Dr. Stephen W. Smith is a faculty physician in the Emergency Medicine Residency at Hennepin County Medical Center (HCMC) in Minneapolis, MN, and Professor of Emergency Medicine at the University of Minnesota. The blog presents ECGs in clinical context. In particular, prehospital and emergency department electrocardiograms (ECGs, EKGs)
I awoke in the morning and discovered a text with this ECG that was sent 6 hours prior by a former resident:
"60 year old with classic chest pain. The cath lab is occupied for the next 90 minutes. Cards says "not a STEMI". Thinking of giving lytics."
What do you think?
What do you do?
I texted back: "Sorry for delay! Was sleeping. This is OMI!! Did you give lytics? Proximal LAD. Great catch!"
There is 0.5 mm of ST Elevation in V3-V6. The T-wave in V4 is far too large for the QRS. The LAD occlusion formula would be very high due to the extremely small R-wave in V4 and QRS in V2, but without the QT I cannot calculate it exactly.
This ECG is diagnostic of LAD OMI. Occlusion Myocardial Infarction.
"Cards was right. It is not a STEMI. But the new paradigm is OMI. And that is what is important. ST Elevation is a very poor way to define myocardial infarction. We have a couple articles, one in press and one in review, that we hope will continue to prompt a change in that inadequate paradigm."
More about the case:
History: 60 yo woman w/ history of smoking but no other cardiac risks who presented to triage w/ CP. She had awoken in the morning w/ bilateral arm paresthesias and by evening called a nurse advice line who told her she may be having a heart attack and to go to ED to be evaluated.
While in her car she developed central chest pressure radiating to right shoulder about 20 min prior to arrival.
She was seen in triage where she had an ECG recorded at T0:
What do you think? (The dx can be made without looking at the baseline ECG, but it is below if you want to see it)?
A baseline ECG was available and is also attached.
Now you know the diagnosis. Acute LAD occlusion.
But the ED is a busy place: "She was hypertensive in the 190s-200s systolic but otherwise had normal VS. The ED was very busy and there were no open rooms.
"The triage ECG was shown to a physician, I don't honestly recall if it was me or one of my partners and labs and CXR were ordered by the provide in triage.
"By the time she was roomed and I assigned myself to her care it was about 1 hr later. She remained very hypertensive and had a nursing note that said she had been too anxious to get a repeat ECG and requesting an order for Ativan.
"As I was reviewing her triage information and initial ECG another pt was roomed who appeared to be critically ill with an STEMI.
"I ordered her aspirin, NTG, fentanyl, a repeat ECG and walked into the room w/ the new STEMI pt.
"As I walked into that room that lab called w/ her initial troponin value of 1.0 (LOD < 0.03). The repeat ECG I ordered is attached here as ECG #2 and was done at T+70."
Tough to interpret
"I activated the cath lab for my 2nd pt and was not able to get to her bedside until about 30 min later. Her pain and HTN were improved but she was still having active CP. I ordered more NTG and fentanyl and obtained another repeat ECG."
(ECG 3-2 at T+100 attached here).
This is the ECG at the top
"I activated the cath lab at this point.
"Our cardiologist came back down to the ED looked at the most recent ECG and said, "That's not a STEMI". I told him I disagreed and thought the patient needed emergent catheterization. He told me that regardless they would be unable to take her for at least 90 min b/c they were just starting the other case I had sent them.
"That's the point at which I texted you.
"We gave heparin, started nitro gtt and was considering giving thrombolytics but our unit coordinator was able to find an accepting cardiologist at the hospital down the street in about 5 minutes.
"She went emergently to cath (not able to figure out exact timing from my chart review) and was found to have 100% thrombotic distal LADD1 which was stented. Her troponin I there was >50 (they don't measure higher). No post cath echo yet."
The question still remains (thrombolytics?):
If there is no cath lab, are thrombolytics indicated? If I were the treating physician, I would give thrombolytics. But that is because I am so certain that this is an LAD occlusion that there is no doubt in my mind that the benefit/risk ratio of thrombolytics favors treatment.
A careful read of all the original thrombolytic literature shows that the "criteria" for giving thrombolytics are extremely inaccurate. Moreover, there is much recent literature showing that acute coronary occlusion frequently does not meet criteria. In the best study to date, published last month, ST Elevation was 35% sensitive for adjudicated STEMI (51% on serial ECGs) and 21% sensitive for OMI (30% on serial ECGs). Cardiologists were 49% sensitive for OMI.
If I diagnose an acute Coronary occlusion, regardless of "STEMI criteria" of an artery that supplies a significant myocardial territory, and the cath lab is not available, I will give thrombolytics if there are not any really serious contraindications. I am not going to recommend that everyone do it because it is very dependent on ECG and other skills to be certain of the diagnosis.
A female in her mid 60s with history of SVT and HTN presented with sudden onset 3/10 chest tightness while lying in bed in the early morning. She had nausea and diaphoresis with this event, as well as tightness between her scapula, and a loose bowel movement.
Here is her initial ECG at presentation to the ED at time zero (no prior available):
What do you think?
Sinus rhythm with significant downsloping STD in V1-V3, maximal in V1-V2. There is also subtle STE in V6 with large-area T-wave with straight/convex ST segment morphology. The T-waves in the inferior leads could be large if a prior ECG were available for comparison.
This ECG is diagnostic of acute MI of the posterior and lateral walls. The most common etiology of this condition is Occlusion MI (OMI) affecting these walls, most likely LCX or other artery in this territory including a diagonal or obtuse marginal, or RCA in some cases.
Because the current STEMI vs. NSTEMI paradigm greatly undermines the understanding and recognition of the STD of posterior OMI, this finding was not initially recognized.
Initial troponin returned slightly elevated at 0.02 ng/mL. This triggered a repeat ECG at t = 50 minutes:
The findings above are still present but slightly improved, however there is still active ischemia on this ECG. OMI is ongoing until proven otherwise.
It is unclear whether the patient still had symptoms at this time.
The patient was admitted to cardiology for NSTEMI. There was no bed in the cardiology unit, so the patient was boarding in the ED.
The second troponin returned at 0.13 ng/mL, prompting another repeat ECG at t = 2 hrs:
Further improvement but still not back to baseline.
CT aorta was negative for dissection.
She was started on heparin.
Trop #3 at t = 6 hrs 30 min = 0.41 ng/mL Trop #4 at 9 hrs = 1.13 ng/mL Trop #5 at 12 hrs = 1.17 ng/mL
Finally, a note from the admitting team states that she will be taken to cath for ongoing chest pain and rising troponins at t = 15 hrs.
Cath at t = 16 hrs:
Mid LCX 100% occlusion with TIMI 0 flow. TIMI 3 after PCI. Also noted triple vessel disease with RCA 70% and LAD mid 90%.
ECG the next day:
First five measurements were before cath, then you can see the spike as sequestered troponin in non-perfused myocardium is released after reperfusion.
STD maximal in V1-V4 with a normal QRS complex (not explained by RBBB, etc) is worrisome for posterior OMI until proven otherwise. Posterior leads may be helpful, but lack of clear elevation in the posterior leads does not obviate concern for posterior OMI when the STD on the anterior leads is diagnostic.
Ongoing ischemia (by symptoms, troponin, or ECG) despite medical management is an indication for emergent cardiac catheterization.
Written and submitted by Ashley Mogul, with edits by Pendell Meyers and Steve Smith
A man in his 40s with recent smoking cessation but otherwise no known past medical history presented due to chest pain since the previous evening. The pain has been constant and associated with vomiting and diaphoresis. He decided to present the following day when the pain had not stopped.
Here is the presenting ECG (no prior available):
What do you think?
Relevant findings include slight STE in V1 with an upright T-wave, slightly large T-waves in V2-3 (possibly hyperacute if compared to baseline), and slight reciprocal depression in II, III, aVF, V4-V6.
Meyers: This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. If clinical picture was anything compatible with ACS I would heart alert it [Ashley and I trained at Stony Brook where we call a "Heart Alert" on a situation/ECG that doesn't meet STEMI criteria but we are nevertheless worried about the need for emergent cath and emergent ACS workup] and get serial ECGs, unless I had access to an identical baseline (not likely in my opinion). Very very subtle one. What happened?"
These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog:
These findings were not initially recognized. Labs were sent and an initial Troponin I resulted at 2.14 ng/mL. At that time, the patient was given 324 mg ASA and sublingual NTG. Cardiology was called and the patient was taken for urgent catheterization with the time from ED arrival to cath about 1 hour and 45 minutes.
100% proximal LAD thrombotic occlusion with TIMI 0 flow was found and stented with excellent angiographic result and TIMI 3 flow. He also had non-acute CAD of the RCA (50%) and LCX (50%).
Before intervention with arrows demonstrating the area of occlusion.
After intervention showing the site of prior occlusion.
ECG a few hours later:
Some leads with STD previously have now resolved. The T-wave in lead V1 is no longer upright, with terminal T-wave inversion which is likely due to reperfusion.
Echo showed akinesis of the anteroseptal and anterior walls as well as the apex with an LVEF of 45%. Troponin I elevated to 3.93 ng/mL but was not trended to peak.
Not all OMI will present as STEMIs. Complete LAD occlusion can be incredibly subtle as in this case. Remember this case and the similar cases (links above) showing this patter of LAD occlusion including subtle STE with upright T-wave in V1-2 with reciprocal STD in lateral and inferior leads. When in doubt, record serial ECGs and watch out for signs of ischemia despite medical management.
A middle aged male called EMS for chest pain. EMS arrived and confirmed that the patient was complaining of chest pain and shortness of breath.
They recorded this prehospital ECG:
What do you think?
Normal QRS complex rhythm with hyperacute T-waves in V2-V6, I and aVL. Slight STE in V2 only, with significant STD and thus de-Winter pattern in V4-V6. Leads II and III show reciprocal depression of the ST segment (II) and T-wave (III). This is diagnostic of acute myocardial infarction of the anterolateral walls, with the most likely etiology being Occlusion of the LAD. In other words, this ECG shows LAD OMI.
Shortly after this ECG, the patient suffered a witnessed VF arrest. ACLS was started and continued without ROSC to the Emergency Department despite several shocks administered.
He arrived still in VF arrest. Several more shocks were administered with no change out of VF arrest. ECMO was not available at this institution, and it is the policy of interventional cardiology not to perform cath with ongoing chest compressions.
Dr. Alva correctly diagnosed "hyperacute T-waves anterolaterally" on the EMS ECG and decided to give tenecteplase as both ECMO and intra-arrest cath were not an option.
ROSC was achieved after two more rounds of CPR.
Here is his initial post-ROSC ECG:
Obvious huge anterior STEMI (obvious OMI). Assuming you correctly found the J-point!
The cath lab was activated based on this obvious STEMI, however cardiology refused and deactivated the cath lab. The reason given was that "the bleeding risk was too high" due to thrombolytics administration (this is nonsensical, see literature review at the end of this post for current applicable STEMI and combination reperfusion strategy guidelines).
Here is his ECG 60 minutes after ROSC:
New RBBB with LPFB, with persistent but improving STE in V2-V5. Decreasing STE and T-wave inversion in leads with STE implies that the artery is open, and reperfusion is in progress.
Here is his ECG 90 minutes after ROSC:
Back to normal QRS complex with continuing improvement of STE. This ECG alone would still be barely diagnostic of hyperacute T-waves in V2-V4 in the right clinical context.
Troponin T rose to 13 ng/mL and then was not further trended (peak troponin unknown).
Cardiac catheterization was performed the next day, approximately 24 hours after arrival, and showed a "hazy 80-90% mid LAD lesion" (TIMI flow not listed) which was successfully stented with resultant TIMI 3 flow and excellent angiographic result.
The patient survived.
Brief review and summary of combination reperfusion strategies:
Combination reperfusion strategies (thrombolytics plus PCI) constitute a large topic with many subcategories, however the relevant summary of our 2013 ACC/AHA STEMI Guidelines is:
Immediate transfer and PCI is recommended for: - all failed reperfusion ("rescue PCI", ST resolution less than 70%) - all high risk patients (hemodynamic / electrical instability) - all other patients may be transfered and PCI delayed for 2-3 hours after thrombolytics
Here is a relevant quote from our 2013 Guidelines:
"22.214.171.124. TRANSFER FOR ROUTINE EARLY CORONARY ANGIOGRAPHY AFTER FIBRINOLYTIC THERAPY With the introduction of coronary stents and aggressive antiplatelet therapies, there has been renewed interest in immediate and early catheterization after fibrinolytic therapy. The advantage of this approach is that it can be initiated at non–PCI-capable hospitals and affords the healthcare system additional time to arrange a “nonemergency” transfer for angiography and PCI. Routine referral for angiography with the intent to perform PCI is supported indirectly by retrospective analyses from trials of fibrinolytic therapy that suggest that patients treated with PCI during the index hospitalization have a lower risk of recurrent MI and a lower 2-year mortality rate (365–367). The results of RCTs evaluating a strategy of routine catheterization after fibrinolysis are limited by small sample sizes or surrogate endpoints and have provided mixed results. Nevertheless, most trials have demonstrated improvement in clinical outcomes in patients transferred for early catheterization, most notably in higher-risk patients (357– 362,368–371) (Table 8 and Figure 3). In the GRACIA (Grup de Analisis de la Cardiopatia Isquemica Aguda) study (362), early catheterization within 6 to 24 hours of successful fibrinolysis in stable patients was compared with an ischemia-guided approach. It resulted in improved outcomes, including a significantly lower rate of death, reinfarction, or ischemia-driven revascularization at 1 year. The TRANSFER-AMI (Trial of Routine Angioplasty and Stenting after Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction) study (360) was the largest (n=1059) of the RCTs evaluating transfer for coronary angiography and revascularization among high-risk patients and showed a significant reduction in the combined primary endpoint of death, recurrent MI, recurrent ischemia, new or worsening HF, or shock at 30 days with immediate transfer for the angiography group compared with conservative care. The findings from this and other studies indicate that high-risk patients with STEMI appear to benefit from immediate transfer for early catheterization, compared with either an ischemia-guided approach or delayed routine catheterization at 24 hours to 2 weeks (360,361). The reported benefits relate to a reduction in the incidence of recurrent infarction or ischemia, thus favoring earlier transfer and revascularization when possible.
In a meta-analysis (359) that included 7 RCTs of early transfer for catheterization, a strategy of routine early catheterization after fibrinolysis was associated with a statistically significant reduction in the incidence of death or MI at 30 days and at 1 year, without an increase in the risk of major bleeding. This meta-analysis was based on a mixture of trials that randomized high-risk patients (360,361,369) and trials that did not mandate the inclusion of high-risk subjects. A meta-regression analysis investigating the relative benefit of an invasive strategy after fibrinolysis according to the baseline risk of the enrolled patients for each trial suggested a larger proportional benefit with early catheterization and PCI in trials enrolling higher-risk patients (359)."
Although there is no specific recommendation regarding a patient who suffered out-of-hospital cardiac arrest, given lytics, and has a STEMI on their initial ROSC ECG, it is clear from the above ACC/AHA recommendations that they would intend for this patient to receive immediate angiography as soon as possible, and at the very least within 2-3 hours.
This patient had witnessed VF arrest with prehospital ECG showing subtle but definite signs of LAD OMI without STEMI criteria. No literature exists yet on this specific population, but common sense tells us that intra-arrest thrombolytics are a reasonable option when both ECMO and intra-CPR cath are not available.
You must learn to recognize these subtle signs of OMI on ECG.
Immediate PCI after thrombolytics is recommended for all high risk patients, as well as those with evidence of thrombolytic failure. For all other patients, catheterization is recommended within 2-3 hours.
A 60-something man with HTN, DM, and hyperlipidemia presented stating he had chest pain starting 48 hours prior to arrival. It was substernal, non-radiating and associated with diaphoresis.
He stated that he had the symptoms throughout the day. He didn't think much of the pain at the time and took some acetaminophen without much relief.
He had similar discomfort 1 day prior to presentation.
Apparently the pain was not continuous.
Patient denies of having any chest pain previously before this episode. No cardiac history.
The patient had no chest pain at the time of arrival.
Here was his triage ECG:
What do you think?
There is inferior ST elevation with reciprocal ST depression in aVL and I. There is ST depression in V2-V4. So this is an infero-posterior STEMI.
However, there are deep QS-waves in II, III, aVF and very tall R-waves in V1-V3. Why?
This ECG correlates perfectly with the history of 48 hours of pain, as this is a classic subacute STEMI. There is completed infarction. The tall R-waves are really Q-waves of the posterior wall as recorded from anterior leads. [For purists, these tall R-waves actually represent "lateral" infarction, (see Bayes de Luna; Journal of Electrocardiology 41 (2008) 413–418.)]
The initial troponin I returned at 11.0 ng/mL. This is a very typical initial troponin for a subacute STEMI. One expects that, after the artery is opened and the trapped troponin is released, that the post PCI troponin will be much higher.
There is significant ST Elevation.
The cath lab was activated even though symptoms were resolved. Is that necessary? Angiogram
There were 2 culprits ("co-culprits"):
1. 99% stenosis in the mid RCA with 90% long stenosis in the ostial and proximal RPDA.
2. Also 99% long stenosis in the distal Left Circumflex and 2nd obtuse marginal (OM2).
These were both opened and stented.
Post PCI ECG, next day:
There is less ST Elevation
Less STE still.
Significantly reduced LVEF (35-40%) on TTE with large inferior and inferolateral (+ apical) regional dysfunction.
A STEMI with early reperfusion may these echocardiogram findings due to reversible myocardial stunning, and then recover much or most its function over the ensuing weeks. On the other hand, in a case of completed transmural infarction, as evidenced by Q-waves (and tall R-waves which signify lateral MI, the poor function and wall motion abnormalities are likely to be permanent.
Fortunately, he did not develop any overt heart failure signs or symptoms while in the hospital, but was initiated on an ACE inhibitor.
Case 2. A 70-something y.o. male w/PMH HTN, HLD, DM2 presented with malaise. On the day prior, he experienced "crushing" chest discomfort and profuse diaphoresis between 1330-1500, accompanied by some lightheadedness. He went home to rest.
On the day of admission, he experienced occipital headache and some vague epigastric abdominal pain and two episodes of non-bloody emesis.
At triage, this was his ECG:
His family brought him to triage. He had an ECG that was concerning for STEMI, so he was immediately moved to the stabilization room.
He was chest pain free on arrival.
An ECG was recorded at triage:
This again shows inferior Q-waves and large R-waves in V2 and V3. There has already been significant infarction, completed. The "coving" (upward convexity with slight STE and inverted T-wave) in inferior leads is diagnostic of inferior MI, and with Q-waves and inverted T-waves, is typical of subacute MI.
The initial troponin I (which also turned out to be the peak) was 39.5 ng/mL.
Angiogram next morning
Because the infarct had happened the previous day, and the patient was asymptomatic at presentation, he was not taken for emergent angiogram. He was taken the next day.
There was a 100% mid circumflex subacute occlusion. It was opened and stented.
Decreased left ventricular systolic performance-mild. The estimated left ventricular ejection fraction is 40-45%. Regional wall motion abnormality-inferior. Regional wall motion abnormality-inferolateral.
Which subacute STEMI should go to the cath lab?
IF there is subacute STEMI by ECG or other criteria AND: 1. Symptoms onset is within 48 hours AND 2. There are persistent symptoms OR persistent ST Elevation
Then the patient should go for emergent angiogram/PCI.
I think it makes sense to extend this beyond 48 hours because ischemia can be so intermittent.
Schomig et al. randomized patients with: STEMI 12-48 hours of symptoms No persistent symptoms Persistent ST Elevation
The patients who received emergent PCI had significantly smaller median left ventricular infarct size (8% vs. 13%, p=0.001) measured by single-photon emission computed tomography study, as well as non-significant but underpowered decrease in the composite of death, recurrent MI, or stroke at 30 days (4.4% vs. 6.6%, p=0.37).
The first patient had no symptoms but did have persistent ST Elevation (and ST depression of posterior MI, which is reciprocal to posterior ST Elevation), so emergent angio was indicated. The wisdom of this is somewhat demonstrated by the dramatic rise in troponin after opening the artery.
The 2nd patient had BOTH resolved ST segments (no ST deviation) and no persistent symptoms, so angiography could be delayed. That emergent angio was not indicated is retrospectively supported by the absence of a rise in troponin after artery opening.
Summary: if there is EITHER symptom or ECG evidence of ongoing ischemia, subacute STEMI should go emergently to the cath lab. If neither, it is ok to wait.
Schomig, A., J. Mehilli, D. Antoniucci, G. Ndrepepa, C. Markwardt, F. Di Pede, S. G. Nekolla, et al. 2005. “Mechanical Reperfusion in Patients with Acute Myocardial Infarction Presenting More than 12 Hours from Symptom Onset: A Randomized Controlled Trial.” JAMA: The Journal of the American Medical Association 293 (23): 2865–72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15956631.
A 60-something woman presented with dyspnea. She had a history of chronic respiratory disease and hypoxia, but hypoxia was no worse than normal.
There is abnormal ST Elevation in I and aVL. Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this.
Therefore, I went to find an old ECG and it looked the same.
The patient ruled out for acute MI with all negative troponins. She had a completely normal formal echo. All previous ECGs were identical.
This was her baseline ST elevation, and I have seen this many times.
Case 2: sent by Dr. James Alva
A man in his 50s with diabetes, hypertension, and hyperlipidemia presented to the ED with chest pain and shortness of breath off and on over the past three days, with associated vomiting. He was slightly tachycardic, otherwise normal vital signs.
Here is his initial ECG (no prior available):
What do you think?
I sent this ECG with no clinical context to Dr. Smith. He commented: "by every measure, this would be RBBB with inferior and lateral STE appearing to be STEMI," but he also noted that there are several features that appear similar to false positives (like the first case above). For example, he noted a lot of what looks like STE in inferior leads in this EKG is really just the end of the QRS complex. "Nevertheless, lead II really does have STE that looks ischemic, and aVR has STD that looks ischemic." There is also much STE in V3-V6, especially V4-V6, that must be considered to be STEMI.
The first troponin (contemporary troponin T) returned at 2.00 ng/mL.
The patient was taken to the cath lab where a 100% occluded OM2 was opened.
Peak troponin was 3.21 ng/mL.
Here is his ECG just after cath:
This is minimally different from the pre-cath ECG. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon). Or it may be simply too early after cath, and subsequent ECGs may show resolution of ischemic findings.
It can be difficult to distinguish true positive vs. false positive ECG findings in RBBB in some cases like these. As a general rule, there is usually no STE in any lead in most normal RBBB. However, some baseline cases of RBBB may sometimes have STE in leads with especially large, slurred S-wave of RBBB (such as V5-6, I, and aVL). When in doubt, these findings should be assumed new until proven otherwise.
Here is an old post with some similar relevant cases:
60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting.
What do you think?
There is inferior ST elevation. Is it normal variant? Is it ischemic (OMI)? [Pericarditis? (NOT!)]
There is one finding that argues against inferior OMI (There is absence of reciprocal ST depression in aVL; STD aVL is extremely sensitive for inferior OMI; Reference: Bischof and Smith). However, there is also straightening of the inferior ST segments, and a straight ST segment in aVF; this is extremely rare in normal variant STE). _______ There is also terminal QRS distortion in II, III, aVF [absence of S-wave and J-wave (notch)]. The significance of this in inferior leads is unknown, but I suspect it is a marker for inferior OMI vs. normal variant.
There is a definite change in the inferior leads, with new ST elevation. Previously, all inferior leads had appropriate upward concavity.
The patient was given aspirin, heparin, and IV nitroglycerine.
Another ECG was recorded at 35 minutes:
It is hard to discern a difference
At this point, the first troponin I returned at 0.55 ng/mL (significantly elevated)
A D dimer was also elevated.
Another ECG was recorded at 58 minutes:
Again, no big difference.
There was concern for aortic dissection, so a CT was done and was negative.
The cath lab was activated:
Result: Thrombotic 95% stenosis at the ostium of a small LPL2 with 70% stenosis at the LPL2/LPDA bifurcation in the distal/AV groove Cx Tubular 70% stenosis in the mid-circumflex. (In other words, inferior MI with some posterior involvement). It was stented.
All ST Elevation is gone (more proof that it was all a result of ischemia)
Normal estimated left ventricular ejection fraction - 55%.
Regional wall motion abnormality-mid and basal inferior .
Troponin I peaked at 12.1 ng/mL.
1. Any inferior ST elevation may be acute OMI, but there are subtle differences between OMI on the one hand, and normal variant on the other. 2. 99% of inferior OMI are either obvious or have some amount of ST depression in aVL. But 1% may be/have neither! 3. In this case, one might say it is "obvious" MI because of a straight ST segment in aVF. A straight ST segment virtually never happens in inferior ST elevation that is NOT due to OMI (normal variant, pericarditis) 4. If a patient presents with symptoms of ACS, has an elevated troponin, and has persistent symptoms in spite of medical therapy [antiplatelet, antithrombotic, and anti-ischemic (nitro)], then cath lab activation is indicated regardless of ECG findings. 5. Compare with an old ECG. 6. Record serial ECGs.
There is no ST elevation, but V2 has a definite hyperacute T-wave. Inferior leads have a tiny bit of ST depression (this is very significant). aVL has a tiny amount of coved ST elevation in the presence of a tiny QRS. These are all very very suspicious for proximal LAD OMI.
They recorded another at 20 minutes:
Evolving anterior OMI, but with barely any ST Elevation. Look at the huge size of the T-wave in V4 relative to the R-wave. Increasing STE in aVL Increasing inferior reciprocal ST depression If you doubted LAD occlusion on the first one, there is no doubt any more. This is diagnostic
Repeat at 25 Minutes:
Further evolution. Absolutely diagnostic of acute LAD occlusion.
And another at 30 minutes:
The computer never noticed the myocardial infarction on any of these ECGs.
The patient arrived in the ED.
This is the first ED ECG (at t = 40 minutes):
Computer did not comment on acute MI. The attending physician brought this to me without any of the other ECGs and asked my opinion: With 3 seconds, I said: Acute LAD Occlusion. It is diagnostic of LAD occlusion all on its own, without even comparing to the others. This is what my partner thought also, but just wanted confirmation.
The cath lab was activated.
2nd ED ECG 60 minutes
Now there is diagnostic ST Elevation, but barely. Computer still did not comment on STEMI
A Proximal LAD occlusion was found and stented.
ECG after reperfusion
Typical Reperfusion T-waves, similar to Wellens' waves (and same pathophysiology), but different in that true Wellens' waves have preservation of R-wave. This has a QS-wave in V2 because of extensive infarction, in spite of rapid reperfusion.
QS-waves with reperfusion T-waves again
Peak trop I 85.6 ng/mL (very large OMI)
Anterior Wall Motion Abnormality
At no point in time did the computer read a STEMI
1. Acute LAD occlusion frequently does not manifest ST Elevation that meets "criteria" 2. Look for hyperacute T-waves (relative to QRS amplitude/voltage) 3. Look for any inferior ST depression, even minimal 4. Do serial ECGs.
These 2 ECGs were texted to me with the words "I think acute MI, but cardiology does not."
I believed these to be 2 serial ECGs:
ECG 1: (later found to be time zero):
Computer read: "minimal ST depression 0.025 mm" There is a small amount of STE in II, III, aVF From less than 0.5 mm - 0.5 mm. There is les than 0.5 mm of reciprocal ST depression in aVL, and an inverted T-wave
And the other: (later found to be time 24 minutes):
Now there is more STE and more STD One very telling finding are the ST segments in V2-V6: ST depression has developed in V2-V6, downsloping in V4-V6. Though minimal, this is very specific adjunctive data for ECG diagnosis of MI.
This was my response:
"It looks like a myocardial infarction...Does the patient have chest pain?"
Syncope in clinic, some vague chest pain.
Not a great history, so we looked for a previous ECG:
From within the last year No STE, no STD. This makes the others diagnostic.
Cardiology had wanted the patient to be admitted, but had not seen evidence of acute MI and had not wanted the cath lab activated.
In spite of this, my partner and I agreed the cath lab should be activated, so he did activate.
Just before transport, another ECG was recorded at time 71 min, prior to cath:
Now obvious inferior and posterior STEMI.
The patient had a ventricular fibrillation arrest before the angiogram, and was resuscitated.
Angiogram: 100% distal RCA occlusion.
After cath, next day:
Reperfusion T-wave in III. STE resolved.
Peak trop 47.4 ng/mL (large MI)
Echo: Regional wall motion abnormality-inferior, EF 60%.
1. In the original thrombolytic trials (the only placebo-controlled reperfusion trials!), especially GISSI-1, treatment of inferior MI with streptokinase did not have a measurable effect on mortality outcome. Here we see what appears to be an electrocardiographically tiny inferior MI, which only later becomes large. The patient arrests and has a very high troponin. So don't be fooled by an apparently small inferior MI. 2. Do serial ECGs. 3. Compare with a previous ECG.
4. You must push to get patients who need it to the cath lab.
5. Cardiologists have a huge amount they have to know, spanning an enormous specialty. They do not always have time to learn the subtleties of OMI on the ECG.