Three normal high sensitivity troponins over 4 hours with a "normal ECG"

Written by Willy Frick

A 46 year old man with a history of type 2 diabetes mellitus presented to urgent care with complaint of "chest burning." The documentation does not describe any additional details of the history. The following ECG was obtained.

ECG 1

What do you think?

The ECG shows sinus bradycardia but is otherwise normal. There is TWI in lead III, but this can be seen in normal ECGs. No labs were obtained. The patient was given a prescription for albuterol and a referral to cardiology.

Smith comment: No patient over 25 years of age with unexplained chest burning should be discharged without a troponin rule out, no matter how normal the ECG.  A diagnosis of "reflux" or "GERD" is never supportable without a troponin rule out.

Over the next three days, he continued to have intermittent symptoms and therefore re-presented to the emergency room. He described the symptom as chest burning with occasional radiation into his throat and jaw. He first noticed it while exercising. The day of presentation, the pain woke him from sleep, which is why he decided to come in. The following ECG was obtained around midnight. The machine read was "Normal sinus rhythm, normal ECG."

ECG 2

What do you think?

Algorithm: GE VU 360

Here is the Queen of Hearts interpretation together with lead-by-lead explainability.

She sees OMI with high confidence. 

I sent this ECG to Dr. Smith with no clinical context, and he said "posterolateral OMI." Just like the Queen of Hearts, Dr. Smith did not have access to the patient's prior ECG at the time. Here are a few selected leads shown side by side:

We can appreciate the following changes:

• Increase in the area under the curve of the T waves in II and aVF as well as V4-V6
• Newly symmetric T waves in the same leads compared to the prior tracing (which showed a more gradual up slope and more abrupt down slope)
• Similar changes in the T waves in V1-2, but inverted (as would be expected in posterior OMI)
• T wave flattening in V3
• Subtle STE in II, aVF, V4-V6 not meeting STEMI criteria
• STD in V1-2
• Relative STD in V3 (slight physiologic elevation before, now almost isoelectric)

The clinician seeing the patient documented "Sinus arrhythmia with a ventricular rate of 71 bpm. Additional findings: No ST elevation." They also documented "Reproducible chest tenderness." (Remember, reproducible chest tenderness should not reassure you in patients with high pre-test probability of OMI. Our patient already has an ECG diagnostic for OMI, so this finding is useless.) HsTnI drawn at that time was 9 ng/L (ref. < 35 ng/L). Repeat hsTnI 2 hours later was 13 ng/L, a slight increase but still within normal limits.

Smith comment: this is an otherwise healthy relatively young man.  It is unlikely, though not at all impossible, that he would have a detectable troponin.  Moreover, an change in troponin ≥ 3 leaves a substantial possibility that subsequent troponins will climb higher.  This is the Abbott hs troponin and you can only rule out MI with 99% NPV if the first trop, drawn at least 3 hours after pain onset, is ＜5 ng/L or the delta is < 3 ng/L.

The patient was given aspirin 324 mg and morphine 4 mg IV. (Morphine does not treat myocardial ischemia but does hide it!) Bedside echocardiogram is described as having "grossly normal systolic function." Due to ongoing symptoms, the patient was given a second dose of morphine 4 mg IV. Repeat ECG is shown below.

ECG 3

Now there is even more evidence of OMI, in the inferior leads and with reciprocal STD in aVL

And here is Queen of Hearts analysis:

Notice the Queen really sees that reciprocal ST depression in aVL

It is not known how the patient's symptoms compared to presentation. Compared to ECG 2, there is new STD in I/aVL which is reciprocal to the inferior changes. However, there is less symmetry and volume in the T waves which suggests that the occlusion may be spontaneously reperfusing.

A dose of NTG 0.4 mg SL is not helpful. A third hsTnI 4 hours after the first was 26 ng/L, still within normal limits. The patient has now had three high sensitivity troponins over the course of four hours that were within normal limits.

Smith comments on these troponins: 

Nevertheless, a change in troponin of this magnitude is far beyond both biological variability and the coefficient of variation.  See paragraph below for discussion of coefficient of variation.  The definition of a high sensitivity troponin assay is really high precision: it can measure the level in at least 50% of normal individuals (levels below the 99th percentile reference) with a minimum coefficient of variation of 10% (high precision) at the 99th percentile.

As for biological variability, the maximum is about 80% from day to day (MUCH less from hour to hour).  In other words, if you measure someone's troponin one day, and then the next, the largest change should be no more than 80%.  Here the first change was from 9 to 13.  This is too much for laboratory variation.  But the difference is possible for biologicial variability.  So it neither rules out myocardial injury, nor rules it out.  However, the 2nd change is from 13 to 26 ng/L.  This would be too great a change even from day to day (> 80%) and definitely too much for hour to hour.  So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardial infarction.)  However, the Definition of MI requires at least one value above the 99th percentile, which for a male is 34 ng/L (16 ng/L for women).  Thus, the patient does not (yet) get a formal diagnosis of MI and must be called unstable angina unless further troponins return above the 99th percentile. 

One must also contend with the coefficient of variation of the troponin test.  This is a measure of reproducibility of the test for the SAME sample.  If you measure twice, will it be the same?  For this test it is VERY low (very good) at 4% at the 99th percentile -- 26 ng/L, but it will not be so good at a level of 9 ng/L.  Thus, one considers a test result that varies by 2 or less to be the same result.  

Thus, these troponins are very concerning for ACS, and subsequent ones will probably be diagnostic of acute MI.

Finally, troponin rises more slowly in patients with a persistently occluded artery.  The troponin is trapped in the myocardium that is not being perfused.  One can see troponins skyrocket after PCI of an occlusion due to release.  So a patient with persistent pain and a low troponin may have a very large MI!

Case continued

Medicine was called for admission. Repeat ECG at around 9 AM is shown below. His symptoms were improving at this time, but this is not particularly helpful since he received a total of 8 mg morphine.

ECG 4

Much improved.  Reperfusion.

And Queen of Hearts explainability:

She sees no OMI with high confidence. As a brief thought experiment, imagine that the patient had waited a few hours to present, and instead this is the first ECG! It could be mistaken for normal, but in fact it is pseudonormal. In fact, all the T waves are more upright than his prior urgent care ECG. Remember that patients with OMI can have normal ECGs! Repeat hsTnI was 183 ng/L, up from 26 ng/L.

Around noon, cardiology was called for evaluation. Repeat ECG at that time is shown. The patient said his chest pain was 4/10, down from 8/10 on presentation.

ECG 5

Repeat hsTnI rose to 1417 ng/L. At this time, despite a normal appearing ECG, cardiology felt that this was a reperfusing OMI. Given ongoing symptoms, they planned immediate cardiac catheterization. Unfortunately, the cath lab was occupied with a complex structural case, so they elected to temporize with tenecteplase. He was also started on continuous heparin and nitroglycerin infusions, and was given metoprolol tartrate 25 mg, captopril 12.5 mg, and clopidogrel 300 mg.

The patient's symptoms did not resolve. A few hours later, he described only mild improvement in his symptoms from 4/10 to 3/10. Repeat ECG is shown below.

ECG 6

It is essentially unchanged from the prior tracing. On the basis of unresolved angina, cardiology decided to perform rescue PCI. His angiogram is shown below.

This is left anterior oblique cranial ("LAO crani"), best to visualize most or all of the RCA. You can identify LAO because the heart is in front of or to the left of the spine.

Here is an annotated still, showing the RCA which bifurcates into the PDA (indicating a right dominant system) and posterolateral (called "PL") branch. There is diffuse disease throughout the RCA with a severe focal lesion at the red arrow. The PDA has a subtotal occlusion very proximally near the bifurcation, indicated by the yellow arrow toward the center of the image.

This is right anterior oblique caudal ("RAO caudal"), best to visualize the LCx and its branches. You can identify RAO because the spine is off the screen to the left (and the heart is to the right of it).

Here we see the LAD, diagonal branches, the LCx, and a large OM. The LCx has diffuse disease (very lumpy, not smooth) with no severe lesions. The OM has a subtotal occlusion indicated by the purple arrow. The proximal LAD has mild disease, but the distal LAD and diagonal branches are not well evaluated in this view.

Finally, this is right anterior oblique cranial ("RAO crani"), best to visualize most of the LAD. Again, the spine is off the screen to the left, and the heart is to the right of it.

Here we see the LAD, diagonal branches, and the distal LCx. The LAD has diffuse disease with a few areas of moderate stenosis but no flow-limiting lesions. The distal LCx is seen, and the OM is not well visualized here.

From angiography, it is not clear what the culprit is. The ECG changes were inferior, posterior, and lateral. Although it is statistically unlikely, multiple plaque ruptures are possible. On intravascular ultrasound (IVUS), the mid RCA plaque was described as "cratered, inflamed, and bulky," and the OM plaque was described as "bulky with evidence of inflammation and probably ulceration." The PDA plaque was also bulky, but was not described as inflamed or ulcerated.

Evidence regarding intervention to non-culprit plaques is mixed and beyond the scope of this blog post. Heitner et al. (DOI:10.1161/CIRCINTERVENTIONS.118.007305), showed that in patients presenting with NSTEMI:

• The infarct related artery is not able to be identified in 37% of patients
• An incorrect artery is identified as the culprit in 31% of patients
• Among patients receiving PCI, 27% got revascularization only to non-culprit arteries

The recent FIRE trial by Biscaglia et al. (conducted in a different patient population) found a benefit to treatment of non-culprit lesions. One wonders whether the benefit might be mediated in part by avoidance of accidentally missing the culprit!

On the combined basis of angiography and IVUS, this patient received stents to his mid RCA, proximal PDA, and OM. While he was in lab, repeat hsTnI jumped from 1417 ng/L to above the upper limit of quantification 60,000 ng/L.

RCA and PDA before and after, arrows indicating stented regions.

OM before and after, arrow indicating stented region.

If his presenting ECG had been identified and treated emergently, his troponin may even have remained within normal limits. One final ECG was obtained the following morning.

ECG 7

And here is Queen of Hearts explainability:

Compared to the prior tracing, we now see:

• Reperfusion biphasic T waves in II and aVF (and perhaps slightly in III)
• Reperfusion biphasic or inverted T waves in V4-V6
• Reperfusion overly upright T waves in V1-3 (reciprocal to posterior TWI)
• Perhaps even subtle reperfusion T waves in I and aVL, supporting the involvement of the OM as (at least) a co-culprit

Learning points:

• NEVER give morphine to suspected ACS unless you are providing symptom relief while awaiting emergent catheterization. Medically refractory angina should have immediate angiography, but this only happens 6.4% of the time.

• Troponin can rise very slowly at first, but this should not reassure you that you have time to waste when symptoms and ECG are suggestive of OMI.

• Patients with OMI can have normal ECGs.

• A pharmacoinvasive approach (tPA followed by catheterization) is sometimes the best option even in a PCI center if the patient is unable to undergo timely angiography.

• Reperfusion findings may not manifest obviously and immediately. Sometimes it can take 12 or 24 hours to see ECG evidence of reperfusion.

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MY Comment, by KEN GRAUER, MD (1/5/2024):

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Superb and thorough discussion by Dr. Frick of today's case! I therefore decided to aim my comment as an editorial lament. We have on many occasions in Dr. Smith's ECG Blog, highlighted the downside of indiscriminate use of morphine in patients who present with new ischemic CP (Chest Pain). Striving for appropriate use of this invaluable, time-honored analgesic medication should be an EASY goal to achieve. The basic facts are these:

• Morphine works. The drug is easily titrated. It is effective in relieving symptoms. And, the drug does provide physiologic benefits for a patient with an acute cardiac event (ie, it helps to relieve anxiety as well as pain — which may decrease activation of autonomic nervous system activity — often resulting in reduced heart rate, blood pressure, venous return and myocardial oxygen demand — Murphy et al: StatPearls, 2023). And, among our chief goals as medical providers — we want to treat pain when this can be safely done!
• 
  
• The above said — Morphine clearly should not be given until the decision is made to expedite diagnostic and therapeutic cardiac catheterization. This because relief of CP in such patients leads to delayed cath (because it removes one of the major indications for prompt cath).
• But the simple fact that our patient is presenting with new, severe cardiac-sounding CP that is persistent — is of itself, clear indication for prompt diagnostic (and potentially therapeutic) cardiac catheterization.
• We know that even high-sensitivity troponin may not exceed the "normal" range for a period of hours in certain patients with acute coronary occlusion. So it is faulty reasoning to withhold morphine because you are waiting "until" troponin turns positive. 
• We also know that initial ECG(s) may be non-diagnostic despite a recent event (ie, IF an acute occlusion spontaneously opens after only a brief period of time — or if the initial ECG is obtained during the "pseudo-normalization" period). 
• 
  
• So — IF medically refractory new, cardiac-sounding CP is a recommended indication for prompt cardiac cath, even if the initial ECG(s) and troponin(s) are normal — Why are interventionists and other front-line providers committing the compound error of — i) Not performing the KEY diagnostic (and therapeutic) intervention which is prompt cardiac cath in these patients that guidelines clearly indicate as recommended? — and, ii) Leaving their patients with continued, severe CP that morphine could relieve?
• 
  
• What the "BOTTOM Line" Should Be: Providers should appreciate that persistent ischemic CP is among recommended indications for prompt cardiac cath. Delay in performing prompt cath once this indication is satisfied gains nothing — and risks loss of viable myocardium. Additional motivation for expeditiously arriving at the decision to perform prompt cath — is that you can then treat your patient's CP with as much morphine as might be needed, as well as saving significant myocardium by prompt PCI when cath confirms OMI. 

 

 

85 year old with chest pain, STEMI negative, then normal troponin but with relatively large delta: discharge?

Written by Jesse McLaren, with comments from Smith

 

An 85 year old with a history of CAD presented with 3 hours of chest pain that feels like heartburn but that radiates to the left arm. Below is the ECG. What do you think?

There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". But there are multiple other abnormalities that when combined are diagnostic of OMI and predictive of RCA occlusion:

1. sinus bradycardia, which is common in RCA occlusion
2. inferior hyperacute T waves (broad based, symmetric, tall relative to the QRS)
3. reciprocal ST depression and T wave inversion in aVL (and I), which is highly specific for inferior OMI
4. primary anterior ST depression, which is posterior OMI until proven otherwise
   

 

Here's the interpretation of the PMcardio AI trained in identifying OMI:

 

Below is the old ECG, showing the first degree AV block, delayed R wave progression and some of the precordial ST depression is old especially in the lateral leads. But the bradycardia and the infero-posterior OMI is definitely new: 

 

 Smith: this also has many abnormalities suggestive of ischemia: many leads have ischemic appearing ST depression

 

The emergency provider followed the sequential steps of the current paradigm:

1.     Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative

2.     Use troponin to rule out non-STEMI: two high sensitivity troponin I performed two hours apart were 4 and 16 ng/L, both in the normal range (upper limit of normal 16 in females and 26 in males).  The assay was Abbott Alinity, which is very similar to Abbott Architect high sensitivity troponin I.  See analysis below.

3.     Arrange follow up for chest pain patients who are “STEMI negative” with “normal troponin”: the patient was referred to outpatient cardiology

 

But 6 hours later the patient returned with recurrent chest pain: 

 

 

Again diagnostic of infero-posterior OMI, though this time it does STEMI criteria, albeit barely.  The cath lab was activated.

 

A repeat ECG was done on way to cath lab:

 

 

"STEMI negative" again. Hyperacute T waves are deflating, suggesting reperfusion but there is still reciprocal change in I/aVL and ST depression in V2, and the bradycardia is worse. On angiogram there was a 90% RCA occlusion. Troponin rose from 600 to 17,000 ng/L.

 

Discharge ECG showed resolution of bradycardia, inferior reperfusion T wave inversion, and baseline precordial ST depression.

 

 

Take home

1.     As the new ACC consensus states (citing the work of Smith/Meyers), "The application of 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, as this may represent abnormal coronary blood flow and/or vessel occlusion."

2.     Using troponin for acute coronary occlusion is like relying on a rear-view mirror to navigate a car pile-up: it shows wreckage behind you that has already happened, but can’t see the road ahead and can give false reassurance when there's a head-on collision happening in real time. It’s common for acute coronary occlusion to present with troponin in the normal range, and the initial rise can’t predict the final damage. Even if the troponin on the first visit had been higher there still would have been delayed reperfusion because it would have been diagnosed as "non-STEMI"

3.     Using risk stratification tools like HEARTS or EDACS may have avoided the initial discharge, but shouldn’t be used if the ECG is already diagnostic of OMI. (See this other post: Chest pain, a ‘normal ECG’ a ‘normal trop’, and low HEART and EDACS score: discharge home? Stress test? Many errors here.) There’s also a hazard of relying on troponins that are in the normal range but above the level of detection. As this study from Dr. Smith concluded: “measurable hs-cTnI concentrations less than or equal to sex-specific URLs have important prognostic implications. Our findings underscore the importance of recognizing cTn as a continuous variable, with the higher the cTn, the higher the probability of MACE. We caution against the clinical use of the terms normal or negative among such patients.” (Clinical features and outcomes of emergency department patients with high-sensitivity cardiac Troponin I concentrations within sex-specific reference intervals.)

Smith comments on troponin:

I've done a lot of research on high sensitivity troponin, with colleagues including Fred Apple and Yader Sandoval.  We have published over 30 articles, most on high sensitivity troponin, mostly on Abbott Architect high sensitivity troponin I.  We have found that, to rule out myocardial infarction (and we mostly only studied Non-OMI), the 2-3 hour delta should be less than 3 ng/L.  This conforms with lots of other research done by the HIGH-STEACS group in Scotland and others.   In this case, the delta was 12 ng/L. 

A delta of 12 ng/L is highly likely to indicate acute MI, even if the value is below the 99th percentile.  How is that possible?  Because the 3rd or 4th troponin is highly likely to be ABOVE the 99th percentile if the 3 hour value has risen from 4 to 16 ng/L.

See this graphic from one of our papers:

The PPV is particularly low relative to the specificity because this was a very low risk population.  In a high risk situation, the PPV would be very high. 

Notice that these deltas are REGARDLESS of the initial value.  But if the initial value is very low, as in this case, a delta of 12 early in the course of chest pain is even more significant.

Conclusion:

This patient should NEVER have been ruled out by troponin.

And the ECG findings, which are diagnostic of OMI, were also missed.

Thus, this is the protocol Fred Apple and I developed for Hennepin for the Abbott Architect:

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My Comment by KEN GRAUER, MD (3/24/2023):

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I like this case by Dr. McLaren — because it allows us to highlight a very important fault of the outdated STEMI paradigm that is all-too-often forgotten — namely, Being sure to obtain and clinically correlate at least 2 serial ECGs before you send the patient home! (with "clinical correlation" meaning lead-by-lead comparison of these serial ECGs — keeping in mind the presence and relative severity of CP at the time each ECG was obtained). 

• For ease of comparison in Figure-1 — I’ve reproduced the first 3 ECGs that were done in today’s case.

In reviewing events transpired in today's case — Obtaining a 2nd ECG and clinical correlation of symptom severity with each ECG that is recorded before discharging the patient was clearly not done on this patient's 1st visit to the ED (Emergency Department). I say this because:

• Considering that today's patient presented with new CP (Chest Pain) — the initial ECG is already diagnostic of an acute event until proven otherwise.
• As noted by Dr. McLaren, compared to the prior tracing — there are a number of new ST-T wave changes in ECG #1.
• There is no notation of whether CP was still present at the time ECG #1 was obtained (and if so, whether CP was increasing, remaining constant, or decreasing). Without this information — it is impossible to understand if the acute-looking ST-T wave changes in ECG #1 might indicate ongoing acute occlusion vs spontaneous reperfusion vs spontaneous reocclusion.
• 
  
• In addition to the above missteps — the Troponin Delta (ie, the increase in Troponin from 4-to-16 ng/L) that was interpreted as “negative” — is not a "normal" result (as discussed in detail by Dr. Smith). Therefore, even without the acute ECG changes seen in this case — full evaluation of this patient would be needed.

Challenging Aspects of Today's CASE:

Perhaps the most challenging aspect of today's case — is knowing HOW to interpret the initial ECG in light of obvious ECG abnormalities in the prior tracing. Addressing this issue raises the question of how to optimally compare serial tracings.

Regarding Comparison of Serial ECGs:

• I favor picking one of the 2 tracings that you are comparing — and systematically interpreting that tracing in its entirety before you look at the 2nd tracing.
• When comparing a current tracing with a prior ECG — we ideally should know the circumstances under which the prior tracing was done (ie, Was the patient stable and without symptoms? — or — Was the prior tracing obtained during chest pain or soon after an infarction?). Unfortunately — We do not know the circumstances under which the prior tracing in today's case was recorded.
• Are ECG parameters in the 2 tracings you are comparing similar? (ie, Is there a change in the frontal plane axis? Is R wave progression similar? Is the heart rate and rhythm in the 2 tracings the same?). Significant change in any of these parameters may result in ST-T wave changes that are not the result of ischemia or infarction.

Comparison of the 3 Tracings in Figure-1:

The first ECG we were shown in today's case is ECG #1:

• As per Dr. McLaren — there is marked sinus bradycardia and arrhythmia (ie, heart rate in the 40s) — with 1st-degree AV block (PR interval ~0.23 second).
• Regarding other intervals — the QRS is narrow — and the QTc is probably normal given the slow rate. The frontal plane axis is normal (about +70 degrees). There is no chamber enlargement.

Regarding Q-R-S-T Changes: There are artifactual undulations in the baseline of ECG #1 — but this does not prevent interpretation of this tracing. 

• There are no significant Q waves (ie, The QS in lead V1 is not abnormal per se). A tiny-but-present initial r wave is seen in lead V2 — with this R wave progressively increasing across the precordium. Transition (where the R wave becomes taller than the S wave is deep) — is slightly delayed (to between leads V3-to-V5).
• ST segments are straightened in multiple leads. In the inferior leads, this is associated with slight J-point ST elevation and clearly hyperacute T waves (that are disproportionately tall, "fat" at their peak — and wider than expected at their base).
• Reciprocal changes (ie, a mirror-image opposite ST-T wave picture) — are seen in lead aVL, and to a lesser extent in lead I. Considering how tiny QRS amplitude is in these high-lateral leads — these have to be considered acute changes until proven otherwise!
• 
  
• In the Chest Leads — ST-T wave changes are equally concerning. There is ST segment coving with T wave inversion in leads V1,V2. We see a distinct straightening with downsloping of the ST segment in leads V3-thru-V6. This is followed by terminal T wave positivity in these leads — with T waves in leads V3,V4,V5 being clearly "hypervoluminous" ("fatter"-at-their-peak and wider-at-their-base than they should be — as well as disproportionately tall in leads V3,V4 considering R wave amplitude in these leads).
• 
  
• IMPRESSION of ECG #1: As per Dr. McLaren — Especially in view of the marked bradycardia, the above ECG findings are diagnostic of acute infero-postero OMI until proven otherwise! The ST segment coving in leads V1,V2 suggests possible acute RV involvement — with acute occlusion of the RCA as the presumed "culprit" artery. Given the history of new chest pain — prompt cath is clearly indicated on the basis of this initial ECG.

Comparison of ECG #1 with the Prior Tracing:

As alluded to earlier — ECG #2 is not a normal tracing. Instead — there is ST segment straightening in multiple leads, sometimes with slight ST depression. T waves look disproportionately large in a number of leads (potentially hyperacute IF the patient was having new chest pain at this time). There is ST segment coving with shallow T wave inversion in lead aVL.

• Several differences in ECG parameters make comparison of ECG #1 with ECG #2 challenging. These include: i) The much faster heart rate in the prior tracing; and, ii) Little change in the frontal plane axis — but clearly increased QRS amplitude in the prior tracing.

Looking first at the Limb Leads: 

• Although straightening of ST segments is not a new finding in ECG #1 — there should be no doubt that the subtle ST elevation in leads III and aVF is real — since if anything, there was slight ST depression in these leads on the prior tracing. Similarly, the hyperacute T wave appearance in these inferior leads is markedly increased in ECG #1.
• Reciprocal ST-T wave depression with T wave inversion is similarly markedly accentuated in leads I and aVL of ECG #1.

In the Chest Leads:

• Although ST segment straightening with prominent T waves was present in the prior tracing — lead-by-lead comparison suggests that the T waves in leads V3-thru-V6 in ECG #1 are relatively taller (considering QRS amplitude in each respective lead) — and definitely "fatter"-at-their-peak and wider-at-their-base (ie, more hyperacute) than they were in the prior tracing.
• 
  
• IMPRESSION: In this 85-year old patient with new chest pain — comparison of the prior tracing with ECG #1 should remove all doubt about the acuity of ECG changes on this initial tracing. Prompt cath is clearly indicated — especially in view of the worrisome bradycardia in ECG #1. The patient should not have been sent home.

The Repeat ECG:

As per Dr. McLaren — the patient was unfortunately discharged from the ED — but returned 6 hours later with a recurrence of chest pain. Millimeter-based STEMI criteria are finally attained.

• Comparison of ECG #3 with the initial ECG done 6 hours earlier — and with the "baseline" (prior) tracing, provides insight into the sequence of ECG changes correlated to patient symptoms.
• There is now definite ST elevation in all 3 inferior leads in ECG #3 — in association with T-QRS-D (Terminal-QRS-Distortion — as the S wave in leads III and aVF has been lifted from the baseline) + an even greater increase in relative size of the hyperacute inferior T waves (The T waves in leads III and aVF now tower over the R waves in these leads — whereas they were approximately the same height as the R waves in ECG #1).
• Reciprocal ST-T wave depression/T wave inversion in high-lateral leads I and aVL has increased a comparable amount to the inferior lead ST elevation.
• 
  
• In contrast — ST-T wave changes look less prominent in ECG #3 than they were on the initial tracing. The evolution of sequential ECG changes during an acute ongoing event is not always homogeneous.

Figure-1: Comparison between the initial ECG in today's case — with a prior tracing — and with the repeat ECG (done 6 hours after ECG #1).

All data suggest unstable angina, but the angiogram is normal. Ken Grauer on stress testing.

A 50-something woman who has a gastric ulcer was experiencing epigastric pain for which she decided to come to the ED.  Then, approxiately one hour prior to arrival, she experienced some chest discomfort which was sharp, central, 10/10, with SOB, diaphoresis, dizziness, and nausea.  Since that time it has been intermittent.   She called 911 and still had pain when the medics arrived, but it resolved with sublingual NTG x 2.   On arrival she was chest pain free, but still had the epigastric pain.

Prehospital vitals:

We could not find the prehospital EKG.

Here is the first ED ECG, recorded while asymptomatic:

There is what appears to be ischemic ST depression in II, III, aVF, and V5, V6.  There is no other good explanation for it.

She did have a previous ECG available:

This confirms that the ST depression is new.  The precordial T-waves were more robust on the previous than they are on the present ECG.

The first high sensitivity troponin I returned at ＜ 4 ng/L (below the LoD, which all but rules out acute MI)

During her ED stay, one hour later, she had recurrent chest pain and another ECG was recorded.

Strangely, the ST depression is GONE during pain and it was present while she was asymptomatic.

I was worried about the ST depression on the first ECG, and then even more worried when I saw that it was dynamic.

The 2nd high sens trop returned at ＜ 4 ng/L, still below the LoD.  Thus, there is no acute MI.

But I know that unstable angina still exists, and I can read an EKG, so I insisted that the patient be admitted.

It turns out that she did indeed have a prehospital ECG recorded also (we could not find it at the time -- this is a common problem, as the EHR systems do not immediately sync, but we can usually find the paper printout).

Here it is:

Similar to the old ECG.

Echo

Normal

Stress Echo:

The patient exercised for 4:37 minutes on the Bruce protocol and achieved a peak heart rate of 144 bpm representing 87% of age predicted maximum heart rate and an estimated work load of 6.4 METs. Test was terminated because of fatigue, nausea and chest pain.

 

Abnormal stress echocardiogram with a moderate degree of certainty.

 

1. No echocardiographic evidence of ischemia at the cardiac workload achieved.

2. Left ventricular function normal at rest, with mild improvement with stress on most views. There was anterior wall hypokinesis with stress and in the 2 chamber view the LV EF appears to worsen with stress.

She was noted to have dynamic EKG changes with ST depressions in lateral leads that later resolved.  She underwent a stress test yesterday during which she exercised for 4.6 minutes achieving 6.4 METS and 87% of age-predicted maximal heart rate.  Her blood pressure increased from 130 mmHg systolic to 221 mmHg systolic.  Her EF was noted to be normal at rest with mild improvement with stress on most views.  There was an anterior wall hypokinesis noted with stress and it seemed the EF may have worsened in some views.  The patient did experience angina with stress.

 

She has multiple risk factors for coronary artery disease including hypertension, dyslipidemia, obesity, family history and tobacco use.  Differential diagnosis for presentation includes coronary artery disease, hypertensive heart disease, gastroesophageal reflux disease or esophageal spasm.  Given her elevated risk of coronary artery disease, it would be reasonable to rule out obstructive disease with a coronary angiogram.

Angiogram:

Normal!!

Based on these results, presentation is most likely attributed to hypertensive urgency and cardiomyopathic response to stress, given marked hypertension on presentation and hypertensive response to stress associated with symptoms of dyspnea and chest pain. It is reassuring there is no obstructive coronary artery disease. Primary prevention is of the utmost importance. 

 

BP was intermittently elevated to 214/91 in the hospital 

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MY Comment by KEN GRAUER, MD (7/2/2022):

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Excellent step-by-step discussion by Dr. Smith of this 50-something year old woman — who presented to the ED for epigastric pain and new-onset chest discomfort.

• I’ve reproduced the initial ECG in today’s case in Figure-1. For clarity — I’ve highlighted the abnormal ST segment flattening and slight-but-real J-point ST depression in the lateral chest leads (parallel BLUE lines — and RED arrows in Figure-1). Similar-looking (albeit more subtle) ST-T wave changes are seen in the inferior leads.
• As per Dr. Smith — these ECG findings have to be interpreted as ischemic until proven otherwise because i) There is no indication of LVH that might alter ST-T wave appearance (ie, if LV “strain” was present); ii) The heart rate is slow (ie, tachycardia may sometimes produce some ST depression); and, iii) This patient’s chest pain had already resolved at the time ECG #1 was obtained — so there was no plausible reason other than ischemia for these ST-T wave changes.
• As per Dr. Smith — the fact that this patient’s prior ECG did not show these ST-T wave changes confirmed the assumption of ischemia on her initial ECG (given her recent chest pain) — until proven otherwise.
• Change (ie, resolution) of the ECG abnormalities seen on ECG #1 during an episode of chest pain while in the ED — solidified the presumption of “dynamic” ST changes during chest pain (until proven otherwise).

Figure-1: I’ve labeled the abnormal ST-T wave findings in the lateral chest leads of the initial ECG in today's case. Of note — the patient's chest pain had already resolved at the time this ECG was recorded (See text).

For me — the most interesting part of today’s case — was the finding of a completely normal cardiac catheterization. MY Thoughts regarding these results were the following:

• The literature suggests more than 50 potential causes of ST-T wave abnormalities. Cardiac entities make up only a minority of these causes. Entities such as tachycardia, electrolyte disorders, hyperventilation, excess sympathetic or parasympathetic tone, emotions, temperature extremes (cold or heat, including the drinking of very cold or hot beverages), fear, pain, and “sick” patient (among others) — have all been associated with ST-T wave abnormalities on ECG.
• 
  
• Evaluation of the patient in today's case progressed appropriately. Since this patient presented to an ED with a complaint of new chest discomfort (especially in view of the above described ECG abnormalities) — 1st priority needed to be given to ruling out an acute event. Once this was done — further evaluation was in order, especially in view of the medical history of this woman in her 50s (ie, with cardiac risk factors of hypertension, hyperlipidemia, obesity, positive family history and tobacco use).
• 
  
• The patient underwent Exercise Stress Testing (EST). She was only able to exercise for 4:37 minutes on the standard Bruce Protocol. Although she attained a maximum exercise heart rate of 144/minute ( = 87% her predicted “max” for age, which indicates a satisfactory exercise effort) — the test was terminated because of fatigue, nausea and chest pain! Regardless of whether or not her EST resulted in exercise-induced ST segment changes — this is an abnormal and very concerning result! The inability of an adult in their 50s to complete at least 6 minutes on the standard Bruce Protocol — with termination of the test at least in part because of chest pain — is consistent with an “early-positive" test. This result clearly increases the post-test likelihood for coronary disease — which means additional evaluation is indicated until significant coronary disease can or cannot be ruled out.
• 
  
• NOTE #1: Assessment of exercise-induced ST segment changes will be difficult in this patient — because her initial ECG in the ED (ie, as shown in Figure-1) is not normal. The validity of assessing the ST segment response to exercise is far less specific when the pre-test ECG already shows lateral lead ST depression as seen here (ie, that in essence, already “looks” like a positive EST with horizontal ST depression).
• Confirmation of an early-positive EST — was attained by the Stress Echo finding of anterior wall hypokinesis with exercise. Cardiac catheterization was clearly indicated as the next step in evaluation.
• 
  
• NOTE #2: As per Dr. Smith — the normal cardiac cath was reassuring in ruling out obstructive coronary disease as the cause of this patient's symptoms. This narrowed down the differential diagnosis.
• 
  
• NOTE #3: This patient’s formal cardiac Echo was reported as “normal”. I would want to see specific indices of her Echo report — since this patient fits the profile for diastolic dysfunction (ie, an overweight, middle-aged or older woman with longstanding hypertension).
• A diagnosis of diastolic dysfunction could explain this patient's normal EF (Ejection Fraction) at rest — despite symptoms of fatigue and chest pain at a relatively low level of exercise. It is also consistent with her hypertensive response to exercise (ie, BP increasing from 130 mm Hg systolic — to 221 mm Hg systolic with exercise).
• In my experience of assessing Echo reports over years in primary care — mention of "diastolic dysfunction" is often not indicated on the final Echo report. Even when direct mention of "reduced compliance" parameters is not made on the Echo report — a likely diagnosis of diastolic dysfunction can be made when a patient with the "right" clinical profile manifests: i) Some degree of concentric hypertrophy without LV chamber dilatation; ii) Left atrial enlargement; and, iii) An estimated normal EF at rest.

Final Thought: Rather than "unstable angina" — I thought of this case as illustrative of appropriate evaluation for this patient who had non-coronary chest pain, probably with diastolic dysfunction. As per Dr. Smith — risk factor modification, with special attention to BP control will be KEY to her longterm outcome.