Tuesday, December 6, 2022

65 year old with syncope and a 'normal' ECG: discharge home?

A 65 year old with diabetes presented with a syncopal episode while sitting, associated with weakness but no chest pain or shortness of breath. Vital signs were normal and first ECG was labeled as normal by the computer and confirmed by the treating emergency physician and  cardiology over-read. What do you think?







 

There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression, and normal voltages with J waves from early repolarization. There's inferior down-up ST segments and hyperacute T waves, with reciprocal up-down T wave in aVL.

 

I sent this "normal" ECG without any information to a number of ECG enthusiasts, who were all concerned about possible OMI - whether subtle high lateral OMI with inferior reciprocal change, or subtle inferior OMI with high lateral reciprocal change.

 

First troponin I came back at 2,800 ng/L (normal <16 in females and <26 in males), and a repeat ECG was done:

 


 


There’s wandering baseline that makes it difficult to interpret, but there's no longer inferior ST depression and T waves are smaller. There is residual minimal ST elevation from early repolarization.

 

Because of the syncope and troponin elevation the patient was referred to cardiology as cardiac syncope. Repeat troponin declined to 2,500 and repeat ECG ECG was done after another 2 hours, also interpreted as normal. Repeat trop declined to 2,500, and another ECG was done:




Similar to prior. The cardiologists were concerned the second ECG might have shows subtle inferior ST elevation indicative, which could be associated with RCA occlusion that could have produced heart block leading to syncope. So they took the patient urgently to cath: 100% occlusion of inferior obtuse marginal branch of the circumflex, with collateral circulation. Had the cardiologists followed NSTEMI or transient STEMI guidelines, which recommend non-urgent cath, the patient could have redeveloped an OMI and had a worse outcome.

 

But this foresight will not be recorded, because the patient was diagnosed as "transient STEMI", even though no ECG ever met STEMI criteria. In fact the only ST elevation was baseline elevation from early repolarization, and relative to that the patient only had ST depression and hyperacute T waves. So this was transient STEMI(-)OMI, not transient STEMI.


Discharge ECG had small inferior T waves and subtle reperfusion TWI in V5-6 

 



Here's a comparison of initial and discharge ECGs:



This confirms the initial ECG had inferior ST depression followed by hyperacute T waves (deWinter), and also lateral hyperacute T waves V4-6. On discharge the inferior deWinter waves resolved and the lateral T waves deflated and inverted.



Take home

1.  Syncope is an uncommon presentation of ACS, but anginal equivalents are more likely in older patients with diabetes

2.  Circumflex occlusions can have subtle to no ECG changes

3.  You can’t trust ECG's labeled "normal"

4.  Hyperacute T waves and reciprocal change can help identify STEMI(-)OMI

5.  Arteries can be totally occluded with flow intermittently maintained by collaterals

6.  deWinter waves can happen in any coronary artery: see this case and this case










==================================
Comment by KEN GRAUER, MD (11/29/2022):
==================================
Important case for discussion by Dr. McLaren — in that today's patient had a definite MI but no chest pain. Instead — the sole symptom was syncope associated with weakness.
  • Infarction was diagnosed in today's case by the findings of i) Significantly elevated Troponin; ii) 100% occlusion of the inferior obtuse marginal branch of the LCx, albeit with collateral circulation; andiii) Subtle ECG changes on serial tracings, including suggestion of reperfusion T waves.

PEARL #1: Not all patients with acute MI report chest pain. The Framingham studies from many years ago taught us that the incidence of Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

  • The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
  • In the other half of this 30% (ie, in ~15% of all patients with MI) — patients found on follow-up ECG to have had infarction did not have chest pain — but they did have “something else” thought to be associated with their MI.
  • The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
  • BOTTOM Line: Be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is sometimes appreciated. Not all patients with acute (or recent) MI have chest pain.

PEARL #2: The overall longterm prognosis after a 1st episode of syncope is good, especially in previously healthy younger adults. That said — the potential for adverse outcome (including death) exists in all age groups. The highest risk group are patients with a cardiac cause of their syncope, in whom 1-year mortality can reach 33% (Koene et al: J Arrhythm 33(6):533-544, 2017).
  • Cardiac syncope was found in ~9% of patients in the Framingham studies. That said — the actual percentage of patients with cardiac syncope was clearly higher than this in Framingham, as up to 1/3 of patients had syncope of unknown cause. This data highlights the point made above by Dr. McLaren — that diagnostic cath of today's patient (despite the lack of STEMI criteria) may have been lifesaving!

  • Syncope is not a common cause of acute MI. That said — syncope more often is encountered as a consequence of an acute MI. Potential mechanisms that may cause syncope in association with acute MI include: i) A cardioinhibitory and vasodepressor reflex response resulting from vagal stimulation (most commonly seen with acute inferior MI); ii) Development of high-grade AV block (also more common with acute inferior MI); and/oriii) Sustained VT (which is fortunately much less common in the acute reperfusion era).

The First 2 ECGs in Today's Case:
I thought it worthwhile to take a final look at the first 2 ECGs in today's case — which for clarity, I have reproduced in Figure-1
  • As per Dr. McLaren — the initial ECG in today's case is cause for concern: i) There are hyperacute T waves in each of the inferior leads — as determined by being "fatter"-at-their-peak and wider-at-their-base than expected (especially in lead III — in which the T wave dwarfs the QRS in this lead); andii) The tiny QRS complex in lead aVL is associated with a decidedly coved ST segment with T wave inversion in a shape that is clearly not normal.
  • Chest lead findings in ECG #1 are nonspecific and not diagnostic.

  • Impression of ECG #1: While it may clearly be challenging to know what to do with this initial ECG in the absence of chest pain — the likelihood of recent or ongoing acute OMI as the cause of this older patient's syncope increased dramatically the moment the 1st troponin came back elevated! 
  • Putting It All Together: Syncope (as the presenting symptom+ hyperacute changes on ECG #1 + a 1st Troponin = 2,800 ng/L — should be enough to indicate the need for prompt cardiac catheterization.

ECG #2 was obtained when the 1st Troponin came back elevated:
  • Fortunately in today's case — the cardiology team became concerned enough about subtle inferior lead ST elevation 2 hours after ECG #2 was done, that they performed cardiac cath which made the diagnosis.

  • MY Point: ECG #2 does not provide clear indication of how to proceed! Although true that it looks as if there now is some inferior lead ST elevation that was not present in ECG #1 — Bad data in means bad data out! — In my opinion, ECG #2 is not interpretable in this patient in whom you are very concerned may be in the midst of an acutely evolving infarction. This is because there is so much artifact in the 5 beats shown in the limb leads as to leave me with no idea about what is "real" vs artifact. This 2nd ECG should have been immediately repeated.

Figure-1: The first 2 ECGs in today's case.




Monday, December 5, 2022

Are these Hyperacute T-waves?

I received this ECG in a text message, with the message:

"Hey, these look like hyperacute T waves to me, what do you think?  It’s an intubated septic nursing home patient."  


"Here is her old ECG:"

What do you think?









Here is my response:

"There is something wrong with this ECG.  It might be another case of pulse tapping artifact. Change the location of the limb Electrodes and repeat the EKG.  All leads except lead I look bizarre."

So he repeated the ECG after moving the limb lead electrodes:

Much less bizarre appearing, and without the suggestion of hyperacute T-waves


Pulse Tapping Artifact

Ever since learning about "Pulse Tapping Artifact," I have begun seeing it more.   It may be that it is much more common than we think but just not recognized.

We have posted Pulse Tapping Artifact 3 times before:

I was shown this ECG without any information. What do you think?








Explanation

All leads are derived from 3 bipolar electrodes and one unipolar electrode.
Leads I, II, and III depend on bipolar leads voltage differences:
--Lead I uses the right and left arm
--Lead II uses the right arm and the leg
--Lead III uses the left arm and the leg.
--The Wilson (or Goldberger) Central Terminal is used to produce the augmented (a) leads:
aVR, aVL, aVF.




The voltages are calculated as follows (Thanks to Ken Grauer for sending these):
  • I = L - R
  • II = F - R
  • III = F - L
  • aVR = R - (L + F/2)
  • aVL = L - (R + F/2)
  • aVF = F - (R + L/2)
As you can see, the only lead that does not use the left arm electrode is lead II.  Since lead II is the only normal lead in this ECG, the left arm electrode must be the affected electrode.  Indeed, the patients dialysis fistula was on the left arm and was pulsating with each heart beat, moving the electrode and causing artifact.

Arterial pulse tapping artifact

https://www.aclsmedicaltraining.com/blog/guide-to-understanding-ecg-artifact/

This online article references the article below by Emre Aslanger, a great guy who occasionally corresponds with me about ECGs.

Aslanger E, Yalin K. Electromechanical association: a subtle electrocardiogram artifact. Journal of Electrocardiology. 2012;45(1):15-17. doi:10.1016/j.jelectrocard.2010.12.162.

Incredibly, this case was just published in Circulation on January 22, 2018 (thanks to Brooks Walsh for finding this!) 
Asymptomatic ST-Segment–Elevation ECG in Patient With Kidney Failure.   https://doi.org/10.1161/CIRCULATIONAHA.117.032657.  Circulation. Originally published January 22, 2018

Here is a case from Circulation year 2000 that was misdiagnosed as due to pancreatitis.  But you can tell from the normal lead III that this was a right arm electrode problem:
http://circ.ahajournals.org/content/101/25/2989.full

It is full text!! 

Why is there also artifact in precordial leads?
Aslanger explains:
“[O]ne may expect that the leads not connected to the electrode affected by the source of disturbance would be free of distortion; but this is not the case. When one of the limb electrodes is affected by a source of disturbance, it distorts not only the corresponding derivation but also [the others] which are all calculated by mathematical equations…”
“…precordial leads [are also affected] because the Wilson central terminal, which constitutes the negative pole of the unipolar leads, is produced by connecting 3 limb electrodes via a simple, resistive network to give an average potential across the body.”





==================================
Comment by KEN GRAUER, MD (12/5/2022):
==================================
I'll start with My Confession: I looked at today's tracing too fast ...
  • I didn’t know the history.
  • I thought the dramatic increase in chest lead amplitudes (ie, very deep S waves in anterior leads — with very tall R waves in V5,V6) — together with tall, peaked anterior T waves — and QTc prolongation with deep symmetric T wave inversion in V5,V6 — could all be explained by marked LVH with LV “strain” and/or ischemia. I thought the overall picture in these 6 chest leads did not look like acute OMI.


I was admittedly stumped by the limb leads:
  • As per Dr. Smith — the limb lead appearance is bizarre. That said — given what I had convinced myself could be a plausible chest lead picture of marked LVH with QTc prolongation — I thought that IF the limb lead appearance was “real” — then the combination markedly peaked inferior lead T waves + reciprocal T wave inversion in lead aVL + extreme QTc prolongation — might reflect Takotsubo Cardiomyopathy. 



PEARLS for Recognizing Pulse-Tap Artifact:
As per Dr. Smith: Now that we know about Pulse-Tap Artifact — We seem to be recognizing it more and more.
  • If ever you see a bizarre appearance for 2 of the 3 standard limb leads (ie, leads I,II,III) — with the 3rd standard limb lead looking relatively (if not completely) appropriate — Think Artifact! This is precisely what we see for the initial ECG in today's case ( = ECG #1 in Figure-1) — in which the huge and bizarrely pointed T waves in lead II and lead III are distinctly out of character compared to the unremarkable flattened ST segment with shallow T wave inversion in lead I.

  • Since the cause of the Pulse-Tap Artifact is contact of one of the limb lead electrodes with a pulsating artery below it — the bizarre deflection that you suspect is artifact will have a fixed relationship to neighboring QRS complexes. This is precisely what we see for ECG #1 — in that the coupling distance from the QRS until the peak of the T wave in leads II and III remains constant for each beat (best seen for each beat in the long lead II rhythm strip at the bottom of the 12-lead).

  • KEY POINT: You can confidently make the diagnosis of Pulse-Tap Artifact by seeing IF the geometric relationships predicted by Einthoven’s Triangle regarding the relative size of artifact deflections holds true. I illustrate this concept in Figure-1 — in which the RED outlines in ECG #1 show the relative size and shape of the "extra deflection" added on by the pulse-tap artifact to the ST-T wave in the various leads.
  • According to the 3-page article by Rowlands and Moore (J Electrocardiology 40: 475-477, 2007 — which I reproduce in the ADDENDUM below) — the amplitude of the artifact is maximal in the unipolar augmented electrode of the "culprit" extremity, which is lead aVF in ECG #1. The amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVL) will be about 1/2 the amplitude of the artifact in lead aVF.
  • That maximal augmented lead artifact is seen in lead aVF — is consistent with the finding in ECG #1 of comparable artifact amplitude in leads II and III — but essentially no artifact in standard lead I. This is because electrical potential from the left leg electrode (ie, aVF) does not influence the QRS complex in lead I (which is derived from the difference in electrical potential between the RA and LA electrodes, without contribution from the LL electrode — as seen in Figure-2 in the ADDENDUM below).
  • Rowlands and Moore go on to emphasize that the amplitude of artifact deflections in the unipolar chest leads (based on the equation cited in the top-right column of page 477) — should be only about 1/3 the size of the maximal artifact distortion that is seen in leads II, III and aVF. This too is consistent with the relative size of the artifact in ECG #1.

  • Finally: You can prove the “culprit extremity” cause of artifact by demonstrating that artifact deflections are no longer present after repositioning the limb lead electrodes (which is evident in ECG #3). A lesser level of baseline artifact does remain in the limb leads of ECG #3 — but this looks nothing like the bizarrely peaked pulse-tap T waves of ECG #1


Figure-1: Comparison of the initial ECG in today's case — with the repeat ECG obtained after repositioning the limb leads. The RED outlines in ECG #1 show the relative size and shape of the "extra deflection" added on in the various leads by the pulse-tap artifact. BLUE arrows correlate the timing of artifact deflections in various leads. The PURPLE arrow shows the absence of pulse-tap artifact in lead I.


=========================


ADDENDUM:

To facilitate visualization of the electrical relationships cited above by Dr. Smith — I've added Figure-2 below. As per Dr. Smith — the fact that the ST-T wave in lead I of ECG #1 does not manifest any artifact distortion rules out the RA (Right Arm) and LA (Left Arm) electrodes — thereby implicating the LL (Left Leg) as the "culprit" extremity producing the artifact.
  • By Einthoven's Triangle — the finding in ECG #1 of maximal amplitude artifact in unipolar lead aVF (compared to the amplitude of artifact in the other 2 augmented leads = aVR and aVL) — confirms that the LL electrode (which is placed on the left foot) is the "culprit" extremity.

Figure-2: Use of Einthoven's Triangle to determine the electrical voltages in the 3 standard limb leads.



NOTE: I reproduce below (in Figures-3, -4 and -5— the 3-page article by Rowlands and Moore (J. Electrocardiology 40: 475-477, 2007) — which is the BEST review I’ve seen on the physiology explaining the relative size of artifact deflections when the cause of the artifact is from a single extremity.

  • As noted by the equations on page 477 in the Rowlands and Moore article: i) The amplitude of the artifact is maximal in the unipolar augmented electrode of the “culprit” extremity — which is lead aVF in ECG #1; andii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVL) is about 1/2 the amplitude of the artifact in lead aVF. These relative artifact sizes are consistent with the amplitudes of ST-T wave distortion seen in ECG #1.

  • The amplitude of artifact deflections in the unipolar chest leads (based on the equation cited in the top-right column of page 477) — should be only about 1/3 the size of the maximal artifact distortion that is seen in leads II, III and aVF. 

 


Figure-3: Page 475 from the Rowlands and Moore article that I reference above.




 

Figure-4: Page 476 from the Rowlands and Moore article that I reference above.


 

Figure-5: Page 477 from the Rowlands and Moore article that I reference above.





Wednesday, November 30, 2022

Upon arrival to the emergency department, a senior emergency physician looked at the ECG and said "Nothing too exciting."

This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. 


This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chest pain. The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. 


A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chest pain. On medic arrival, she walked out of the house in no distress, but was diaphoretic. She described intermittent chest discomfort for a week, and went to the clinic one day prior where a 12-lead was recorded and reportedly "normal." Today's pain felt similar to previous episodes of "Reflux;" it radiated to her neck and jaw.


VS were: BP 188/72, HR 88 and 99% SPO2 on room air.


Our first 12 lead ECG was then recorded at 0926.

What do you think?








Here is Spencer's interpretation:

There
is a sinus rhythm with narrow QRS complexes and a normal axis. V1 has 0.5 mm of ST segment elevation, V2 and V3 have 1 mm of elevation, v4 has 2 mm of elevation and v5 around 1.5 mm of elevation. More notably there are hyperacute T waves in V3 through V5. These T waves are too large in proportion to their QRS complexes with broad bases, and they are symmetric or nearly symmetric in appearance.

There is also T wave inversion In aVL with a very small amount of ST segment depression. The T waves in the inferior leads appear to be turning hyperacute with broad bases and proportionally large size in comparison to their QRS complexes. The inferior T waves also appear to have a quick take off from the J point with a near symmetrical appearance.


These findings are suggestive of Occlusion of a wraparound LAD.


Smith: I would be more emphatic. These findings are diagnostic of an apical OMI as a result of LAD Occlusion.


Another ECG was recorded 5 minutes later just before arrival at the hospital:

Similar


The patient was transported to a nearby suburban hospital with PCI capabilities while my partner cared for her.


Upon arrival to the emergency department, a senior emergency physician looked at the ECG and said "Nothing too exciting."


Then she began complaining of severe dizziness and quickly went into ventricular fibrillation and resuscitation was initiated by hospital staff. She was defibrillated and resuscitated.


It is apparently fortunate that she had a cardiac arrest; otherwise, her ECG would have been ignored.


Smith: this ECG and clinical presentation is diagnostic of LAD Occlusion. I need to innoculate you against the subsequent opinions below. by making it clear to everyone that this is NOT an EKG that one sees with takotsubo cardiomyopathy. It is also NOT the clinical scenario of takotsubo (a week of intermittent chest pain). Takotsubo is a sudden event, not one with crescendo angina. An apical OMI has the same ultrasound findings as takotsubo, and thus mimics takotsubo.


Hospital Course

The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy.

Here is the cath report:


Echocardiogram:
There is severe hypokinesis of entire LV apex and apical segment of all the walls.  
EF is 30-35%

Troponins 
The high sensitivity troponin I peaked at 9,324 ng/L 
(approximately equivalent to 9.32 ng/mL by 4th generation and older assays.)

This is important because troponin I elevations in takotsubo are not that high.  In a recent article (J Electrocardiol this year, see reference below), peak troponin I levels in takotsubo presenting with ST Elevation were median 1.02 ng/mL [IQR: 0.46, 2.35].  

Note 1: Levels were significantly lower in takotsubo that presented with T-wave inversion.
Note 2: This article fails to specify whether it was troponin I or T, but I contacted the institution and they used exclusively troponin I during that time period.

Reference on Troponins: Xenogiannis I, Vemmou E, Nikolakopoulos I, et al. The impact of ST-segment elevation on the prognosis of patients with Takotsubo cardiomyopathy. J Electrocardiol [Internet] 2022;Available from: http://dx.doi.org/10.1016/j.jelectrocard.2022.09.009

Cardiology opinion: 
Takotsubo Cardiomyopathy (EF 30-35%)
V Fib Cardiac arrest
Prolonged QTC
NSTEMI (Smith comment: is it NSTEMI or is it Takotsubo?  -- these are entirely different)
Moderate single-vessel CAD.

Then they did an MRI:

Patient underwent cardiac MRI on 10/4 that showed mildly reduced BiV systolic function. LVEF 51% and RVEF 49% with severe hypokinesis of distal septal, distal anterior, apical and distal inferior segments.  

Noted increased myocardial and pericardial fluid content. Delayed enhancement reveals small, subendocardial scar in the distal septal, apical and distal inferior segments consistent with scar in the LAD distribution. Findings consistent with infarct in LAD distribution (likely recent). 

Just to add more evidence, here is the post reperfusion ECG:
There is terminal T-wave inversion (identical to Wellens' Pattern A).
Although one sees diffuse symmetric T-wave inversion develop in takotsubo, with a long QT, one does NOT see Wellens' pattern A in takotsubo.


I could have told you this (and did tell you this) without an MRI.  This entire case is not consistent with takotsubo.  Just because you don't see hemodynamically significant CAD on angiogram does not mean it is not OMI.  To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS).  An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!  It can only be seen by IVUS.

Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries).  MINOCA has many etiologies. One of the most common is rupture of a non-obstructive plaque, with thrombus formation and OMI that spontaneously lyses and leaves a wide open artery.  We can tell from the history and ECG that this case is MINOCA that was a result of transient LAD Occlusion with thrombus that subsequently lysed.  One need not have obstructive coronary disease to have occlusive thrombus!  In fact, the majority of acute MI occur in coronary arteries that do not have hemodynamically significant stenoses (see New England Journal Review below)

Here is a quote from a review article in NEJM:

Pathogenesis of Acute Coronary Syndromes

Findings from clinical and pathological studies have challenged these commonly held notions of the pathophysiological features of coronary atherosclerosis and its treatment.1-4 Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery. In a prospective angiographic study involving patients undergoing percutaneous intervention for coronary artery disease, only half the subsequent events arose from lesions with sufficient stenosis to have warranted intervention at the time of revascularization.5 Computed tomographic (CT) angiography, which permits evaluation of the arterial wall (not just the lumen), has shown that the characteristics of plaque associated with acute coronary syndromes include low attenuation (i.e., little or no calcification) and outward expansion of the artery wall, a process that tends to accommodate the growth of plaque while minimizing luminal encroachment.6-8 Intravascular ultrasonography has shown that in acute coronary syndromes, the culprits often lie proximal to the sites of maximal stenosis — the traditional targets of revascularization therapies.9 This dissociation between the degree of stenosis and the propensity to provoke an acute coronary syndrome helps to explain why myocardial infarction often occurs without being heralded by the demand-induced symptoms of angina that would result from a high-grade stenosis.



Learning Points:
1. Learn to Recognize Hyperacute T-waves
2. Many paramedics are far better than any physician (Emergency or Cardiology) at diagnosing OM
3. Do not let your consultants diagnose takotsubo when it is clearly OMI.





I do not have the bandwidth here to write a review of MINOCA.

But a few items: 

The definition of MINOCA is predicated on the patient fulfilling all three main diagnostic criteria, namely: 
1) the Universal Definition of Acute MI (which requires ischemia); 
2) the presence of non-obstructive coronary artery on angiography (defined as no coronary artery stenosis ≥50%) in any potential infarct-related artery; and 
3) the absence of another specific, clinically overt cause for the acute presentation. 

MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli, and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies.

We know that most type 1 acute MI due to plaque rupture and thrombosis occurs in lesions that are less than 50% (see Libby reference).  This is in spite of the known proclivity of tighter stenoses to thrombose.  The reason for this is population-based: there are many more moderate stenoses out in the population than there are tight stenoses, and so more MIs are generated from these moderate ones.  

Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event.  However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram.  Coronary thrombosis with complete lysis is clearly possible, but its contribution to MINOCA is really not known because adequate investigation is rarely undertaken.  The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram.

Furthermore, the clinical presentation of sudden chest pain, typical ECG findings of occlusion (hyperacute T-waves in this case), ECG findings in a coronary distribution, rise and fall of troponin with peak in the typical range for STEMI/OMI, and new wall motion abnormality in the area indicated by the ECG, must be considered to be due to coronary thrombosis.   The degree of stenosis is not a great predictor of thrombosis, and culprits may not be visible.  Even if there is a tight stenosis, it is not proof of culprit, as many individuals have tight fixed stenoses at baseline.  There may be a chronic tight stenosis and a non-obstructed lesion that thrombosed.  

Contemporary research studies of MINOCA have evaluated the prognosis of these patients, reporting a 12-month all-cause mortality of 4.7% (95% confidence interval, 2.6–6.9),3 with comparative studies consistently demonstrating a better prognosis than for those who experience AMI associated with obstructive coronary artery disease.

Lindahl et al. associated typical Myocardial Infarction therapies such as statins and ACE inhibitors with significantly decreased 1 year mortality in MINOCA patients, which suggests that they do indeed have a similar pathophysiology to MI patients with obstructive coronary disease.


From UpToDate:

Acute thrombosis at the site of non-obstructive eccentric plaque thrombosis — Many atherosclerotic plaques expand outward rather than encroaching on the arterial lumen. These ”positively-remodelled” plaques are often lipid rich and have a thin fibrous cap; they are vulnerable to rupture into the lumen [1,9,10]. Transient and partial thrombosis at the site of a non-obstructive plaque with subsequent spontaneous fibrinolysis and distal embolization may be one of the mechanisms responsible for the occurrence of MINOCA. Similarly, coronary erosion with loss of surface endothelium, possibly due to hyaluronan and neutrophil accumulation, can also cause MINOCA [1,11]. (See "Mechanisms of acute coronary syndromes related to atherosclerosis".)

The reason for these cases to be labeled as MINOCA is that angiography is of limited utility for the purpose of elucidating plaque-related thrombosis as a cause of thrombosis due to its low resolution as well as the fact that it does not interrogate the lumen of the vessel. Thus, intracoronary imaging modalities are crucial in this setting. Plaque rupture or erosion has been diagnosed by intravascular ultrasound in about 40 percent of women with MINOCA [12]. Optical coherence tomography, due to its high resolution, may provide additional information [10,13].

As MINOCA is associated with a risk of recurrent cardiovascular events over time, comparable with that of patients with acute coronary syndromes (ACS) and obstructive atherosclerosis [5,14,15], these patients require dual antiplatelet treatment for 12 months and statins. In particular, long-term lipid-lowering therapy with statins after MI is associated with a significant increase of the fibrous-cap thickness, paralleling the reduction of the lipid content of the plaque [16]. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)



From Gue at al.


STEMI MINOCA versus NSTEMI MINOCA 

STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. In patients presenting with non-ST-segment elevation MI (NSTEMI), the infarct is subendocardial. This pathophysiological difference also seems to be present within the MINOCA cohort. Registry data indicate that 6–11% of patients with acute MI have nonobstructive coronary arteries.  Within the literature, MINOCA tends to present more commonly as NSTEMI than STEMI: the incidence of MINOCA reported in patients presenting with NSTEMI is about 8–10% and in STEMI cohorts it is 2.8–4.4%. This has resulted in an under-representation of STEMI MINOCA patients in the literature. Most studies examine undifferentiated ACS cohorts, with only a handful providing separate data. These studies indicate that the 1-year mortality of MINOCA presenting as STEMI is 4.5%, in contrast to the mortality of unselected MINOCA ACS patients who have a mortality of 4.7%. The underlying aetiology of MINOCA is similar among those presenting with STEMI and in all-comer MINOCA patients with ACS, with non-coronary aetiology responsible for presentation in 60–70% of individuals with STEMI and in 76% of unselected ACS patients. 


References:

1.  Lindahl B, Baron T, Erlinge D, et al. Medical Therapy for Secondary Prevention and Long-Term Outcome in Patients With Myocardial Infarction With Nonobstructive Coronary Artery Disease. Circulation [Internet] 2017;135(16):1481–9. Available from: http://dx.doi.org/10.1161/CIRCULATIONAHA.116.026336   https://www.ahajournals.org/doi/epdf/10.1161/CIRCULATIONAHA.116.026336

2. Pasupathy S, Tavella R, Beltrame JF. Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA): The Past, Present, and Future Management [Internet]. Circulation. 2017;135(16):1490–3. Available from: http://dx.doi.org/10.1161/CIRCULATIONAHA.117.027666 https://www.ahajournals.org/doi/epdf/10.1161/CIRCULATIONAHA.117.027666

3. Gue YX, Kanji R, Gati S, Gorog DA. MI with Non-obstructive Coronary Artery Presenting with STEMI: A Review of Incidence, Aetiology, Assessment and Treatment. Eur Cardiol [Internet] 2020;15:e20. Available from: http://dx.doi.org/10.15420/ecr.2019.13

4. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med [Internet] 2013;368(21):2004–13. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=23697515





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My Comment by KEN GRAUER, MD (11/30/2022):
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Today's case is one to remember — as it shatters previous misconceptions regarding the patient who despite non-occlusive disease on cath — may nevertheless have just completed having an extensive acute infarction. As per the brilliant discussion above by Dr. Smith — all-too-many clinicians remain unaware of this possibility. 
  • My focus today is on brief additional commentary regarding the ECGs in this case — and — some thoughts about MINOCA (MI with Non-Obstructive Coronary Arteries).

The ECGs in Today's Case:
Superb interpretation by Spencer Schwartz of the initial ECG in today's case! ( = ECG #1 in Figure-1). To this — I would add the following points.
  • Even more leads than were mentioned show acute changes in today's case! While this point is not essential for initial management (ie, Spencer emphasized his suspicion for acute OMI — with need for transport to a facility with PCI capability) — there are plenty of cases in which recognition of how many leads actually show acute changes is important for accurate diagnosis.
  • As per Spencer — the most notable changes in ECG #1 — are the hyperacute ST-T waves in anterior leads V3-thru-V5.

  • Regarding the chest leads: By the concept of "neighboring leads" — the T waves in leads V2 and V6 are also hyperacute. By this I mean that in isolation — the T waves in leads V2 and V6 might not seem abnormal. But both of these leads do show a T wave that is "fatter"-at-its-peak and wider-at-its-base than it should be — so in the context of obviously hyperacute ST-T waves in leads V3-V5 — I interpreted the range of acute ST-T wave changes as encompassing leads V2-thru-V6.

  • In addition — the deep and wide Q waves in leads V1,V2 (with no more than the tiniest of initial r wave in lead V3) — suggests significant myocardial injury has already occurred in the anterior myocardium.

  • Regarding the limb leads: More than just "turning" hyperacute — the ST-T waves in each of the inferior leads are hyperacute for the very reasons that Spencer mentions ( = these inferior T waves are too large in proportion to their QRS complexes — with broad bases) — as well as also being "fatter"-than-they-should-be at their peak. My point being simply that while I might not be certain from the inferior lead ST-T wave appearance alone that there are acute changes — I know that there are acute inferior lead changes in the context of the obviously hyperacute chest lead changes (supported as per Spencer — by reciprocal T wave inversion in lead aVL).

  • Spencer correctly identified key abnormalities while expediting transport to a PCI-capable facility. But as per Dr. Smith — it is worth emphasizing that in a patient who presents with new chest pain (as in today's case) — the findings in ECG #1 are truly diagnostic of acute LAD OMI until you prove otherwise
  • To Emphasize: The reason definitive diagnosis is important in today's case — is that the senior ED physician interpreted ECG #1 as "nothing too exciting". It is essential to impress upon that physician that we are not dealing with a "maybe" — but rather with an ECG that provides definitive diagnosis of acute LAD OMI in need of immediate cath until proven otherwise.

  • Beyond-The-Core: As discussed in the November 13, 2022 post by Emre Aslanger in Dr. Smith's ECG Blog — ST elevation in both anterior and inferior leads does not necessarily indicate an LAD "wraparound" lesion, as used to be thought (Bozbeyoğlu, Yildirimtürk, Aslanger et al — Anatol J Cardiol 21:253-8, 2019).

The Post-Reperfusion ECG:
Today's case illustrates the confusion that may arise in diagnosis of acute chest pain patients who do not manifest coronary occlusion (or a likely "culprit" artery) at the time of acute cath.
  • As per Dr. Smith — the cardiology opinion following evaluative testing on today's patient was contradictory — because "NSTEMI" is a very different entity from Takotsubo Cardiomyopathy.

  • PEARL #1: As we have often emphasized on Dr. Smith's ECG Blog — Because of the common (albeit still not well appreciated) phenomenon of spontaneous reperfusion of the "culprit" coronary artery (which may sometimes reopen and reocclude multiple times) — more than a single ECG is often needed to identify a recent OMI that shows a relatively normal initial tracing as a result of the "pseudonormalization" that may be seen when acute chest pain resolves because the "culprit" artery has spontaneously reperfused. In order to fully appreciate the sequence of events — serial timed ECGs that are all correlated to serial timed troponin assays and chest pain severity scores may be needed.

  • As per Dr. Smith — the post-reperfusion ECG seen in Figure-1 is not consistent with the expected findings of Takotsubo Cardiomyopathy(For review of ECG findings expected with Takotsubo Cardiomyopathy — Please see My Comment at the bottom of the page in the March 25, 2020 post in Dr. Smith's ECG Blog). Instead — We see typical reperfusion T waves in the diffuse distribution of what was hyperacute ST-T wave changes on the initial tracing.
  • The "good news" — is that anterior R wave progression has improved since the initial tracing (ie, There are now definite initial R waves in leads V2 and V3 of ECG #3 — without loss of R wave amplitude in other leads)

Figure-1: Comparison of the initial ECG in today's case — with the post-reperfusion ECG(To improve visualization — I've digitized the original ECG using PMcardio).



The Unappreciated Entity of MINOCA:
Dr. Smith reviews the all-too-often ignored entity known as MINOCA. For clarity in Figure-2 — I've adapted the Table from the article by Sykes et al that reviews the diagnostic entities to consider in the patient with an acute MI despite non-obstructive coronary arteries.
  • As per Dr. Smith — Perhaps the most common etiology of MINOCA is plaque rupture with thrombus formation and OMI that spontaneously lyses, resulting in a patent "culprit" artery at the time of cardiac catheterization.

  • Putting Today's Case Together: The history of intermittent chest discomfort over the course of 1 week — together with the initial and post-reperfusion ECG findings — is most consistent with acute apical OMI. This impression was confirmed on cardiac MRI.

  • PEARL #2: The fact that the initial ECG in today's case showed hyperacute changes in at least 9 leads in the infero-antero-lateral distribution is consistent with acute apical OMI. As per Dr. Smith — it's important to appreciate that Echo findings of an extensive apical OMI may mimic those of Takotsubo Cardiomyopathy!

  • PEARL #3: The importance of Figure-2 — is that it highlights the need to open ourselves to a series of diagnostic entities when confronted with a patient showing positive troponins and an ECG suggestive of acute MI despite the finding of non-obstructive coronary disease on cath.

Figure-2: Classification of Underlying Diagnoses in Patients with MINOCA (Adapted from Table-1 in Sykes et al: Interventional Cardiology Review: 16:e10, 2021)NOTE: As per Sykes et al — The entities listed under "Other Etiology" may be diagnosed following further investigation and should be considered separately (because they are typically associated with myocardial injury but not considered an MI by the 4th universal definition of MI). This is an important indication for cardiac MRI in patients suspected of MINOCA.



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