Thursday, July 11, 2024

See how bad the outcome can be if you don't know OMI findings on the ECG, and don't use the Queen of Hearts

This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech.  

How is it possible that a kid who has not even started medical school can know so much about EKGs and cardiology?  Because:

1) He has been reading this blog for a long time.  

2) He is curious

This is how Pendell got started.


A 43 year old male with a history of DM II, hyperlipidemia, and a family history of myocardial infarction presented to a family clinic with two days of epigastric pain that started after consuming a meal. He described the pain as a “crushing and discomforting” feeling with no radiation. He reported that the pain was worse with exertion and nothing relieved it. His BP was 138/88 and his HR was 77 BPM. He had an EKG taken at the clinic:

What do you think?

There was no old EKG for comparison, however, this EKG alone is diagnostic of LAD occlusion. 

The T waves in V1-V4 are hyperacute. There is positively sloped ST-segment straightening in V2 and V3. There is a fragmented QS complex in V2. Lead aVL has a very subtly convex T wave with terminal T wave inversion. There is very slight horizontal ST segment straightening in leads III and aVF. These inferior leads could be normal, however, in combination with the hyperacute anterior T waves, they should be interpreted as showing reciprocal changes. V6 also has very slight ST depression. This EKG shows precordial swirl pattern (STE in V1-2 with STD in V5-6).

Smith: there is also a Q-wave in V2 and a small amount of STE.  STE is almost never normal in the context of a Q-wave.  Also, there is STD in V5-6. STE in V1-V4 is never normal if there is also STD anywhere except aVR.  There are many reasons that this ECG is diagnostic of LAD OMI.

Thus, this is yet another case of "Precordial Swirl".

An argument can be made that the reciprocal changes here are not prominent enough to call, but it is important to remember that many LAD occlusions do not show reciprocal changes at all. 

The computer diagnostic algorithm diagnosed “Sinus rhythm. Normal EKG”. The attending provider wrote “Agree with electrocardiogram interpretation”.  The cardiologist overread was: Sinus Rhythm. Normal ECG.

Smith: All physicians, including cardiologists, have a hard time with subtle OMI ECG findings.  This result is common and not surprising. 

In general, family medicine physicians may not have the same amount of exposure to EKGs as an emergency medicine specialist or a cardiologist, but they shouldn’t have to rely on the traditional diagnostic computer algorithm. 

Had the physician instead used the Queen of Hearts, who diagnoses OMI with high confidence, the outcome may have been different:

OMI with High Confidence

Click here to sign up for Queen of Hearts Access

Case continued

Unfortunately, this EKG went unnoticed, and the atypical symptoms with which the patient presented did not prompt any further cardiac workup. A CBC and a metabolic panel were ordered, and both were unremarkable, save for hyperglycemia. The patient was sent home with a prescription for omeprazole to treat presumed peptic disease. He spent the following weeks with continued episodic heartburn and worsening dyspnea on exertion.

No patient with chest pain should be sent home without troponin testing.  Even if you miss the ECG, at least you'll be able to diagnose an MI with troponins, though if it is OMI, you may lose a lot of myocardium before making the diagnosis.  

He re-presented to the family clinic for a follow-up visit a month after his original appointment. His BP was now 82/68, and his HR was 112. On this visit, he expressed worsening exercise tolerance, new orthopnea, and he told his provider that the omeprazole did not relieve any symptoms. An EKG was taken again:

This EKG shows a completed anterior wall infarction! There are hardly any R waves in any of the precordial leads!

The provider recognized the dramatic changes between this tracing and the tracing taken a month prior. He sent the patient to the ED for further evaluation. A chest x-ray in the ED found bilateral pleural effusions. The patient’s BNP was 738, and his D-dimer was elevated, prompting a CT scan to rule out PE. The scan did not find PE, but showed evidence of coronary plaque:

There are areas of dense white in the LAD (red and blue circles) and in the first diagonal (green circle).

An echocardiogram showed severely reduced global systolic function with an EF of 20-25% and an LV apical thrombus. Troponin I values trended from 0.262 to 0.746 ng/mL in 6 hours (URL for this assay is 0.034 ng/mL). The patient was admitted from the ED and finally had an angiogram the next morning:


Image 1:

This is the LAO caudal, or spider projection. The red arrow shows a roughly 80% stenosis of the proximal LAD. The blue arrow shows another stenosis of the LAD distal to the first diagonal branch of about 99%. The green arrow shows a 95% stenosis of the ostium of the first diagonal branch. 

Image 2:

This is the LAO cranial projection. Here, the mid LAD (blue arrow) and the ostial first diagonal (green arrow) stenoses are better visualized. All three lesions had TIMI 2 flow prior to stenting.

This is an RAO cranial projection of the left coronary vessels after thrombectomy and stenting. The blue arrow indicates the LAD, and the green arrow indicates the first diagonal. There is now TIMI 3 flow through all lesions, but there is widespread vasoconstriction.

This is the RAO caudal projection. The LAD (blue) and first diagonal (green) are noticeably narrower than the other vessels.

Here is the post-cath EKG:

There is no change. The LV aneurysm morphology persists. There was hardly much viable myocardium left to be saved by PCI after a month of occlusion.

On day three of his hospital admission, he had a cardiac MRI taken:

The MRI showed:

  • Increased LV volume

  • Severe segmental LV dysfunction with a calculated EF of 26%

  • Thinning and akinesis of the entire anterior wall, apical segments, entire anterior septum, and the mid inferior wall.

  • Large multiloculated apical thrombus (black mass at the apex)

  • Transmural infarction showing nonviable myocardium throughout the entire anterior distribution and all apical segments

The patient was eventually discharged from the hospital. Three months later, he had a follow up appointment for a reassessment of his LV function. An echocardiogram showed an EF of 20-25%. At this point, there was no improvement in LV function and he was out of the convalescent phase of his MI, so the decision was made to install an ICD for arrhythmia prophylaxis.

One month after ICD implantation, an EKG was taken:

Notably, the T wave inversions are now resolved. The R waves have not recovered, however.

He now has regular appointments with the heart failure team.

Learning Points

All of this could have been avoided by:

1.  Expert ECG interpretation -- this is too much to ask of any clinician

2.  Queen of Hearts --  makes the diagnosis easy

3.  The patient should have had serial troponins.  These would have made the diagnosis of MI earlier, but it might still be labeled "NSTEMI" and not get intervention until all that myocardium is lost.


MY Comment, by KEN GRAUER, MD (7/11/2024):

I reviewed today's case from the perspective of a family physician educator with prior experience teaching ECG interpretation nationally to primary care clinicians over a period of 3+ decades.
  • In our primary care residency program, despite our faculty's competency in the basics of reading primary care X-rays — all of our X-rays were overread by a radiologist.
  • I overread all ECGs for our 35 providers.

  • BOTTOM Line: Unless primary care clinicians attain a level of excellence in the interpretation of outpatient X-rays and ECGs — these tests should be routinely overread by physicians with recognized expertise in this interpretation.

Editorial Comment: I begin my thoughts on today's Blog post with the above reflections to provide perspective for my concerns about this case.
  • This patient should not have been sent home from the primary clinic with the history he gave and today's initial ECG (that I've reproduced and labeled in Figure-1).
  • A 2-day history of a "crushing and discomforting feeling" that is worse with exertion and not relieved by any home measures that are tried — even if primarily "epigastric" in location — is a potential presentation for ACS (Acute Coronary Syndrome) that needs to be recognized.
  • Primary care clinicians are trained in the basics of ECG interpretation. While not expected to be experts if such clinicians limit their practice to an ambulatory setting in which they rarely order outpatient ECGs — these primary care clinicians are expected to recognize that in a patient with new symptoms (as in today's case) — the ECG in Figure-1 is not "normal".
  • If the training of primary care clinicians is such that they are unable to recognize that today's initial ECG is not normal — then before the patient is sent home, there should be some form of backup overread. As per Dr. Smith — Queen of Hearts offers one form of immediate backup overread with impressive accuracy for identifying OMI on ECG.
  • Alternatively (and ideally, in addition to QOH) — in 2024, ready access to on-line consultation with either a local or remote expert in ECG interpretation should be available to any primary care clinician within minutes.
  • The above said — of even more concern in today's case, is that the cardiologist overread of today's initial ECG completely missed the diagnosisThis oversight by cardiology is hard to justify.

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

Today's Initial ECG: 
As per Dr. Smith — the ECG in Figure-1 is diagnostic of acute LAD OMI.
  • I've enclosed the reason today's initial ECG should not be overlooked within the RED rectangle. There is simply no way that the QRS complex and ST-T wave in lead V2 can be interpreted as "normal". The hyperacute ST-T wave in this lead completely dwarfs the tiny QRS complex. A repolarization variant will never do this. In addition to its height — this ST-T wave manifests an extremely wide base and straightening of the ST segment takeoff (RED arrow).
  • As a more subtle point — the QRS complex in lead V2 is abnormal. Although there is variation in QRS morphology for each of the complexes in this lead — the "theme" is fragmentation of the QRS, with no more than a tiny vestige for an r wave that I interpret as a Q wave "equivalent" in this patient who has had symptoms already for 2 days.

  • In the context of this marked abnormality in lead V2 — the 2 neighboring leads within the RED rectangle are also clearly abnormal. Lead V1 never normally manifests this much ST elevation, nor this tall of a T wave. And, given these abnormalities in leads V1,V2 — the ST-T wave in lead V3 is also hyperacute (taller and wider-at-its-base than expected, given modest amplitude of the QRS in this lead).
  • In support of this ECG representing acute proximal LAD OMI — is the clearly abnormal complex in lead aVL (within the BLUE rectangle) — which shows a surprisingly wide and deep Q wave (given tiny size of the QRS in this lead) — as well as slight-but-real ST elevation of coved morphology with terminal T wave inversion. Acute ECG findings of this nature in lead aVL is a common accompaniment of proximal LAD OMI. The Q in aVL and the Q-wave "equivalent" fragmentation in lead V2 suggest in this patient with a 2-day history of symptoms — that infarction has already taken place.
  • Finally, as per Dr. Smith — the subtle-but-real ST segment flattening in each of the inferior leads (BLUE arrowsis consistent with representing reciprocal ST depression. To Emphasize — As an isolated finding, I would be uncertain about the clinical significance of the ST-T waves in the inferior leads. But in the context of leads V1,V2,V3 and aVL being diagnostic of acute LAD OMI — the subtle degree of ST flattening in leads II,III,aVF is clearly consistent with reciprocal ST-T wave changes.

In Conclusion: Today's case is concerning because of unfortunate oversights that should not have occurred. The consequence of these oversights is the need for lifelong commitment of this patient to the heart failure clinic.

Tuesday, July 9, 2024

A man in his 50s with unwitnessed VF arrest, defibrillated to ROSC, and no STEMI criteria on post ROSC ECG. Should he get emergent angiogram?

Written by Pendell Meyers

A man in his 50s was found by his family in cardiac arrest of unknown duration. His family started CPR and called EMS, who arrived to find him in ventricular fibrillation. 15 minutes after EMS arrival, after at least 6 defibrillations, the patient achieved sustained ROSC. He arrived to the ED with severe hypotension, heart rate in the 70s, unable to follow commands but moving all extremities requiring restraint and sedation, respiratory rate around 24/min being supported with bag valve mask, with significant hypoxemia.

He underwent resuscitation including vasopressors, inotropic support, and intubation. Here is his ECG after stabilization of vitals (at least 30 minutes since sustained ROSC).

What do you think?

The ECG is diagnostic of acute LAD occlusion MI. This is the "precordial swirl" pattern of LAD OMI that we are planning to publish soon, with STE and HATW in V1-V2, with reciprocal STD/TWI in V5-V6. AVL is also suspicious, and with reciprocal STD in the inferior leads. Anterolateral OMI.

Here is the Queen of Hearts (version 1) interpretation:

Angiogram images before and after intervention:

Another view (before and after intervention):

The patient was confirmed to be in cardiogenic shock, placed on ECMO, also with impella assist device. 

Only one hs troponin I was measured on arrival: 323 ng/L

Initial echo showed10% EF, diffuse severe hypokinesis.

Post angiogram ECG

The patient was eventually able to be weaned off of ECMO and impella. He was extubated, following commands, talking to his family soon. Further information is not available. 

See this recent case which also explains in more detail the guidelines for post arrest NSTEMI management: 

See these many examples of Swirl and of LVH (which has some features of swirl, but is different):


MY Comment, by KEN GRAUER, MD (7/9/2024):

Interpretation of the ECG following resuscitation from cardiac arrest can often be challenging. Despite anticipation by many that the initial post-resuscitation ECG will show an obvious acute infarction — this expected "STEMI picture" is often not seen.
  • For clarity in Figure-1 — I've reproduced the initial ECG in today's case, obtained at least 30 minutes after achieving ROSC in this patient requiring multiple shocks for recurrent VFib.

The Post-Resuscitation ECG:
I thought the initial ECG in today's case was not obvious. Indeed, careful attention to detail is needed to appreciate the important findings. That said, as per Dr. Meyers — this ECG is diagnostic of the Precordial Swirl Pattern (so wonderfully described and illustrated by Drs. Meyers and Smith in the October 15, 2022 post of Dr. Smith's ECG Blog).
  • Restoration of sinus rhythm is evident in Figure-1.
  • Artifact attributable to some repetitive movement/action in the LL (Left Legextremity impairs our assessment of multiple complexes (Maximal artifact in leads II,III,aVF — 1/2-size artifact in aVR,aVL — and no artifact in lead I isolates the "culprit" extremity to the LL).

As per My Comment in the above-cited Oct. 15, 2022 post — I like to focus on the ST-T wave appearance in leads V1 and V6 to facilitate recognition of Precordial Swirl.
  • Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected! 
  • As highlighted within the RED rectangle in Figure-1 — There is no way the ST segment straightening, elevation and peaked T wave in lead V1 is normal.
  • Once we know that the ST-T wave appearance of lead V1 is abnormal — it becomes easier to appreciate that neighboring lead V2 (within the BLUE rectangle) shows similar (albeit less marked) abnormalities.

The other major component of Precordial Swirl — is the ST-T wave appearance in leads V5,V6. I focus first on lead V6(I expand on this concept in My Comment at the bottom of the page in the Oct. 15, 2022 post).
  • CAVEAT: When considering Swirl — Keep in mind that it is EASY to be fooled by LVH, which may produce ST-T wave changes of LV "strain" not only in leads V5,V6 — but also in anterior leads, in the form of an elevated ST-T wave. This is not an issue in today's case, because as seen in Figure-1 — S wave voltage in leads V1,V2 and R wave voltage in leads V5,V6 is small. There is no hint of LVH in today's initial ECG — and as a result, the certainty of abnormality in ST-T wave appearance in leads V1,V2 and V5,V6 is reinforced.
  • PEARL: In general — the shape of the ST-T wave depression in lead V6 with Swirl does not look like it typically does with LV "strain", in which the depressed ST segment will often be downsloping. Instead — the depressed ST segment with Swirl tends to be flatter, at least in lead V6 (BLUE arrow in this V6 lead).

Additional ECG findings in Figure-1 that support the diagnosis of LAD OMI and Swirl include:
  • Reciprocal ST depression in each of the inferior leads (YELLOW arrows).
  • Subtle-but-real ST elevation in lead aVL (dark BLUE arrow in this lead)

Figure-1: I've labeled the initial ECG in today's case.

Sunday, July 7, 2024

60 year old with chest pain, STEMI negative. What should the discharge diagnosis be?

 Written by Jesse McLaren


A previously healthy 60 year old developed exertional chest pain with diaphoresis, and called EMS. Here’s the EMS ECG, digitized with PM cardio. What do you think?





There’s sinus arrhythmia with normal conduction, normal axis and normal voltages. There’s loss of R waves in V2-3 with hyperacute waves V1-5. There’s no significant ST elevation but there are two forms of ST depression: deWinter T wave V3-5 and precordial swirl with ST depression V6 reciprocal to subtle STE in V1. In the limb leads there’s no ST elevation, but there are hyperacute T waves in I/aVL with reciprocal inferior ST depression. So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion.


Queen of Hearts PMCardio AI system was highly confident in OMI based on the hyperacute T waves and ST depression, despite absence of STEMI criteria:

The paramedics called a code STEMI from the field, and gave the patient aspirin and three sprays of nitro. They arrived in the ED 30 minutes later to meet the cardiology team, where an ECG was repeated:


Again no STEMI criteria, and there has been improvement in the deWinter and swirl pattern. But there are ongoing precordial hyperacute T waves and ongoing inferior ST depression, and this is reciprocal to subtle straight ST elevation in aVL. The final blinded cardiology interpretation noted only the minimal inferior ST depression, but the ECG is still diagnostic of proximal LAD occlusion.


Fortunately, the treating cardiology team noted the hyperacute T waves and subtle STE in aVL and continued with the plan for emergent angiography: 100% proximal LAD occlusion. First trop was 7,000ng/L (normal <26 in males in <16 in females) which goes along with the loss of R waves, and peak was 94,000 ng/L. Echo showed EF reduced to 35% with anteroseptal hypokinesis and akinetic apex. Discharge ECG showed antero-lateral reperfusion T wave inversion:

The discharge diagnosis was ‘STEMI’ but no ECG met STEMI criteria, and blinded cardiology interpretation of the ED ECG was also STEMI negative. 

In the current paradigm it would make more sense to call this Non-STEMI because the patient had a type 1 MI without any ECG meeting STEMI criteria. But that wouldn’t account for why the cath lab was activated emergently, because this is supposed to be reserved for patients with STEMI.  So the discharge diagnosis ‘STEMI’ was more a reflection of the time to treatment (emergent cath) rather than current diagnostic dichotomy (STEMI vs Non-STEMI). It is an example of a frequent occurrence: clinicians call OMI "STEMI."  So this is a STEMI(-)OMI which was treated like a STEMI, with rapid reperfusion despite the current paradigm.


Discharge diagnosis: STEMI/NSTEMI vs OMI/NOMI


Why this matters is that > 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion. Their discharge diagnosis also better reflects time to treatment (non-urgent cath), rather than diagnosis. 

These discharge diagnoses create a bias in STEMI/Non-STEMI databases: not only are STEMI(-)OMI with delayed reperfusion buried in Non-STEMI databases along with non-occlusive MIs, which prevents us learning from missed occlusions; but also, STEMI(-)OMI that are rapidly reperfused are buried in STEMI databases, which prevents us from learning from great cases like this. 

Both reinforce the false STEMI/non-STEMI dichotomy, and are barriers to shifting towards the OMI paradigm.


For comparison, see this similar case of a 60 year old with chest pain, with cath lab activated from the field:



Also diagnostic of LAD occlusion, with anterior hyperacute T waves, precordial swirl, and subtle inferior ST depression. The patient also had a 100% proximal LAD occlusion, with a peak troponin of 100,000 ng/L. But because Code STEMI was cancelled on arrival and the patient had delayed angiography, the discharge diagnosis was 'non-STEMI' despite having the exact same pathology. 

Rather than calling the first 'STEMI' because of rapid reperfusion and the second 'non-STEMI' because of delayed reperfusion, both should be called what they are: OMI - and then we can learn from both.


The new ACC expert consensus explains that: “STEMI ECG criteria on a standard 12-lead ECG alone will miss a significant minority of patients who have acute coronary occlusion. Therefore, the ECG should be closely examined for subtle changes that may represent initial ECG signs of vessel occlusion, such as hyperacute T waves or ST-segment elevation <1 mm, particularly when combined with reciprocal ST-segment depression.” But if STEMI criteria is a poor surrogate marker, and if what we care about is acute coronary occlusion, then discharge diagnoses should change to reflect a new classification of OMI/NOMI rather than STEMI/Non-STEMI.


Take home

1. STEMI criteria has poor sensitivity for acute coronary occlusion

2. Other signs of occlusion include hyperacute T waves, deWinter pattern, precordial swirl, and ST depression reciprocal to subtle ST elevation/hyperacute T 

3. Discharge diagnoses and MI classification should reflect patient outcomes of Occlusion vs non-Occlusion MI, not arbitrary STE vs Non-STE criteria, or rapid vs delayed time to cath. All OMIs can then be reviewed to identify which were missed and which were rapidly reperfused, in order to learn from both


MY Comment, by KEN GRAUER, MD (7/7/2024):

Today’s post by Dr. McLaren is an important one — in that emphasizes by means of 2 clinical example cases, shortcomings of the outdated and problematic STEMI paradigm.
  • Regular followers of Dr. Smith’s ECG Blog will be well familiar with scores of cases we’ve presented illustrating the trials and tribulations of the millimeter-based STEMI paradigm. All-too-many clinicians (including cardiologists) — remain “stuck” on this STEMI paradigm out of force of habit and failure to appreciate the now well-defined pathophysiology of what happens during the course of an evolving ACO (Acute Coronary Occlusion) — which is what we call an OMI (Occlusion Myocardial Infarction).
  • As per the 2 cases presented today by Dr. McLaren — the consequences of this current fallacious approach are many and far-reaching.

An expanding literature has now convincingly shown the following: 
  • Rigid adherence to millimeter-based STEMI criteria misses at least 1/3 of OMIs (Meyers, Smith et al — Ann Emerg Med 74(4): S26, 2019 — and — Meyers, Smith et al — Int J Cardiol Heart Vasc, 2021)
  • We know STEMI criteria are problematic — because clinicians trained to assess other ECG parameters (instead of relying solely on a given amount of millimeters of ST elevation) — are able to accurately identify OMIs that adherence to STEMI criteria will miss (McLaren, Meyers, Smith — Canad J Emerg Med 24: 250-255, 2022) — and — Westafer L — ACEP Now, Dec., 2022 — and — Kontos et al; 2022 ACC Expert Consensus — JACC 80(20):1925-1960, 2022).
  • More than simple failure to identfy STEMI-/OMI+ cases — adherence to the outdated STEMI paradigm may result in delayed diagnosis of many patients with acute coronary occlusion who did not manifest enough ST elevation to “qualify” for a STEMI at the time they were seen.
  • The clinical reality of this delayed diagnosis distorts data in the literature by overestimating the accuracy of the STEMI paradigm. This happens because some patients who are STEMI- initially — eventually do develop enough ST elevation to “qualify” as a STEMI — yet delay by a period of hours (and sometimes delay for up to a day or more!) — means significant loss of viable myocardium in these OMI+ patients, who should have been recognized and treated with PCI long before they finally developed "enough" ST elevation to qualify as a STEMI (McLaren, Meyers, Smith — J Electrocardiol 76: 39-44, 2023).
  • Another way in which the current literature is distorted in favor of the failed STEMI paradigm — is that there are no false negatives among STEMI- patients (McLaren, Meyers, Smith — J Electrocardiol 76: 39-44, 2023). This is because failure to satisfy millimeter-based STEMI criteria is erroneously accepted as the absence of acute coronary occlusion — and then misclassified as a "NSTEMI". Unfortunately, this methodological flaw perpetuates false conclusions about the overrated accuracy of STEMI criteria.

Clinicians and the STEMI Paradigm both ignore OMI Pathophysiology:
Based on cases submitted to us at Dr. Smith’s ECG Blog — the overwhelming majority of clinicians (including cardiologists) ignore the basic pathophysiology of what happens during the course of an acutely evolving OMI. Consider the following:
  • Not uncommonly — the “culprit” artery may suddenly occlude — then spontaneously reopen (sometimes prior to the patient seeking medical attention) — and on occasion, continue to open and close spontaneously a number of times. Interpreting serial ECGs that are correlated to the patient’s History — can tell us the state of the “culprit” vessel (thereby helping us greatly to understand and interpret ECGs that may not be showing frank ST elevation).
  • With acute occlusion — the patient typically develops CP (Chest Pain) — and — ST segments over the area of infarction tend to elevate, while in opposite areas of the heart, there is typically reciprocal ST depression.
  • With spontaneous reopening of the “culprit” vessel — CP decreases (or resolves) — and — ST segment deviations (elevation and depression) improve or normalize.
  • KEY Point: What spontaneously opens — may just as easily (and at any time) spontaneously reclose. It is for this reason that even if a patient who had ST elevation is now pain-free and now without ST elevation — that prompt cath with PCI is still indicated, because that patient may still at any time spontaneously reocclude.
  • CAVEAT: Even a recent STEMI may fail to show ST elevation at the time the ECG you are looking at was done IF — prior to this, there has been an ongoing process of intermittent occlusion, followed by spontaneous reopening. Remember that in between the phase of acute ST elevation and development of reperfusion T waves (with T wave inversion) — may come a phase of pseudo-normalization, in which the ECG may look surprisingly unremarkable.
  • Many of these patients with positive troponin and unremarkable or nonspecific changes on ECG at the time their tracing was recorded — are misdiagnosed as having had a "NSTEMI" — when in fact they had acute coronary occlusion. Failure to correlate symptoms with each ECG (stemming from a failure to appreciate the pathophysiology described above, of an acutely evolving OMI) is the reason for gross overuse of the term, "NSTEMI".
  • Finally, depending on WHEN the cath was done during the course of a “transient” STEMI — the “culprit” artery may not always still be occluded at the time of cardiac catheterization (ie, a less than totally occluded artery on cath might still be the "culprit" artery that caused the infarction).

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