focused on consistent electrode lead placement. Also relevant in this case as a potential cause for change in transition zone and chest lead QRS amplitude, is intermittent LAD occlusion with spontaneous reperfusion.
  • Often unappreciated is the fact that change in the incline of the patient’s bed may account for QRS axis shifts. How often are ECGs done on acute care patients who have difficulty lying in a completely flat bed? How you ever seen the angulation in degrees of the patient’s bed noted on the ECG when cardiograms are done on patients who are not completely flat? I have always suspected change in angulation of the bed over serial tracings to be one of the common causes of inferior lead Q waves that are sometimes seen one day and gone the next …

Tuesday, June 26, 2018

Palpitations and Chest Tightness: Should You Activate the Cath Lab (or Give Thrombolytics)?

This case was sent by Jessica Carmichael, and Emergency Physician  on active duty at Irwin Army Community Hospital in Fort Riley, Kansas.  She trained at Brooke Army Medical Center.

ECG and Case

I was sent this ECG with some information, but I looked only at the ECG before reading the text:

What do you think?

My response was this:

"I have not read the text of your email yet, but I would say that this is benign normal variant STE."

(There is also atrial fibrillation without a rapid ventricular response.)

"Now I will read your text:"

Here is the text:

"The following ECG was sent to me by a former resident yesterday and seems timely given your recent post [You Diagnose Pericarditis at your Peril (at the Patient's Peril!)]. The resident was berated by cardiology for activating the cath lab as he felt it was obviously pericarditis. I was concerned that there wasn't a truly discernible J or S wave in V3 [note: there is both a J-wave and an S-wave in V3, so there is NOT terminal QRS distortion]. Given that there is no acceptable miss rate for MI, I felt activating the cath lab was absolutely appropriate."

This was my response:

It is NOT pericarditis.  It is normal variant.
It is reasonable to activate. I would have instead done a contrast echo to prove no wall motion abnormality.

Comment: The very high QRS voltage, the very marked J-waves in many leads, and the short QT interval make this very unlikely to be LAD occlusion.  But it does meet STEMI "criteria" in multiple leads.

Here is the full history:

"Basics: 28 yo AA male who had a history of WPW who had sudden onset of heart palpitations and chest tightness 5/10 at rest. Had had ablation in 2016. No issues since. Presented with no other associated ROS, save for lightheadedness. Denies drug use, UDS neg. No family history.  Physically fit. Systolic BP 112. Sats normal.  Takes daily beta blocker. Denied recent illness, exertional chest pain or fever. No PE risk factors." 

"Found to be in new afib with multiple concerning EKGs.  Rate from 50s to 80s, irregular."

"Old EKG with early repol, but in my opinion new EKG much more drastic/changed." 

"Called a STEMI and discussed with cards who initally advised me of early repol findings. Requested they evaluate EKG. After, they remarked it looked like pericarditis, which I argued didn’t fit the clinical picture. He admitted the EKG was abnormal but was skeptical. Went ahead with our protocol for him to get heparin, TNKase, plavix, ASA and flew to outlying hospital." 

"Initial troponin about 1 hour after symptom onset was neg. CKMB was mildly elevated at 2.5 ish. CK 1300. After the pericarditis statement by cards, I added CRP and ESR after patient left, which came back negative.  Unfortunately, didn’t think to do a bedside echo before he left. "

"Cards texted me later and said he was fine, still in afib and that they felt his EKG was unchanged from old and consistent with early repol.  Cath lab deferred. Didn’t get report on if second troponin was done. "

Happy to get further follow up? I have about 4 EKGs from his brief stay in my ER as well as a one previous from his records. 

Found the recent blog post interesting in light of this case!
[You Diagnose Pericarditis at your Peril (at the Patient's Peril!)]

Jessica Carmichael, MD

Further analysis:

Dr. Carmichael performed 4 serial ECGs and they were all unchanged.   The QTc was between 385 ms and 402 ms.

Here is one of them:
No significant change
Notice the computer calls it pericarditis.
On other identical ECGs in the same series, the computer calls it ***STEMI***

What if we had used the 3- or 4-variable formulas?

STE60V3 = 4 mm
RAV4 = 33 mm
QTc = 400 ms
QRSV2 = 15 mm

3-Variable: = 17.62, which is far below the cutoff of 23.4
4-Variable: = 13.93, which is far below the cutoff of 18.2

The formulas would have predicted benign normal variant STE (early repol).


Angiogram was normal.
All trops negative.

By the way this is NOT pericarditis.

Learning Points:

1. It is never acceptable to berate another physician who is doing their best for the patient.  Obviously Dr. Carmichael was providing excellent care.

2. This ECG clearly meets STEMI "criteria" of 2.5 mm of STE in 2 consecutive right precordial leads, in addition to meeting STEMI criteria of 1 mm in lateral leads.

3.  There are features that can clue you in to benign ST Elevation: High voltage, profound J-waves, and short QT

4. Use the formulas.  They are very helpful.  (by the way, the formulas have now been externally validated in a large cohort; publication pending.  The 4-variable formula is now proven as the best!!)

5. One can avoid angiogram by performing a formal contrast echo.  Had Dr. Carmichael had access to one and been able to perform it, it would have shown no wall motion abnormality.  This would have ruled out LAD occlusion as the etiology of the STE, and she would have been able to avoid giving potentially harmful TNK-tPA.

Comment by KEN GRAUER, MD (6/26/2018):
Interesting case and write-up submitted by Dr. Jessica Carmichael — with excellent Comments by Dr. Smith. The concern was ST elevation felt to be significantly more than on a previous tracing. As a result, a STEMI was called. Cardiology initially favored acute pericarditis.
  • As per Dr. Smith — features suggesting this was not an acute OMI ( = Occlusion-related Myocardial Infarction) include the very high QRS voltage; the very marked J-waves in multiple leads; the short QTc — and extremely low values in Dr. Smith’s 3- and 4-variable formulas. That said, given ST elevation with new symptoms — diagnostic cath was reasonable. That said, given the above ECG features — obtaining an Echo during symptoms that failed to show wall motion abnormality could have avoided a cath ...
For the purpose of academic discussion — I’ll add the following thoughts:
  • The principal factor that prompted cath lab activation was concern that the ST elevation in Figure-1 was significantly increased from a prior ECG that showed early repolarization. Cardiology later thought there was no significant change between the 2 tracings. While impossible to comment on this comparison (since we are not given the prior ECG) — caveats to be aware of that may affect lead-to-lead comparison of serial tracings, are the need to make note of any change in: i) frontal plane axis; ii) in R wave progression; andiii) in QRS amplitude in the various leads. Change in any of these features complicates judgment about serial differences. Clearly, the amount of ST elevation seen in Figure-1 is marked (at least 4mm in lead V3). But QRS amplitude in leads V3-through-V6 is also dramatically increased (off the page in lead V4, and overlapping neighboring leads in V3, V4, V5). As a result, the amount of ST elevation relative to QRS amplitude in a given lead is proportionately not so excessive. Was QRS amplitude equally large as it is here on the prior tracing?
  • The History is KEY in this case. As per Dr. Carmichael — “sudden onset of heart palpitations and chest tightness at rest” is not a typical history for acute pericarditis. Often overlooked is awareness that new-onset arrhythmias (including faster SVT rhythms, as well as slow AFib) may present to the ED as chest discomfort. It would be interesting to know more about the nature of this patient’s chest pressure and palpitations — including whether both started at the same time, whether both were ongoing in the ED, and whether the patient was aware of when he had a regular vs irregular heart rate. Such historical information can sometimes prove invaluable in suggesting when chest discomfort might be the result an arrhythmia.
  • An additional ECG feature against the diagnosis of acute pericarditis is the finding in lead V2 of beginning T wave inversion at the same time that there is still significant ST elevation in this lead (BLUE arrows within the blue rectangle in Figure-1). With the typical evolution of acute pericarditis — ST segments first return to the baseline before T wave inversion occurs. In contrast — T wave inversion at the same time as there is ST elevation is common with acute infarction, and may be seen in some types of repolarization variants.
  • Additional ECG features against acute OMI — are how generalized the ST elevation is, and the lack of reciprocal ST-T wave depression. Granted, reciprocal ST depression is not always present with OMI — and it is possible to have OMI superimposed on a baseline tracing of early repolarization … This is the reason access to Echo in the ED at the time of symptoms is so valuable. In view of a predominance of ECG features in this case against OMI — the absence of a wall motion abnormality on Echo obtained during symptoms would essentially rule out OMI.
Figure-1: Initial ECG obtained in the ED on a 28-year old man with new symptoms (See text for details).
Final Thought: Is there group beating in Figure-1? This 28yo man has a history of WPW with prior ablation — but presumably was in sinus rhythm prior to the day of admission. He is now in AFib at a surprisingly low heart rate for new-onset of this arrhythmia. Is the dose of ß-blocker that he is on high enough to produce this much heart rate slowing with new AFib? Or could there be Wenckebach block out of the AV node, resulting in the similar short-long cycling for the first 5 beats in Figure-1 — with Wenckebach periodicity also seen toward the end of the rhythm strip (ie, progressively decreasing R-R intervals from beats #7-thru-10; and similar duration pauses between beats #2-3; 4-5; 6-7; 10-11 that are all less than twice the shortest R-R interval). 
  • Clearly, a longer period of monitoring is needed to know for sure — and the suggestion of group beating that we see could all be coincidence. But it IS worthwhile pointing out that recognition of group beating with atrial fibrillation or atrial flutter should suggest the possibility of Wenckebach conduction out of one or more levels within the AV node.

Sunday, June 24, 2018

Insulin Overdose: Does this ECG help to Guide your Management?

This patient with diabetes, but no other health problem, presented after a large insulin overdose.

What finding fits with insulin overdose?
And how does it help to manage the patient?

Answer:  There are down-up waves in several leads, especially V3.  The upright part is a U-wave, not a T-wave.  The diagnosis is hypokalemia.  K was confirmed low at 2.6 mEq/L.  The ECG finding may persuade you to partially correct the K in spite of the absence of total body K deficit.

Insulin, as you remember, lowers potassium by helping to "shift" postassium from the extracellular space (including intravascular) to the intracellular space.  We treat hyperkalemia with insulin and dextrose in order to lower the extracellular K.

But of course this does not change the total body K.  When the overdose resolves, all that intravascular K will again become extravascular.

So should we treat the hypokalemia with potassium?  Treating with potassium will increase total body K, and put the patient at risk for "potassium rebound" (hyperkalemia) when the overdose resolves.  (See the case below of a patient with Thyrotoxic Hypokalemic Periodic Paralysis who was treated with K supplementation and became severely hyperkalemic and died after the attack resolved).

But the presence of U-waves shows that this low K is having an effect on the heart.  Does this prove that the risk of dysrhythmia due to hypokalemia is higher than without hypokalemic ECG abnormalities?   I think so, but without hard evidence.

I can find very little data correlating the ECG with dysrhythmias in hypokalemia.  It is established as a truism that hypokalemia causes fatal ventricular dysrhythmias, and I don't seriously doubt it, but it is remarkable how little actual data there is.   I personally have treated several cases of fatal and non-fatal ventricular fibrillation in which the only apparent cause was hypokalemia.

I am not aware of any hard data correlating ECG findings of hypokalemia with dysrhythmias.  It is my belief that if the ECG has manifestations of hypokalemia, including ST depression, prolonged QT and U-waves, that the risk of dysrhythmias is higher.

Thus, it is my belief that these U-waves are a marker for dysrhythmias in this patient and one reason to supplement with potassium, in spite of the risk of K rebound.

In a patient with good renal function, one can generally use furosemide to aid in the renal excretion of excess potassium.  But that did not prevent the death of the patient described in the report below.

An interesting alternative to giving K in such patients is the use of beta blockade.  This may work for periodic paralysis, as the mechanism of action in thyrotoxic periodic paralysis involves beta agonist effects.  It probably would not have any siginificant effect in raising the K in a patient with insulin overdose.

In any case, one must be very careful with K supplementation when hypokalemia is a result of shift rather than a result of increased total body K.  I would not supplement if the ECG showed no evidence of hypoK, as I believe the risk of hypokalemic dysrthythmia would be small.

The patient was given supplementation with potassium and had a good outcome.

What are other causes of hypokalemia without a total body K deficit?
--Beta aderenergic agonists, including bronchodilators and epinephrine, result in potassium shift (and are thus also used for hyperkalemia).  Patients in out of hospital cardiac arrest frequently present with hypokalemia because of the prehospital epinephrine.
--Hypokalemic Periodic Paralysis.


The best evidence that I am aware of for dysrhythmias in hypokalemia:
Diuretics, serum and intracellular electrolyte levels, and ventricular arrhythmias in hypertensive men
Those whose diuretic therapy resulted in occasional K values less than 3.0 developed, on Holter Monitoring, "complex ventricular arrhythmias," including 7 episodes of VT, at twice the rate of the other patients.   

Fatal Dysrhythmia Following Potassium Replacement for Hypokalemic Periodic Paralysis.
--Treating with K led to rise in K from 1.5 to 10, and death of the patient
Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis. 
--more potassium supplementation led to faster recovery, but also to higher K levels after recovery
Pathophysiology of hypokalemia and Dysrhythmias
"Electrolyte Disorders and Arrhythmogenesis"

Etiology and symptoms of severe hypokalemia in emergency department patients

Comment by KEN GRAUER, MD (6/24/2018):
Nice illustration by Dr. Smith in this case on “the art of medicine” — in which he explains his rationale for how logical presumptions (albeit without hard evidence) can be applied to ECG interpretation for assistance in management of a patient with insulin overdose. I’d add the following points regarding this case.
  • In addition to the U waves — there are other ECG findings in this tracing that are consistent with hypokalemia. These are: i) ST segment flattening; andii) slight J-point ST depression. Both findings are present in multiple leads — which is consistent with the metabolic disturbance of hypokalemia.
  • In my experience, correlation of the ECG for the presence and severity of hypokalemia is less than perfect. That said, by the time U waves overtake underlying T waves (as is the case in this tracing) — the likelihood of hypokalemia is greatly enhanced.
  • Interpretation of the tracing shown in this case might be quite different if instead of a patient with diabetes “but no other health problem” — the history was from an older individual with increasing angina over the past few days. In this later case, the diffuse ST segment flattening with slight depression + ST elevation in lead aVR should prompt concern about ischemia with potentially significant underlying coronary disease. Serum electrolytes would clearly need to be checked — but even if serum K+ was low, one would still be left with the question of whether there might be superimposed coronary disease with recent ischemia. Clinical correlation, finding a baseline tracing on the patient, and follow-up tracings once serum K+ was corrected might be needed to sort things out.
  • This differential diagnosis is clearly of less concern in the current case in which the patient has no prior or recent history suggesting coronary disease. That said — serial tracings may still prove very helpful in guiding management. With K+ replacement — one would expect reduction in U wave amplitude, with restoration of clear definition between the end of the T wave and beginning of the U wave. ST segments should also normalize (or at least improve). Following the rational proposed in this case — reduction of ECG findings consistent with hypokalemia on follow-up may assist in signaling when to stop supplemental K+.

Friday, June 22, 2018

A 60-something year old man with chest pain and a wide QRS

Written by Pendell Meyers, with edits by Steve Smith

A man in his 60s with history of CAD s/p PCI, HTN, presented with chest pain which started while doing construction on his house several hours prior to arrival.

Here is his ECG on arrival at 2052:
What do you think? Should you activate the cath lab?

Yes, because there is an acute coronary occlusion causing OMI of the inferior wall. This is evident based on the LBBB with excessively discordant STE in leads II, III, and aVF, with reciprocal findings in I and aVL.

But the current guidelines do not use the modified Sgarbossa criteria, but rather the original Sgarbossa criteria. Because the STE in the inferior leads does not meet the 5mm threshold, it is negative by the original Sgarbossa criteria, as there is no concordant STE or STD.

The patient was given ASA and NTG drip with improvement but not full resolution of pain.

Initial troponin T was undetectable.

Troponin T at 2200 was 0.10 ng/dL (elevated).

Here is his repeat ECG several hours later at 0022:
There has been interval marked improvement of OMI findings, implying the artery has reperfused.

 Another repeat at 0248:
Still no signs of reocclusion.

Troponin T at 0306 was 0.80 ng/dL.

Troponin T at 0649 was 1.60 ng/dL.

The patient was admitted to cardiology for urgent cath.

1629: Cath shows an acute thrombotic ostial RCA in-stent restenosis culprit, 95% stenosed at the time of cath with TIMI 3 flow. Stent placed with good angiographic result. He also had a 70% chronic mid LAD stenosis, as well as 30% LCX.
Left main, LCX, and LAD, no large vessel occlusions.
LAD lesion described above.

RCA showing 95% ostial stenosis immediately after the tip of the catheter.

Another view showing the ostial RCA stenosis.

Intervention on ostial RCA lesion underway.

Post intervention with good angiographic result.

Troponin T peaked at 3.75 ng/mL the next morning (large MI). The characteristics of this lesion and the highly elevated troponin meet our definition of acute coronary occlusion surrogate criteria (when the angiogram is not performed at the time of the occlusion) used in the derivation and validation of the modified Sgarbossa criteria studies.

I looked back in the chart and found an almost identical presentation 4 years prior. He presented at that time with chest pain.

Presentation ECG at 2317:
Even more obviously positive for the modified Sgarbossa criteria with very excessive discordant STE in II, III, and aVF, with reciprocal findings in aVL and I. Notice how the original Sgarbossa criteria are falsely negative in this case both times.

Cath showed a 90% in stent thrombosis in the proximal RCA, described as "severely thrombotic." TIMI flow was increased from 2 to 3 after intervention.

Findings resolving.

Ongoing resolution with a hint of terminal T wave inversion in the inferior leads.

Serial Troponin T rose from undetectable to 3.63 ng/dL over the course of about 16 hours.

Learning Points: 

Use the modified Sgarbossa criteria to look for OMI in LBBB. The modified criteria are more sensitive than the original criteria as evidenced by cases like this.

Just because there is not complete occlusion at the time of cath does not mean there wasn't complete occlusion at the time of the ECG prior to cath. This is why we have criteria for OMI when the angiogram is not performed at the same time as the ECG evidence of occlusion. Finally, complete transmural ischemia (what happens when there is OMI without collateral circulation) does not even require complete occlusion. A near-occlusion with TIMI 1 flow without collateral circulation may result in similar amount and speed of myocardial loss, and therefore similar benefit of immediate reperfusion therapy until proven otherwise.

Unlike most diagnostic tests, the modified Sgarbossa criteria are also more specific than the unweighted Sgarbossa criteria.  It is unusual to find a test that is both more sensitive and specific than the original test, but this is one.  

Here is the table from the validation cohort:
Compare lines 1 and 4
Comment by KEN GRAUER, MD (6/23/2018):
Highly insightful case by Drs. Meyers & Smith regarding the clinical utility of Modified Smith-Sgarbossa Criteria for diagnosis acute OMI in the setting of LBBB. Details in the paper by Dr. Smith et al on use of these modified criteria is found under the Rules + Equations Tab on this blog. I will play “Devil’s Advocate", and offer the following points:
  • As emphasized by Dr. Meyers — Use of the Modified Smith-Sgarbossa Criteria are clearly diagnostic in this case!
  • Another way to arrive at the same conclusion that the 1st ECG (@ 20:52) is diagnostic of acute OMI is qualitative — by recognizing the presence of ST segment elevation in leads in which it just should not be there. This is seen in all 3 inferior leads in ECG #1 (Figure-1). Support that this ST elevation is acute is provided by the presence of “mirror-image” reciprocal ST-T wave changes in lead aVL.
  • IF any doubt existed about the acuity of the initial ECG — lead-to-lead comparison with the 2nd ECG that was done (@ 00:22) should have clarified the picture. While slight-but-definite differences in QRS morphology make interpretation of ST-T wave changes challenging for the chest leads in the 2 tracings shown in Figure-1 — there is unmistakable reduction in inferior lead ST elevation, and in high lateral lead (ie, leads I, aVL) reduction in reciprocal changes. Given associated reduction in chest pain — the clinical picture of OMI with spontaneous reperfusion is irrefutable with this 2nd ECG done at 00:22.
Figure-1: Simultaneous view of the 1st 2 ECGs in this case to facilitate lead-to-lead comparison and appreciation of qualitative ST-T wave changes.
My purpose in posting the first 2 ECGs recorded together in Figure-1, is that this combination tells a story. For those clinicians not yet as comfortable with qualitative ST-T wave assessment — a picture is worth 1,000 words.
  • Although correctly classified as LBBB — ECG #1 is an atypical form of LBBB because: i) there is excessive fragmenting; ii) there is no predominant upright R wave in any of the lateral leads; and iii) the initial Q waves seen in the inferior leads are not “normal” for LBBB in view of the positive, then negative deflections that follow (ie, a qrS is not a “normal” inferior lead morphology with simple LBBB). In this context — there is inferior ST elevation that should not be there in each of the 3 inferior leads in ECG #1.
  • Perhaps the most markedly abnormal-appearing ST-T wave in ECG #1 is seen in lead I. Despite the artifact and tiny overall QRS complex in this lead — the depressed and straightened ST segment “shelf”, that then rises to a disproportionately tall and peaked terminal T wave has to be assumed acute until you prove otherwise.
We often learn the most from challenging cases that do not go the way we might optimally want them to go. Soul-searching is tough work. Armchair quarterbacking the next day is far easier. Our THANKS to Drs. Meyers and Smith for this highly insightful and instructive case, in which the cath lab should have been activated after ECG #1 (@ 20:52) — and if for any reason not then — then after ECG #2. In the “retrospectoscope” — a 2nd tracing would have been ordered before 00:22. Finally, appreciation of qualitative ST-T wave changes can facilitate optimal application of modified Smith-Sgarbossa Criteria.

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