Monday, October 3, 2022

Chest pain one day after a negative stress test

 Written by Dominic Nicacio MD, with edits by Pendell Meyers and Steve Smith

A man in his early 50s with known CAD and prior stent presented to the ED via EMS one day after hospital discharge for a chest pain admission with a negative stress test. He experienced recurrent chest pain the night following his hospital discharge and called EMS. He was noted by EMS to be frankly diaphoretic. He was given sublingual nitroglycerin and full dose aspirin. EMS called in over the radio and reported patient was having chest pain with concerning findings in his anterior ECG leads. The ECG was transmitted to ED providers by EMS. 

But when we received this ECG from EMS, we had no knowledge of any of the history above, other than acute chest pain and diaphoresis.

ECG sent by EMS to ED Providers at 1752:

What do you think?

- Borderline LAFB, normal precordial R wave progression
- slight STE in aVL, 1 mm STE V1, 2-2.5 mm STE V2-V4
-baseline movement makes it hard to say if there is STD in III and aVF
- Very tall, asymmetric T waves in V2-V5, which do not have excessive area under the curve for their height; the differential for these T waves is: normal variant, hyperacute, or potentially hyperkalemic
- QT interval WNL

The differential is anterior OMI vs. normal variant vs. hyperkalemia.

Meyers note: Usually, the defining feature of hyperacute T waves is that they are abnormally fat and broad, as if being inflated with air from below, causing increased area under the curve of the ST-T waves. I teach that hyperacute T waves look like they are being inflated with air, while hyperkalemic T waves look like a tent being pitched with a pole. I also teach that hyperacute T waves resemble the US capitol building, compared to hyperkalemic T waves which look like the Eiffel tower. Hyperacute T waves are often quite tall, but not always. When I saw this ECG without any other context, I initially had a moment when I wasn't totally sure of OMI, in part because I thought these T waves weren't as fat and broad as most hyperacute T waves. So I sought out the patient's prior ECG. 

STE60V3 = 3.0 mm
QTc (computer) = 419 ms
R wave V4 = 15 mm
QRS amplitude V2 = 19.5 mm
Result = 18.01 (barely less than highly specific cutoff of 18.2) 
As with all dichotomous rules: "The closer the score is to 18.2 (e.g. between 17.7 and 18.7) the more likely it is to be a false negative or false positive"
So this result of 18.01 is not reassuring.

I was surprised to find that his most recent ECG was from yesterday (this is when we discovered that he had just been discharged):

Barely 0.5 mm STE in V2-V4, normal T waves.

Compared to this "prior" (1 day ago) ECG, the EMS ECG above is obviously diagnostic of acute LAD OMI.

Based on this, we activated the cath lab prior to patient arrival.

On arrival to the ER he was diaphoretic and uncomfortable appearing, and he was immediately rolled into a room in our ED high acuity area.

First set of vitals: BP 153/109 mm Hg, HR 67 bpm, RR 18/min, O2 96% on room air

Physical Exam:
General: Diaphoretic, uncomfortable appearing
Cardiovascular: Regular rate and rhythm, 2+ radial and DP pulses, brisk capillary refill
Respiratory: Clear to auscultation in bilateral anterior lung fields with normal work of breathing
Abdomen: Soft, non-tender
Neuro: Alert and oriented, but with paucity of speech and eyes closed unless prompted

On arrival, EMS showed us all their ECGs over 30 minutes:

Very tough! without comparison to the prior ECG, I would not be immediately certain that this was early LAD OMI.

1752 (the one they transmitted, shown above)
Interpretation above. Again, compared to prior ECG yesterday, completely diagnostic of LAD OMI.

Very similar to 1747 ECG above, meaning interval reperfusion since 1752.

Obvious STEMI(+) OMI, re-occluded since 1809. Notice the RBBB beats with concordant STE in V1-V3.

The interventionalist did a small double-take when we told him about the negative stress test yesterday, but of course agreed to take the patient immediately to lab.

While awaiting cath lab readiness, we obtained some ultrasound images:


- Normal appearing LV and RV systolic function
- No signs of acute right heart strain
- No pericardial effusion
- No obvious dissection flap in PSL view
- IVC is collapsible
- There may be an anterolateral WMA on limited PSS view

While the patient was in the cath lab, I was curious to review this admission from yesterday with chest pain, to see if this could have been predicted or prevented:


Prior Visit (one day prior):
Pt presented for sharp left chest pain lasting 20 minutes while walking at work, immediately called EMS and presented to ED within less than 1 hour of the episode, resolved upon ED evaluation. He stated that these symptoms were identical to prior MI (for which he received an LAD stent).

Here is his ECG on presentation:

I see a tiny bit of STD in V6, II, III, and aVF. Otherwise, I see no other convincing features of ischemia. There was no ECG on file before this one, nothing to compare to.

Initial high sensitivity troponin I was 6 ng/L (limit of detection less than 6, and URL for men 20 ng/L)
Second troponin was 9 ng/L.
Third troponin was 16 ng/L. NO MORE TROPONINS WERE ORDERED!!!!!!

He was admitted to medicine

Cardiology was consulted: "Episode of exertional chest pain with typical and atypical features. ECG demonstrates no acute ischemic changes. He ruled out for myocardial infarction by serial high-sensitivity troponin values....He has history of prior proximal LAD drug-eluting stent....He will be scheduled to have vasodilator stress myocardial perfusion study in the morning for evaluation of myocardial ischemia and LV systolic function. If he has recurrent chest pain or significant ischemia on stress myocardial perfusion study, he will be referred for left heart catheterization."

"Adenosine stress myocardial perfusion study performed and demonstrated normal myocardial perfusion with no ischemia or prior infarction. Gated SPECT demonstrated normal LV systolic function with no wall motion abnormalities and calculated LVEF 59%. There was no chest discomfort or diagnostic ECG changes noted during study. The patient may be discharged home with outpatient follow-up in our office in 2 to 3 weeks."

Meyers note: "ruled out for MI?" You can't just stop measuring rising troponins and declare that there was no AMI. A patient with clear ACS symptoms and rising troponin (not stable angina, suggestive of a ruptured plaque) should not be subjected to a stress test. This is risky and would never be done intentionally if providers suspected acute type 1 ACS with plaque rupture and risk of reocclusion or significant worsening of ischemia during stress. Luckily for the patient, he had no adverse events during the stress test.

Another ECG was obtained on the day of discharge:

Similar to the ECG above on initial presentation. STD in III and aVF is abnormal, but I do not see clear high lateral OMI causing reciprocal findings. Could it be the subtlest south african flag pattern? But by all accounts, the patient had no further pain at all, even during stress. And also no reperfusion (Wellens morphology), probably because the ischemia was too brief.


Clinical Course:

He was found to have a proximal LAD stent with acute thrombotic 99% in-stent restenosis, also non-culprit 90% proximal RCA, 40% distal stenosis of his LM, and otherwise mild diffuse CAD. He had PCI performed on his proximal LAD and RCA with TIMI-3 flow after intervention. Formal echocardiography after LHC showed and LVEF 58% with hypokinesis of the basal-mid inferolateral myocardium as well as the basal inferior and inferoseptal myocardium (I find this to be an unexpected area of wall motion abnormality considering the ECG and angiogram). He was started on dual antiplatelet therapy, did well post procedure, and was discharged the next day.

Troponins during our visit:

Initial ED troponin: 12 ng/L (!!! because so little time between onset of symptoms and blood draw)
none further measured (this is a significant problem in our retrospective research, because we are unable to quantify this patient's peak troponin).

Case Discussion Points:

The patient’s ECG transmitted to ED providers by EMS showed T waves that are easily confused with the peaked T waves of hyperkalemia. Sometimes hyperacute T waves have this slimmer, taller appearance, and it can be difficult to distinguish them in these cases. The new STE in anterior leads helps to understand these as hyperacute. Also, other signs of hyperkalemia were absent, as there was no P wave flattening or QRS broadening, bradycardia, new AV blocks or NSIVCD, bizarre QRS morphology, or Brugada patterning. Additionally the clinical context was clearly ACS in this case, and if there were remaining question of hyperkalemia a point of care VBG could be performed to obtain a rapid K+ level.

Comparison to prior ECGs is an absolutely critical piece of information that will help you distinguish OMIs from normal variant STE. Serial ECGs are just as important or more so.

When comparing the present ECG to a prior ECG, it is important to understand the clinical context at the time the prior ECG was captured, as it may not represent a true “baseline ECG”

Rising troponins that have not yet crossed the upper reference limit does not mean that AMI has been ruled out!

Dr. Smith's data using a different high sensitivity troponin assay showed that MI is not ruled out with 100% sensitivity unless all values are less than the URL at 9 hours.  If the first 2 troponins have a very small delta (change < 2-3 ng/L depending on the hs-cTnI assay), that tells you that the peak troponin will not continue to rise. But if the delta on the first troponins is>2 (≥ 3), that implies that the peak could continue to rise until it is greater than the URL.  Moreover, any such larger changes below the URL are real changes (that is, they are not due to biologicial variation or laboratory imprecision), and need explanation.  So, if the 9 hour troponin were still below the URL (and the ECG were not diagnostic as it is!), it would be reasonable to do further testing with a stress test (but a CT coronary angiogram is far better).  

Even high sensitivity troponins will be frequently within normal range in the first few hours of symptoms. In both presentations, even during active LAD occlusion, the initial troponins in these presentations were both within normal limits.

Do not perform stress tests on patients who may have acute type 1 ACS with ruptured plaque and risk of reocclusion or further ischemia during stress.

Stress test data obviously does not apply to patients who are in the throes of active acute coronary syndrome, as this has never been studied and shouldn't be studied. Once Acute MI has been ruled out, a negative stress test can identify patients who have a lower incidence of ACS events in the future. HOWEVER, when such patients later return to the ED with subsequent acute chest pain, then their prior negative stress test has no protective value as to whether their new chest pain is ACS or not (see references below). The pitfall is that providers may believe that the prior negative stress test has negative predictive value for ACS during the new chest pain event. 

For some more discussion about the "recent negative stress test", here is an excellent excerpt from a very relevant post a few years ago, written by Salim Rezaie for Dr. Smith's ECG Blog:

"Teaching Point #1: Uselessness of “Negative” Stress Tests
Many emergency providers have taken care of patients with true acute coronary syndrome or even primary cardiac arrest despite having had a recent “negative” stress test.  I know I have.  Overreliance on “negative” stress tests can be a common reason for misdiagnosis or delays in patient care.  It is important to remember that coronary artery disease can arise from atherosclerotic lesions that are only mildly stenotic with unstable plaques that rupture and not picked up by standard stress testing. There is a huge misconception about “negative” stress tests in the health care industry and by laypersons. The sensitivities and specificities for stress testing are often reported between 65 – 90% depending on which study you read.  Here are two trials that stress this exact fact:

Study #1 [1]: This was a retrospective chart review of 164 patients with either a “negative” stress test (122 patients) or a “normal” indeterminate stress test (42 patients) over the past 3 years.  34 patients (20.7%) from the total cohort were determined to have significant coronary artery disease in the next 30 days. Significant coronary artery disease was defined as myocardial infarction identified by positive cardiac markers, subsequent positive stress test of any type, cardiac catheterization requiring intervention, CABG, or death due to medical cardiac arrest.  Here is the troubling part…8/34 (23.5%) had their most recent stress test within 1 month prior to admission 7/34 (20.6%) had their stress test between 1 – 3 months, and 11/34 (32.4%) had their stress test between 6mo – 1 year.  Of the total cohort of 164 patients, 13 patients (7.9%) had an AMI.

Study #2 [2]: This was a prospective evaluation of 186 patients who had been referred for coronary angiography for suspected stable angina.  All patients had a normal ECG at rest, none had undergone coronary revascularization, or have diabetes mellitus. 50% of women and 25% of men who had reversible perfusion defects on radionuclide stress imaging had completely normal exercise electrocardiographic findings.  ECG stress is very insensitive.

Teaching Point #1 Bottom Line: Stress testing is used to identify critical stenosis causing obstruction to coronary blood flow, however in the setting of acute myocardial infarction the underlying pathophysiology is plaque rupture and thrombus formation.  Coronary lesions may not have been significant enough to be detected on stress testing.  Therefore a prior “negative” stress test should not be used to determine the disposition of your patients. If you think they are having ACS, then disposition them appropriately regardless of the prior “negative” stress test."

  1. Walker J et al. coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
  2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
  3. Marwick TH et al. Techniques for Comprehensive Two Dimensional Echocardiographic Assessment of left Ventricular Systolic Function. Heart 2003. PMID: 14594869
  4. Smith SW et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment elevation Myocardial Infarction. Ann Emerg Med 2012. PMID: 22520989

MY Comment by KEN GRAUER, MD (10/3/2020):
Superb and comprehensive case by Drs. Nacacio, Meyers and Smith — which emphasizes the following points.
  • Even high-sensitivity troponins will frequently be within the normal range during the first few hours after the onset of symptoms (as was the case for today's patient in both of his presentations).
  • An increase in hs-troponin — even if still "within" the upper reference range — is not a "normal" finding. In a patient with suspected ACS — an increasing hs-troponin trend mandates continued evaluation. Unfortunately this was not done in today's case.
  • Stress Testing is contraindicated during suspected ACS. If there has been spontaneous reperfusion of the "culprit" artery — then a Stress Test may result in a false-negative result. If the "culprit" vessel is still occluded — then a Stress Test could result in a much larger infarction. 

What About the Cardiac Rhythm?
Although not essential for diagnosis and management of today's case — I found the rhythm in the 4th EMS tracing to be fascinating. I focus my comment on in depth discussion of this tracing — because the KEY points are relevant to diagnosis and management of other cases that readers of Dr. Smith's Blog will encounter!
  • NOTE: What follows below includes some advanced concepts on rhythm interpretation! Are YOU up for the challenge?

Technical Note: There are a total of 8 ECGs shown in the above discussion by Drs. Nicacio, Meyers and Smith. For clarity — I have numbered these ECGs in the sequence that they are shown above:
  • I focus my comment on ECGs #1 and #6 — which I have put together and labeled in Figure-1.

  • ECG #1 — is the 1st ECG shown above in today's case. This is the 2nd prehospital ECG, which was recorded by the EMS team at 17:52.
  • ECG #1 is the same tracing as ECG #4. I chose to show ECG #1 — because the resolution of this ECG is better than the black and white version of this tracing.

  • ECG #6 — is the 4th prehospital ECG, which was recorded by the EMS team at 18:09 (or 17 minutes after ECG #1). This is the very challenging tracing that I focus my attention on.

What is going on with the rhythm in ECG #6? The complete answer to this question entails several components — each important in its own right:
  • HINT: The reason I added ECG #1 to Figure-1 — is that ECG #1 is essential for figuring out what is going on with ECG #6.
  • There are 14 beats in the long lead II rhythm strip of ECG #6. How many beats are shown in the 12-lead ECG?
  • What is the advantage of this type of ECG recording system? What might some disadvantages of this system be?
  • WHY is QRS morphology changing in ECG #6?

  • By itself — Is ECG #6 diagnostic of acute LAD OMI? IF so — WHICH beats are most definitive for this diagnosis? 

Figure-1: The 1st and 6th ECGs in today's case (which correspond to the 1st and 4th ECGs obtained prehospital by the EMS team).

MY Thoughts on the Rhythm in ECG #1:
When presented with a tracing that has both a 12-lead ECG and a long lead rhythm strip — I favor starting with the long lead rhythm strip — at least to gain a quick initial impression of the rhythm.
  • The underlying rhythm in the long lead II rhythm strip of ECG #1 is sinus — as upright P waves with a constant PR interval precede all but 2 of the beats on the tracing (ie, No P wave precedes beats #1 and 4).
  • The QRS morphology of these 2 non-sinus beats (beats #1 and 4) is different! The question is why?

KEY Points:
To assess the etiology of non-sinus beats — it is invaluable to be able to view QRS morphology in other simultaneously-recorded leads. This is EASY to do with most monitoring systems that I am familiar with — because long lead rhythms strips are typically recorded simultaneous with the 12-lead ECG above it. But this is not what is happening in ECG #1 !!!
  • Note that beat #4 is clearly not simultaneous with the 12-lead tracing above it — because no QRS complex is seen directly vertical above beat #4 in leads aVR, aVL and aVF! This means that the long lead rhythm strip was not recorded at the same time as the 12-lead tracing above it!
  • It turns out that the type of ECG recording system used in ECG #1 (and in each of the 4 prehospital tracings posted above in today's case!) shows the last 3 beats in the long lead rhythm strip ( = beats #12, 13 and 14 in ECG #1) in each of the 4 lead groups. With this type of system — only 3 beats are seen in the 12 lead ECG!

  • As I noted earlier — 12 beats are seen in the long lead rhythm strip for ECG #1, so we do have ample opportunity to get a true "feel" for the regularity of the rhythm. But we are not able to look at simultaneously-recorded leads for 9 of these 12 beats. The obvious disadvantage of this type of ECG recording system — is that we have no idea of what beat #1 looks like in leads I,II,III — nor of what beat #4 looks like in leads aVR,aVL,aVF.

To EMPHASIZE — Clinically, this does not matter for ECG #1 — because the overall rhythm is sinus, and there are only 2 non-sinus beats.
  • I interpreted beats #1 and #4 in the long lead II rhythm strip of ECG #1 as PJCs (Premature Junctional Contractions) — because they are not preceded by P waves, and the QRS of beats #1 and 4 is narrow (albeit somewhat different in morphology from sinus-conducted beats — probably due to some aberrant conduction).

  • Editorial Comment: Among the literally thousands of ECGs I've interpreted on international ECG forums over the years — I have not encountered this type of monitoring system often. I hate this system. I find it totally confusing — because it is usually not at all apparent which (if any) beats on the rhythm strip correspond to which beats on the 12-lead ECG. Simply stated — this system negates the invaluable assistance simultaneous recording of all beats on a rhythm strip can provide for determining the etiology of an arrhythmia.

  • So WHY make a big deal about this recording system? The answer to this question lies with interpretation of ECG #6, that is shown in Figure-1.

Regarding the Rhythm in ECG #6:
Starting with the long lead II rhythm strip in ECG #6 — it should be apparent that every-other-beat occurs early!
  • Once again — it should be clear that the long lead II rhythm strip in ECG #6 is not a "simultaneous" recording. Given that there are at least 3 different QRS morphologies in this long lead II (some of which manifest QRS widening) — I initially had no idea as to what these beats were. For interpretation of ECG #6 — it is important to appreciate the type of ECG recording system being used!

  • Once again — it is only the last 3 beats in the long lead rhythm strip ( = beats #12,13,14 of ECG #6) — that are shown simultaneously in the 12-lead ECG. These same last 3 beats are actually seen in each of the 12 leads! That is — While the long lead II rhythm strip in ECG #6 shows 14 beats — only 3 of these beats (#12,13,14) are seen in the 12 lead tracing.

Applying this Information to ECG #6:
The most characteristic of the widened early beats is the 2nd QRS complex in lead V1 of ECG #6. This rsR' complex, with small initial r wave — followed by S wave that descends below the baseline — finishing with a slender taller "right rabbit ear" R' deflection is absolutely characteristic of supraventricular conduction with RBBB!

  • To Emphasize — this 2nd QRS complex in lead V1 — corresponds to beat #13 in the long lead II rhythm strip! 
  • The predominantly negative QRS of beat #13 in the long lead II rhythm strip — is consistent with LAHB conduction. That LAHB conduction is present — is confirmed, because the 2nd QRS complex in both leads II and III — and the 2nd QRS complex in lead aVF all manifest LAHB morphology.
  • Additional support that a supraventricular pattern of RBBB conduction is present in ECG #6 — is forthcoming from noting that the 2nd QRS complex in lead V6 (which corresponds to beat #13 in the long lead II rhythm strip) — manifests the wide terminal S wave that is characteristic of RBBB.

Putting It All Together:
Knowing that the underlying rhythm in ECG #1 was sinus with some PJCs — helps us greatly in deducing what is probably going on in ECG #6.
  • NOTE: Interpretation of the rhythm in ECG #6 is especially difficult from a technical perspective — because there is LOTS of baseline artifact — and, because the tracing is slightly slanted and therefore distorted (so that R-R intervals and coupling intervals are not consistent).

  • That said — the overall rhythm in the long lead II of ECG #6 manifests bigeminy (ie, every-other-beat occurs earlier than expected). Since we demonstrated that beat #4 in ECG #1 was a PJC — it is most likely that every-other-beat in ECG #6 is also a PJC

  • BOTTOM LINE: The rhythm in ECG #6 is most probably Junctional Bigeminy — in which every-other-beat manifests some combination of RBBB with/without LAHB aberration (accounting for the varying width and varying morphology of beats #1,3,5,7,9,11 and 13 in the long lead II rhythm strip).

  • Relevance to Today's Case: Given that all early beats are supraventricular (ie, PJCs) — we can reliably assess ST-T wave morphology of these beats. The marked ST elevation of the 2nd QRS complex in leads V2-thru-V5 (with T-QRS-D = Terminal QRS Distortion in V2,V3,V4) — is absolutely diagnostic of acute LAD OMI.

Friday, September 30, 2022

Are all of these ST-T findings due to LVH?

 I was texted this ECG:

What do you think?  What did I text back?

The ECG is diagnostic of acute inferior-posterior OMI.  This is what I texted back:

"It is tricky because it is in the setting of left ventricular hypertrophy. And I worry the cardiologist will say that it is all LVH. But I am quite certain that it is diagnostic of acute OMI.   And if you find an old one, it will not look like this."  

"See V2: there is downsloping ST segment .  The T wave in lead III Is too big for that small S wave. There is terminal QRS distortion in aVF.  The STT in aVF is not discordant as you would expect with LVH, and there is a straight ST segment."

I sent it to Pendell, and he immediately texted back:

"Nice inferior-posterior OMI.  Likely to be missed."

The MD who sent it to me is a highly skilled, fellowship trained ED ultrasonographer.  She did a bedside echo and did not see any wall motion abnormality.

Later, I heard the history:

A 40-something male with past medical history significant only for hypertension presented to the ED with acute onset of chest pain, associated with diaphoretic and shortness of breath.

At the time of the 2nd ECG, his chest pain is improving however still present.  No similar episodes of chest pain in the past. 

He had presented through triage (not by ambulance) 1.25 hours after pain onset, and the ECG was recorded another 27 minutes later (our ED is completely overwhelmed with patients who are "boarding" in the ED and in triage is thus also overwhelmed on a daily basis)

The cath lab was activated, and a 2nd ECG was recorded 55 minutes after the first one, while waiting for the cath team:

Slight increase in the previous findings.


RCA: dominant. It supplies a medium sized RPDA (right posterior descending) and small RPLA (right posterolateral). It is thrombotically or embolically occluded in the distal segment at the bifurcation to the RPDA and RPLA.  It was successfully stented.

Formal Echo with Definity Bubble Contrast:

Decreased left ventricular systolic performance, mild; estimated left ventricular ejection fraction is 45%.

Regional wall motion abnormality- mid to distal inferior segments ("posterior" is no longer recognized as an echocardiogram wall, but this amounts to an inferior and posterior MI)

Highest hs troponin I measured (at 6 hours, after PCI -- which releases "pent up" troponin) = 24, 500 ng/L.

An ECG was recorded the next day:

Inferior Q-waves and reperfusion T-waves (inverted) with reperfusion T-waves in V2 and V3 (upright, enlarged)

1. LVH can mimic or obscure the findings of OMI
2. Not all large OMI that are evident on ECG can be seen on bedside echo.  Formal echo with bubble contrast is the only way to rule out wall motion abnormality.  It may be that Speckle Tracking could be nearly as good.

See these posts of Speckle Tracking Cardiac Echo in the ED:


MY Comment, by KEN GRAUER, MD (9/30/2022):


Today's post by Dr. Smith reinforces an important and always challenging concept — How to assess for OMI in a patient with LVH?
  • I focus my comment on a few additional aspects to those discussed above by Dr. Smith that I hope will be useful for approaching this diagnostic dilemma.
  • For clarity in Figure-1 — I've reproduced the initial ECG that was texted to Dr. Smith without the benefit of any history. For comparison — I have added the chest leads from a patient with LVH but no acute OMI (taken from the July 29, 2022 post in Dr. Smith's ECG Blog).

Figure-1: The initial ECG that was texted to Dr. Smith ( = ECG #1). Compare the chest leads of ECG #1 — with the chest leads in ECG #2 (which I've taken from the 1st case presented in Dr. McLaren's July 29, 2022 post in Dr. Smith's ECG Blog).

MY Thoughts on Today's Case:
As per Dr. Smith: Reasons why despite LVH — ECG #1 is diagnostic of acute infero-postero OMI include the following:
  • Per Dr. Smith: "There is a downsloping ST segment in lead V2"
  • Per Dr. Smith: "The T wave in lead III is too big for that small S wave. There is terminal QRS distortion in lead aVF — and the ST segment in this lead is straight".

To Dr. Smith's comments — I'd add the following:
  • The abnormal shape of the ST-T wave in lead V2 constitutes a positive Mirror Test. Even without LVH — the taller-than-expected initial R wave in lead V2 and the ST-T wave appearance in this lead instantly suggested to me that posterior OMI was likely  (Please see My Comment at the bottom of the page in our recent September 21, 2022 post — in which I review in detail my use of the Mirror Test).
  • In a normal tracing (ie, without LVH) — the ST segment in leads V2 and V3 is very often slightly elevated, with a gentle upsloping — that leads into a positive T wave. So in addition to the definitely abnormal shape of the ST-T wave in lead V2 — I immediately thought lead V3 in ECG #1 was highly suspicious of a continuation of an acute process.

  • Knowing that leads V2 and V3 were abnormal quickly convinced me that the disproportionately large (hypervoluminous) ST-T wave in lead III almost certainly represented a hyperacute T wave. And as soon as I found out that the patient in question presented with new-onset chest pain — the diagnosis of acute infero-postero OMI was assured until proven otherwise.

  • PEARL: In my experience, the fragmented QrS complex in lead III is virtually diagnostic of infarction at some point in time. Much more than a simple negative deflection (ie, Q wave) — the finding of an initial negative deflection (Q wave) — that then briefly turns positive (the small r that we see in lead III) — but which then promptly descends again (into the deep S wave) — is indicative of scar, and most often of infarction at some point in time. Given the hyperacute ST-T wave in lead III — this strongly suggests an ongoing acute process!

What Should ST-T Waves Look Like with LVH?
I've reviewed my approach to the ECG diagnosis of LVH on many occasions in Dr. Smith's ECG Blog (See My Comment in the June 20, 2020 post in Dr. Smith's Blog — among many others).
  • The presence of increased voltage on ECG without ST-T wave abnormality consistent with LV "strain" (or a "strain equivalent" pattern) — is not specific for true LV chamber enlargement. In such cases (IF there is a need to know) — Echo would be needed to distinguish between benign increased QRS amplitude on ECG vs true chamber enlargement.
  • In contrast — in a patient with the "right disease" (ie, heart failure, longstanding hypertension) — who is of a certain age (ie, younger adults often manifest increased QRS amplitude not due to chamber enlargement) — the finding of voltage criteria for LVH + ST-T wave changes of "strain" is more than 90% specific for true LV enlargement!

More about the Effect of LVH on the ECG:
Patients with marked LVH often manifest ST-T wave changes of LV "strain" in one or more leads.
  • Not all patients with Echo-proven LVH manifest LV "strain" on ECG. The Framingham Studies taught us that longterm prognosis is adversely affected when both voltage and repolarization changes of "strain" are present on ECG.
  • ST-T wave changes of LV "strain" are most commonly seen in one or more of the lateral leads (ie, in leads I, aVL; and/or V4, V5, V6). Typically — there is slow descent of the ST segment, with a more rapid rise at the end of the ST segment.
  • Some patients with LVH (especially if the frontal plane axis is vertical) — also manifest ST-T changes of LV "strain" in the inferior leads.
  • Some patients with especially deep anterior S waves — manifest the "mirror-image" picture of LV "strain" in the form of an upright ST-T wave, often with some ST elevation in these anterior leads.
  • The other major effect produced by LVH on ECG is that the increase in leftward and posterior forces forces may overshadow baseline anterior forces — with a "net result" that R wave progression is delayed (sometimes to the point of producing QS complexes in one or more anterior leads).

LV "Strain" — What About Today's Case?
The 2 ECG examples I provide in Figure-1 synthesize the above concepts:

ECG #1 in Figure-1:
  • Voltage criteria for LVH are fulfilled in multiple leads in ECG #1. These include: i) One or more limb leads with an R wave ≥20 mm; ii) R in aVL ≥12 mm; iii) Deepest S in V1,V2 + tallest R in V5,V6 ≥35; andiv) R in V6 ≥18 mm.
  • A classic LV "strain" pattern is seen in lead aVL (and to a lesser extent in lead I)To Emphasize — the slowly downsloping ST segment shape with more rapid return to baseline in lead aVL is so typical, that even with possible added effect from reciprocal OMI changes — I interpreted this ST-T wave appearance in these high-lateral leads as typical for LV "strain".
  • The patient in today's case is 40-year old man who has hypertension — therefore, he is clearly in a higher prevalence group likely to have true LVH.

  • KEY Point: Despite multiple leads showing markedly increased voltage — the chest leads in ECG #1 are remarkable because: i) There is no ST-T wave elevation in any of the anterior leads; andii) Although there is shallow T wave inversion in leads V5 and V6 — there is virtually no slowly downsloping ST segment depression in these leads (as would be expected in a patient such as this with so much other ECG evidence for true LVH with "strain").

  • BOTTOM LINE re ECG #1: Given the history of new-onset severe chest pain — the logical conclusion is that the lack of the typical LV "strain" changes in anterior and lateral chest leads is because the acute infero-postero OMI produced opposing ST-T wave changes that attenuated what we otherwise would have seen from LV "strain".

The Chest Leads in ECG #2 in Figure-1:
  • As mentioned above — the 6 chest leads in ECG #2 are from a patient with marked LVH but no acute OMI.

  • As sometimes happens — Instead of manifesting increased lateral chest lead R wave amplitude — this patient manifests exceedingly deep anterior S waves in leads V1 and especially V2 (I've outlined in RED the huge >30 mm S wave in lead V2).
  • Considering how deep the S wave in lead V2 is — the ST elevation with large, peaked T wave in this lead is not disproportionate — and was purely the result of marked LVH.
  • Although lateral chest leads V5 and V6 show no more than modest R wave amplitude — these leads nevertheless manifest an ST-T wave shape highly typical for LV "strain".

  • In CONCLUSION: Contrast a final time the appearance of ST-T waves consistent with LV "strain" in the anterior and lateral chest leads of ECG #2 — with the lack of such changes in the chest leads of ECG #1 (in which ST-T wave changes were attenuated by the opposing effect of the ongoing acute infero-postero OMI).

Sunday, September 25, 2022

A 50 year old with chest pain? What is going on? By Emre Aslanger.

Posted by Emre Aslanger, our newest blog Editor. Emre is a distinguished cardiologist in Turkey, and has published widely on the ECG in OMI and other areas.

Emre Aslanger Google Scholar Profile

A 50-year-old male with a 20 years’ history of diabetes mellitus treated with metformin only presents with chest pain that started 20 minutes ago. The pain radiates to left inner arm and is now about to resolve. His admission ECG is given below.

What do you think?

You can click on it to make it larger, but let's make it a bit easier to see here:

What do you think? (you can still click on it to make it larger)

Although the wandering baseline makes it a bit hard to interpret, ST-segment depression in inferior leads are quite evident. This should immediately urge the interpreter to look at high lateral (lead I and aVF) and anterior leads for subtle ST-segment elevation. There seems to be a subtle ST-segment elevation in aVL, which can be easily overlooked if interpreted in isolation. The ST-segment elevation in V1-3 is also highly suspicious. Moreover there is ST-segment depression in V4-6. All indicate a proximal left anterior descending artery (LAD) occlusion myocardial infarction (OMI), which sadly does not meet ST-elevation myocardial infarction (STEMI) criteria.

Despite this, the automated interpretation suggests acute STEMI!  

If you were use the LAD-normal variant STE formula (which is not advised when there is ST depression, which make normal variant all but impossible), you would get 18.89, which indicates LAD occlusion.


Smith comment: This is strange because the millimeter criteria for STEMI are not met.  How did this conventional algorithm (not a neural network) diagnose STEMI?


Smith and Meyers comment: We have posted several prior cases of STE in V1 with STD in V5, 6 due to LAD occlusion.  These seem to indicate septal MI, proximal to septal perforator (see below for other cases).  We have coined the term "Procordial Swirl" pattern based on the upward ST-segment shift usually seen in V1-V2/V3 and downward shift in V4/V5-V6, as shown in another example below. Please note: the most important mimic of the precordial swirl sign is seen in cases of LVH, which routinely have STD in lateral leads and STE in V1-V2. 

Here is another example of "Precordial Swirl":


The clinician in charge was not sure and ordered ECG and troponin follow-up.

A second ECG was taken after 15 minutes. The patient said the pain was almost resolved. 

What do you think?

The subtle ST-segment elevation in lead I, aVL and V2 continues. The ST-segments in inferolateral leads are resolving, but there is still significant ST depression especially in lead III (this should always be considered to be reciprocal to high lateral STE, whether that STE is evident or not -- it is NOT "inferior (subendocardial) ischemia"!!  . Also note the tiny Q wave in V2. Even this ECG is highly suspicious, if not diagnostic, for anterior OMI !


Smith comment

Since I started writing this blog, I have been making the point that "ST depression does not localize," meaning that ST depression in inferior, anterior, or lateral leads does NOT tell you that there is subendocardial ischemia in those leads.  This has been proven by many studies of stress ECGs.  ST depression in II, III, aVF is generally reciprocal to (often unseen) STE in aVL.

ST depression limited to Inferior leads is reciprocal to high lateral wall and represents STEMI

ST depression does not localize: 2 cases of "inferior" ST depression diagnostic of high lateral STEMI (references can be found here)


The first troponin (hsTnT) turned out to be 9 pg/dL (normal <14 pg/dL). [This is the same as the ng/L, the units used in most of the US and Europe].  As pain was then completely resolved, they decided to wait for a second troponin. 


Smith comment: If the ECG is diagnostic, as it is here, waiting for the troponin is only acceptable if BOTH ECG and symptoms have resolved


The second troponin came 69 pg/dL. A diagnosis of non-STEMI was made and a search for a PCI-capable center was commenced. 

Another ECG was taken at 4th hour.

Nearly all ST segment changes returned to normal. Note spontaneous reperfusion caused T-wave inversion in aVL and relatively bulky T-waves in inferior leads ("reciprocal reperfusion T-waves".) 

The patient was transferred to PCI-capable center. A third troponin at three hours after admission turned out to be 320 pg/dL.

Angiogram showed exactly what is expected: a thrombosed stenosis just before the first septal and diagonal artery. 

LAD lesion was successfully stented. The next day echocardiogram showed mid and apical anterior and septal dyskinesia with an ejection fraction of 40%. 


Take home messages:

  • A subtle ECG does not mean a mild, unimportant lesion.
  • Troponin lags and does not reflect the seriousness of the situation. 
  • Although this lesion is spontaneously reperfused, the risk of reocclusion is quite high and if it occurred, a significant amount of myocardium would be lost before reaching to catheter laboratory. These patients should urgently be taken to catheterization laboratory.
Research on the ECG in OMI:
If this case were in one of our studies, it would be considered a false positive EKG!!  Our methods in determining retrospectively if the artery was occluded at the time of the ECG recording require EITHER 1) TIMI 0/1 or sometimes 0/1/2 flow OR a culprit PLUS a very high troponin, which for high sensitivity Troponin T is above 1000 ng/L.  In this case, reperfusion was so fast that the peak was at 320 ng/L, and this case would be considered a false positive in one of our studies!!

See these other cases with precordial swirl sign:

A man in his 50s with "gas pain"

Comment by KEN GRAUER, MD (9/25/2022):
We welcome Dr. Emre Aslanger as our newest Associate Editor to Dr. Smith's ECG Blog! The problem he addresses in today's case relates to a "theme" well known to our readers: Recognizing subtle signs of an acute OMI that does not meet "STEMI criteria" — but which nevertheless needs prompt intervention.

For clarity and ease of comparison — I have reproduced the 3 serial tracings in today's case in Figure-1.
  • I find it easiest to appreciate the serial ECG findings highlighted by Dr. Aslanger — by lead-to-lead comparison — in association with close correlation to the clinical history.

Figure-1: Comparison of the 3 serial ECGs in today's case.

MY Thoughts on the Serial ECGs in Today's Case:
As is so often true — the History in today's case is KEY: The patient is a 50-year old man with the longstanding risk factor of diabetes. He presented to the ED with new-onset chest pain that began just 20 minutes prior to ECG #1
  • Not only does the presentation of today's patient immediately place him in a "high-prevalence" group for a likely coronary event — but the fact that he presented to the ED so soon (ie, within 20 minutes!) after the onset of symptoms: i) Makes it quite possible that any ECG findings found on his initial tracing will be subtle and not yet fully evolved; andii) Makes this patient an optimal candidate for maximum benefit from prompt intervention IF it turns out that he is in the process of evolving an acute cardiac event.

ECG #1:
The rhythm in ECG #1 is sinus arrhythmia at ~90/minute. The axis is normal at +15 degrees. The PR, QRS and QTc intervals are normal. No chamber enlargement.
  • Q waves — A tiny, narrow q wave is seen in lead aVL.
  • R Wave Progression — Transition (ie, where the R wave becomes taller than the S wave is deep) — is slightly delayed, occurring between leads V5-to-V6. Of NOTE (and potentially relevant given this patient's clinical course!) — is the fact that the R wave increases from lead V1-to-V2 — but then decreases from V2-to-V3 — increasing again in lead V4 — but inexplicably decreasing one more time from V4-to-V5. I thought this repetitive increasing-then-decreasing R wave progression strongly suggested one or more errors with chest lead electrode placement.

Regarding ST-T Wave Changes in ECG #1:
I counted ST-T wave abnormalities in no less than 11/12 leads!
  • I thought the most "eye-catching" ST-T wave abnormality was in lead V2. Although slight ST elevation is commonly seen as a normal finding in anterior leads V2 and V3 — this usually does not attain 2 mm, as seen in lead V2 of ECG #1. Even more remarkable is the disproportionately enlarged T wave in lead V2 (with respect to the QRS complex in this lead) — that in a patient with new-onset chest pain strongly suggests a hyperacute change.

  • Neighboring leads V1 and V3 also manifest taller-than-they-should-be T waves — that I interpreted as a continuation of the hyperacute change seen in lead V2.
  • Leads V4 and V5 manifest the unusual appearance of an initially downward-sloping ST segment — that evolves into disproportionate taller-and-fatter-than-they-should-be T waves.
  • This appearance of the ST-T waves in leads V4 and V5 made more sense to me when I considered anterior neighboring leads V1,V2,V3 (all of which show hyperacute T waves) — and the neighboring lateral chest lead V6, which shows primarily reciprocal ST depression (ie, leads V4 and V5 being obviously acute — manifest an intermediate picture to its anterior and lateral neighboring leads).

  • As per Dr. Aslanger — the overall picture of ECG #1 in this patient with new-onset chest pain strongly suggests acute proximal LAD OMI. This impression of proximal LAD occlusion is further supported by the subtle-but-real ST elevation in high-lateral leads I and aVL — and the reciprocal ST depression in all 3 of the inferior leads

  • QUESTION: How might the appearance of the acute ST-T wave changes seen in all 6 of the chest leads been altered — IF chest lead electrodes had been correctly placed?

  • BOTTOM LINE: Even before troponin results come back positive — this high-risk clinical presentation in today's patient with new-onset chest pain + abnormal ST-T waves in 11/12 leads, including multiple leads with hyperacute T waves — clearly justifies prompt cath after this 1st ECG.

ECG #2:
It's important to emphasize how optimal it is that the initial ECG was repeated in just 15 minutes! The need for quickly repeating the initial ECG became especially important in today's case when the patient's clinical condition changed! (ie, His chest pain had almost resolved within 15 minutes after ECG #1 was done!).
  • Interpretation of ECG #2 is best accomplished by direct lead-by-lead comparison (which is facilitated by side-by-side viewing of the first 2 ECGs in today's case, as shown in Figure-1).
  • Although subtle — there is definitely less ST elevation in lead V2 of ECG #2 — and there is no longer any ST elevation at all in lead V3. The T waves in these 2 leads clearly look less hyperacute.
  • In lead V1 — Not only has the ST elevation completely resolved in ECG #2 — but instead of the straight ST segment takeoff seen in the 1st ECG, the ST segment is now distinctly flat.
  • In the lateral chest leads (V4,V5,V6) — although T wave size has not appreciably changed — there is no longer ST segment flattening or depression in any of these leads.
  • In the inferior leads — the reciprocal ST depression previously seen in ECG #1 has now almost resolved.
  • In lead aVL — the T wave has become smaller in ECG #2.
  • The only lead not to show any ST-T wave change is lead I.

Putting It All Together:
Although only 15 minutes passed between the time that ECG #1 and ECG #2 were recorded — the patient's chest pain virtually resolved during this period and at the same time, there was improvement in ST-T wave morphology in 10/11 leads that showed abnormalities in ECG #1. This qualifies as clear evidence of "dynamic" ST-T wave changes in a patient who presented to the ED for new chest pain less than 1 hour earlier.
  • As per Dr. Aslanger — Acute proximal LAD OMI should be assumed until proven otherwise. Although relief of chest pain and resolution of acute ST-T wave changes suggests spontaneous reperfusion of the occluded vessel — the risk of reocclusion remains high.
  • Troponin may not become significantly elevated if the period of vessel occlusion is very brief (ie, when there is rapid spontaneous reperfusion). The decision to perform cardiac catheterization should not have to wait for troponin to become elevated.
  • Clinically in Today's Case Conditions could not have been better for potential optimal benefit from prompt cath with PCI of the "culprit" vessel to prevent reocclusion.

ECG #3:
To Emphasize — Prompt cath was indicated in today's case, if not immediately (after ECG #1) — then 15 minutes later after ECG #2.
  • Although ECG #3 was not needed for diagnostic purposes — interpretation of this 3rd tracing adds further support to the conclusions drawn from review of the first 2 ECGs. As per Dr. Aslanger — Chest lead ST-T wave changes have essentially normalized in ECG #3 — with reperfusion changes evident in the limb leads (ie, T wave inversion in lead aVL — and flat ST segments with bulky inferior T waves).

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