A male in his 60s with chest pain

Case sent in by Alex Bracey, written by Pendell Meyers, edited by Smith:

A male in his 60s woke up from sleep with chest pain radiating to the back with nausea. There was no vomiting, diaphoresis, palpitations, or other associated symptoms. Vitals were within normal limits, and the exam was unremarkable, the patient appeared well.

He arrived in the ED approximately 1 hour after onset of pain. Here is the initial ECG, as well as the prior ECG on file from several months ago which was immediately available:

What is your interpretation? 

Presentation ECG interpreted alone: 
Sinus rhythm at approximately 60bpm, with normal QRS complex. No pathologic Q-waves. Without the prior ECG for comaparison, the T-waves are not clearly hyperacute. There is slight STE in V3-V5. There is 1-2mm STE in II, III, and aVF with slight J-point depression in aVL and marked, large T-wave inversion in aVL.

If you consider only the ST elevation in the inferior leads out of context, this amount and morphology would not be incompatible with a baseline ECG of a young man with high voltage and diffuse baseline ST elevation.

The ST depression and T-wave inversion in aVL, however, is NOT compatible with a baseline abnormality, and makes the ECG diagnostic of acute coronary occlusion. As has been shown through many prior cases and publications by Dr. Smith, lead aVL holds the key to understanding inferior ST elevation. ST depression in aVL should always be assumed to be due to inferior MI, unless there is: limb lead LVH, WPW, LBBB, paced rhythm, etc. If there are well-formed Q-waves, it could be due to inferior LV aneurysm as well.

For review, see Dr. Smith's study comparing the findings of lead aVL in inferior ACO versus pericarditis, showing almost perfect reliability of aVL in this scenario:
http://www.sciencedirect.com/science/article/pii/S0735675715008189

Although the study did not incorporate a cohort with normal variant inferior ST elevation, it is extremely unusual to have reciprocal ST depression in aVL in this setting.



Comparison with baseline ECG: 
The STE in the inferior leads is larger than baseline, but only by a small amount. The inferior T-waves are hyperacute in comparison to the baseline. Although there was a very small negative T-wave at baseline, the STD and large bulky negative T-waves seen on the presentation ECG are clearly new changes and must be taken to be reciprocal evidence of inferior ACO. The precordial leads are basically at baseline, and specifically there is no obvious evidence of posterior or lateral ACO accompanying the inferior ACO.


Case Continued:

The ED physicians were immediately suspicious of inferior STE and reciprocal STD and inverted T wave in aVL. They called the interventional cardiologist and began recording serial ECGs.

T=20 mins from presentation: the ST segments in III and aVF show straightening, which further confirms inferior ACO.

T=30 mins from presentation: STE in the inferior leads increasing. 

T=40 mins from presentation: STD in aVL increasing. Q-waves in III and aVF starting to increase in size and width.

Bedside echo was limited but showed no effusion, no obvious wall motion abnormality.

The initial troponin was undetectable (as you would expect for an acute coronary occlusion of less than 2 hours duration).

The patient was taken for emergent cardiac cath and found to have 100% in-stent restenosis of his prior RCA stent (this history was withheld above for educational purposes).

Here are the cath images:

The LAD appears patent. What is missing in this picture?

The right coronary artery shows occlusion of the mid-RCA stent. What is that other vessel right at the osmium? The patient has an anomalous circumflex artery which arises from the RCA rather than the left main. The LCX RCX is patent. 

The RCA is now patent after intervention.

Here are the post-cath ECGs:

STE resolving, Q waves continuing to form. aVL normalizing.

Continued normalization. No terminal T-wave inversions yet in the affected leads.

Troponin T was first positive approximately four hours after onset of symptoms, and peaked at 2.09 ng/dL approximately 10 hours after onset.

Echo later that day showed EF 59%, with severe hyperkinesis of the basal inferior wall and inferior septum.

Leads II and III from all ECGs, side by side, showing the progression of changes from baseline to ACO to post-PCI. BL= baseline. Reperfusion was not available as no more ECGs were obtained. 

The progression above shows the morphology changes of ACO over time in this case. Visualize the STE, inflating T-waves, straightening of the ST-segments, all of which contribute to the overall increasing amount of area under the curve of the ST-T segment compared to the QRS complex, which then resolves after intervention.

Side note: We believe that the ratio of "area under the curve" from the J-point to the end of the T-wave (compared to the baseline) to the overall size and width of the QRS complex is a great way to visualize and monitor the ST-T segment changes of acute coronary occlusion. This concept incorporates the subtleties of hyperacute T-waves, proportionality, and is illustrated by almost all cases of ACO on this blog. If it could be quantified by a computer (rather than qualified by the eyes of an experienced electrocardiographer as it is now), I believe it would perform much better than the standard STEMI criteria that is currently recommended by guidelines.

Learning Points:

• Lead aVL almost always holds the key to evaluating subtle inferior STE
• Serial ECGs interpreted by those who know what to look for are invaluable

Test almost all of your most important ECG rhythm interpretation skills with this case.

Sent by Anonymous, written by Meyers, edits by Smith:

A female in her 70s with history of HTN woke up around 2am with severe shortness of breath. EMS found the patient in moderate respiratory distress, hypoxemic on room air, with diffuse rales. CPAP was initiated. The prehospital ECG is unavailable but reportedly showed a wide complex regular tachycardia at around 150 bpm. 150mg amiodarone was given for presumed VT with no obvious effect.

She arrived at the ED at 2:52 AM. She had normal mental status, and was in moderate respiratory distress with diffuse rales, with respiratory rate 30/min, and initial blood pressure 129/60.  Her oxygen saturations were in the 90's. Bedside US showed severely reduced global LV function and bilateral diffuse B-lines. 

Here is her initial ECG (no prior for comparison, she's on vacation from out of town to visit family, with no other available history): 

What do you think?

At this point in the case you face some very interesting and difficult questions:

1) Is the patient stable or unstable? 

2) What do you think the ECGs show? What is the rhythm?

3) Do you think the rhythm is the cause of the symptoms? What is happening pathophysiologically with this patient?

4) Given the above, how will you proceed?


Stable or Unstable:
By the ACC/AHA definitions, the patient could be called "unstable" based upon the presence of acute heart failure (assuming you attribute the acute heart failure to the rhythm). 

Regardless, this patient has a normal mental status, is tolerating BiPAP, and is no longer hypoxic -- is she peri-arrest?? No. You have some time.

The ECG:
Regular wide complex tachycardia at ~140 bpm. The differential is then VT, SVT with abnormal conduction, Sinus tach with abnormal conduction, or any of these with or without the ever-important hyperkalemia. The QRS complex morphology is very similar to LBBB, with the only outliers being leads V5 and V6, which are negative instead of positive as would normally be seen in perfect lead placement in LBBB.  However, I and aVL do have monophasic R-waves typical of LBBB -- that V6 does not agree with I and aVL raises the suspicion of possible lead misplacement, as they normally share a common general axis.

The beginning of the QRS shows rapid depolarization, with the time from onset of QRS to the nadir of the S-wave in V1-V4 approximately 40ms (generally fast enough to suggest the use of specialized conduction system rather than the slowly creeping cell-to-cell myocardial propagation of a PVC; less than 50 ms is typical of true LBBB). With nearly perfect LBBB morphology and very fast initial QRS depolarization, this QRS complex is very likely to be created by depolarization anterogradely down the Right Bundle Branch, meaning it is either supraventricular with LBBB or originates within the Right Bundle itself (rare). 

In V1 between the QRS complexes there is a distinct large negative deflection which is likely atrial activity. Using the rhythm strip of V1 to trace this activity to other leads, you can see an "extra bump" in the T-waves in the corresponding location in leads V6 and II. This also prompts the question whether there is an extra set of P/flutter waves hidden in the QRS. It is difficult to tell. Lewis leads are an option that may help in this scenario by clarifying P-waves or revealing flutter waves.

Despite these characteristics, there is no way to exclude VT based on this ECG. Other than wide complex QRS, there are no particular features suggesting hyperK. There are no signs of ischemia superimposed onto this abnormal QRS complex with appropriately discordant ST-T segments.



The Pathophysiology:
There are at least two main competing explanations for this patient's overall clinical picture:

1) Primary acute onset SVT/VT, in the setting of unrecognized poor LV function -- acute heart failure with pulmonary edema

2) Primary acute hypertensive pulmonary edema ("SCAPE" -- Sympathetic Crashing Acute Pulmonary Edema), which is facilitated by history of hypertension with poor LV function; compensatory sinus tachycardia with baseline or rate-related aberrancy

Either explanation could also be caused by ischemia from ACS, or could result in demand-related ischemia.

Factors that may help differentiate:

• A 75-80 year old female should have a theoretical maximum sinus tachycardia around 140-150 bpm (220-75=145). This patient's rate of 139 bpm is not so fast that we should doubt sinus tach based on the rate.
• SVT is usually, but not always, faster than 140 bpm. The exception of course is atrial flutter, which is commonly 135-160 bpm. 
• A rate of 139 bpm is unlikely to cause hemodynamic compromise in a young structurally normal heart (which is not the case here)
• SCAPE usually presents with sinus tachycardia

Factors that don't help differentiate:

• Bedside US showing poor LV function and diffuse B-lines does not help differentiate these two, because poor LV fct and pulmonary edema may be associated with both. These findings are consistent with underlying heart disease that would predispose to "Sympathetic Crashing Acute Pulmonary Edema" ("SCAPE"), but they would also help explain why a primary arrhythmia with rate of 139 bpm could be so poorly tolerated.
• Blood pressure is "normal" or "pseudo-normal." Some will say she is not hypertensive enough to have SCAPE at 129/60. Of course, she has already been receiving NTG drip and BiPAP. External BP measurement is also unreliable, but even if it were the true arterial pressure, it still may not help differentiate here. When a patient with acute heart failure has "normal" or low BP, it may represent cardiogenic shock, especially in a patient who likely has HTN at baseline. 
• Cardiogenic shock may be the result of the rate, or the rate may be the appropriate expected response to the cardiogenic shock, pulmonary edema, and sympathetic response of SCAPE. 

How to Proceed with this Patient:
You have to either choose whether you think the rhythm is the cause, or proceed with management that is based on acknowledging both possibilities simultaneously. Options for this patient with wide complex regular tachycardia and some signs of hemodynamic compromise but not peri-arrest include: 

Immediate attempted intervention on the rhythm:
 - Synchronized electrical cardioversion
 - Adenosine and/or vagal maneuvers
 - Medical cardioversion (procainamide, amiodarone, etc)

These options all incur some small risk (sedation for cardioversion, very small risk of deterioration in rhythm with adenosine, hypotension or rhythm deterioration with amiodarone/procainamide), while having the potential benefits of cardioversion (if the rhythm is not Sinus Tach) and further diagnostic information for the rhythm. 

Observe the patient on NTG drip and BiPAP for a short time (~10 minutes at bedside):
Observe for improvement with the current ongoing interventions, more historical or EMR information, serial ECGs, and bedside features that help differentiate the rhythm including variation in rate, occasional dropped beats revealing flutter waves, etc. The risk of this strategy is prolonging hemodynamic insult and demand ischemia if the rhythm is the cause, and the benefit is potentially avoiding the risks of immediate interventions above if the rhythm is sinus tach and not the cause.


My (Meyers) personal belief given the information currently available in this case is that any of the above options above are reasonable if you are not able to prospectively determine that this is sinus rhythm. Electrical cardioversion in particular offers a rapid and effective diagnostic challenge in this scenario, and is very safe when performed by well-trained emergency physicians. On the other hand, the patient is not peri-arrest and the presentation sounds very much like the almost daily 3am wake-up SCAPErs that we all know so well, who improve rapidly in the first 10 minutes of arrival on NTG and NIV.

Smith comment: I think the P-waves in leads V1 and II are very clear, and that this is sinus tachycardia. I would not cardiovert. It is always tempting for emergency physicians to do something, but we must resist that temptation when doing something that makes the situation worse. Give the patient a bit of time and support, and you will see the rate slowly drift down, which does NOT happen in the other re-entrant etiologies of wide complex tachycardia, such as VT or SVT with aberrancy or atrial flutter. Only the automatic rhythm sinus tachycardia will have a slowly decreasing rate. If the patient worsens, it is time for endotracheal intubation.


Back to the Case:

BiPAP and low dose NTG drip were continued on arrival. The ED team was split on whether this represented VT or SVT with aberrancy, but nobody thought it was sinus tach and they agreed on their suspicion that the rhythm was the cause of the acute heart failure. 

The resident on the case states they watched the heart rate for approximately 15 minutes and it fluctuated only between 138 and 142 bpm. They then sedated with etomidate and attempted cardioversion, with BiPAP and NTG continued throughout. After these interventions, here is the next available ECG:

The QRS morphology is identical (confirming supraventricular origin), but the rate is now 118 bpm and the possible atrial activity seen on the initial ECG is clear and definitive now at the lower heart rate. It appears to be sinus tachycardia, and further raises the suspicion that the prior ECG also represented sinus tachycardia.

After sedation, BIPAP, and shock, the rate continued to drift down, leveled off around 105-110bpm and stayed there for the duration of the ED stay. BiPAP was weaned off about an hour later.

Here is a repeat ECG:

The QRS complex in V6 is now upright, while other leads remain identical to prior ECGs. This suggests a change in lead placement, and now the morphology is even more consistent with classic LBBB.

Unfortunately, the decrease in rate after shock also does not help differentiate SVT from SCAPE with compensatory sinus tach: If it was SVT, then the shock may have caused cardioversion with subsequent lowering of the rate; if it was SCAPE with compensatory sinus tach, then the decrease in rate could easily be explained by ongoing therapy with BiPAP, NTG drip, sedation with etomidate taking away the sympathetic surge that was feeding the positive feedback loop of SCAPE and compensatory sinus tach.

Retrospectively, I believe that SCAPE with compensatory sinus tachycardia is much more likely to have been the case here, based on the identical QRS and P-wave morphology seen later in definitive sinus rhythm.

Case Resolution, Part 1:

Troponin T rose from undetectable initially to around 0.17 ng/mL over the first couple hours then fell again. CXR showed severe pulmonary vascular congestion and pulmonary edema. A CT pulmonary embolism protocol failed to demonstrate any acute PE. She was admitted to the cardiac step down unit.

Cardiac catheterization revealed minimal CAD (10-30% stenoses in several small vessels, with no lesions deemed acute culprits) and severely reduced global systolic function with EF 29%.

During the first few days of her hospitalization she was observed to have flash pulmonary edema almost every night around 1-3am. She received escalating doses of lasix with improvement, and was put on 40mg lasix BID indefinitely. Outside records revealed only additional history of type 2 diabetes (already on metformin) which was also optimized and the patient's metformin dose was increased. She was discharged on hospital day 9. 


Case, Part II: Patient returns to ED:

But the patient apparently just won't quit teaching us about ECGs while on her vacation, and re-presented 1 week later complaining of an acute episode of chest pain with shortness of breath, with several days of preceding nausea and diarrhea. Vitals and exam were unremarkable, with no respiratory distress. Her pain had decreased just prior to her initial ECG:

What do you think? Are there signs of ischemia to explain her chest pain? Is is possible to have acute coronary occlusion with a recent "non obstructive" cath? Any non-ischemic abnormalities?

Of course it is possible to have acute coronary occlusion with a recent "non obstructive" cath. There are many etiologies, including simply a good old-fashioned plaque rupture of a lesion that was less than 30% stenotic. Not to mention the possibility of extra-luminal atherosclerosis, coronary spasm, or complications from the cath itself.

But there are no original or modified Sgarbossa criteria present. Sinus rhythm with (almost perfect) LBBB. The QRS is identical in its morphologic components compared to the prior discharge ECG, but there is still a very important difference in the QRS complex. Do you see it?

It's significantly wider. Prior QRS duration was 136-142 msec consistently during last admission. Today it's 168 msec. So that must trigger your hyperK cognitive hard stop alarm, which prompts you to then look for the other signs of hyperK. The T-waves are not dramatically more peaked than prior. The rhythm is sinus, not junctional or lower. But the PR interval is 200 msec, compared to 164 on the discharge ECG from 1 week ago. So we have a new wider QRS and new longer PR interval. This is strong but subtle evidence of hyperkalemia and must be acted upon, especially in any patient who complains of weakness. FYI, there is also new fragmented QRS, which suggests old infarction and is not associated with hyperK. This could be simply the way the QRS looks when it is stretched out, uncovering components of the QRS morphology that were not visible before. 

The hyperkalemic changes were not recognized, and no treatment was started yet.

Initial labs returned grossly abnormal:

Na = 114

K *unavailable*

Cl = 82

Bicarb = 9

Glucose = 209

Creatinine = 1.24 (baseline 0.80)

Anion Gap = 21

Troponin T = undetectable

Lactate 3.8

Another example of why you can't wait on the K level to diagnose and treat hyperK. Of course, the more important reason is that the patient may decompensate before the level comes back (if you're lucky enough for a true, non-erroneous level to ever come back). This is supported by the findings of Durfey et al in the newest retrospective cohort study of hyperkalemia which will be reviewed on this blog soon. 

Hyperkalemia was still not suspected, and there was concern that these very abnormal lab values were erroneous as the patient seemed extremely well appearing and was actually asymptomatic except for persistent vague weakness.

Repeat labs were sent for clarification, and returned at 1400 (approximately 3 hours after presentation):

Na = 118

K 7.2

Cl = 81

Bicarb = 12

Glucose = 209

Creatinine = 1.42

Anion Gap = 21

With the K now resulted, hyperkalemia was suspected and a repeat ECG was performed:

The QRS is slightly wider still, with QRS duration 178 msec. PR interval is still 200 msec. No obvious change in T-wave morphology. This is mildly worse than presentation.

At this point the patient received 2gm calcium gluconate, 500 mL lactated ringers, 40mg lasix IV, 10U insulin, and 10mg albuterol nebulizer. Kayexalate was also given later.

Repeat ECG several hours later:

QRS duration has decreased significantly, now 148 msec, which is near the baseline from last admission which was recorded with normal potassium level. PR interval has decreased 182 msec. 

Luckily she did not experience any rhythm or cardiovascular deterioration before hyperkalemia therapy, and the treatment was successful in lowering the K. Labs two hours after treatments showed K = 7.0, which is barely improved from 7.2, implying that the K would have risen even higher without such aggressive therapy. Two hours later the K was measured at 5.9, and continued to decrease from there.

She was transferred to the MICU where she continued to improve with supportive care, without the need of dialysis or other aggressive interventions. She was discharged on day 6. Her presentation and lab abnormalities were explained likely as multifactorial including:

1) initiation of lisinopril 5mg and spironolactone 25 daily (which had been titrated in tandem with lasix during last admission)

2) possible metformin-induced lactic acidosis in the setting of recently increased metformin dose, with possible inciting factors such as IV contrast loads given for CT PE scan and coronary catheterization; resulting in the high lactic acid level and associated nausea, vomiting, fatigue, dehydration with resultant decreased clearance of lisinipril/spironolactone, etc

3) possible euglycemic DKA (beta hydroxybutryate = 0.38 on initial labs)

ECG at discharge. QRS duration back down to 140msec, PR interval to 162 msec.

She did well, but this probably wasn't her idea of a relaxing vacation with her family. 

Learning Points:

1. "Stable vs unstable" per current guidelines is misleading; if the patient is not peri-arrest or in extremis, there may be more time or options than ACLS would have you believe.
2. Differentiating rhythm etiologies of wide complex tachycardias can be very difficult, but the approach to management can proceed safely without knowing the exact rhythm.
3. Make a habit of watching the leads being placed. Don't let lead misplacement make these cases even more difficult.
4. Shocking ST is better than missing VT, but in situations like this there may be a little more time to figure out all your options.
5. The importance of recognizing and treating hyperkalemia cannot be overstated.

A Very Elderly Male with a Fall and no Chest Pain

A very elderly man fell and injured his face.  There is always the possibility of syncope as the etiology of a fall, especially in an elderly person.

I was consulted on his ECG.

He had no chest pain, nor chest pain shortly before presentation.

What do you think?
This is what the treating physicians wrote:
"Syncope workup notable shows abnormal EKG with Wellens' waves in V2 and V3."

My opinion was this:  

"There are no R-waves in V2 and V3, so it is not Wellens'.  Furthermore, it can't be Wellens' syndrome even if the ECG is true Wellens' morphology: Wellens' syndrome requires that the ECG be recorded after an episode of chest pain that is now resolved.  This patient had no pain at any time."

I asked:

"Is there a previous ECG for comparison?" (No, there was not)

Continued

"The QS-waves and shallow T-wave inversion are typical of a dense old transmural anterior MI, and may represent an aneurysm of the LV anterior wall.  There could be some acute NonSTEMI superimposed on old MI, but the ECG does not make me worried for LAD acute coronary syndrome and not for acute coronary occlusion.  If these T-waves are due to acute ischemia, then the troponin will be positive.  So just get serial troponins."

Outcome

The patient ruled out for MI, with all troponins below the level of detection.

A previous echocardiogram was found, which showed
Regional wall motion abnormality-distal septum, anterior and apex, hypokinetic, large.

Bizarre T-wave Inversions in a Patient without Chest Pain

This was sent by a recent ultrasound fellow, asking for my ECG diagnosis.

He stated that it is "an acute change from previous" in an elderly smoker with hypertension, syncope, and abdominal pain.

First, there is some lead placement problem with V2, but I'm not sure exactly where it belongs!
There is ST elevation in I, II, III, aVF, V2, V3, V4, V5, and V6.
There is bizarre T-wave inversion with very long QT in all these leads
What is this?

My response:
"These are typical of Takotsubo or CNS catastrophe.
Obviously it is clinically not a CNS catastrophe, so it must be Takotsubo.

You must have done an echo?

Apical ballooning?"

His answer:

"It was Takotsubo!  Sadly I did not perform my own echo.  It was a busy shift, fewer US machines are available here, so I could not find one in that moment.  Cards came to see the patient and brought their machine down, and he had clear apical ballooning and the cath lab was activated in the middle of the night (a little begrudgingly).  The angiogram was negative."

Comment

Notice that I did not even put ACS on my differential?  These ECGs, in my experience, are not seen  in ACS.  

However, there are morphologies of Takotsubo that cannot be distinguished from STEMI.  See below.

Here are some examples:

1.

Takotsubo Stress Cardiomyopathy that mimics LAD occlusion
Cath was clean.

 2.

Central Nervous System T-waves. This one is called:

"Spiked Helmet Sign"

3.

Takotsubo
Typical Takotsubo, very unlikely to be ACS because of extremely long QT
Presented with altered mental status, hypotension, and mild chest discomfort
Peak trop 0.15
Angiogram is not necessary if there is apical ballooning.

4.

Takotsubo
This looks like and infero-posterior STEMI, but the QT is bizarrely long.
In the right clinical situation, this could actually be STEMI (not very typical though).
This patient presented with altered mental status and seizure, so the diagnosis of Takotsubo can be made without angiography or even echo.

5. Diffuse ST Elevation with Apical Ballooning: is it Takotsubo Stress Cardiomyopathy?

33 yo male with 2 days of chest pain

This was an anterior STEMI that had apical ballooning and was wrongly thought to be Takotsubo

Diffuse ST Elevation with Apical Ballooning: is it Takotsubo Stress Cardiomyopathy?

Patient had a presentation of chest pain and this ECG is much more likely to be LAD occlusion of a wraparound (type III) LAD to the inferior wall.  The only reason to think it might be Takotsubo is the apical ballooning on echo, but that is often seen with occlusion of a wraparound LAD. 

LAD Occlusion

6. Chest pain presentation: Takotsubo mimics LAD occlusion

Chest pain presentation: Takotsubo mimics LAD occlusion
Because the presentation is chest pain, an angiogram was done to be certain this is not a wraparound LAD
Cath lab activated, coronaries clean, apical ballooning on echo.

30-something with chest pain, a fragmented QRS, and ST Elevation.

A young man presented with acute chest pain.  He had no cardiac history.  He had no medical history at all.  His vital signs were normal.

Here was his first ED ECG:

What do you think?

What do you think?

Here is an old one, from 2 months prior:

What do you think?

What do you think?

Here I will show them again, with comment:

This is very abnormal.
There are deep QS-waves in V1-V3.  QR-waves in V4 and I, aVL
There is a fragmented QRS in V3, which is all but diagnostic of old infarction
There is ST depression in II, III, aVF.

This looks like a very large old MI, but it also looks acute, as the T-waves are tall, too tall to assume this is LV aneurysm (persistent STE after old MI; see this post).

If the T/QRS ratio in any of leads V1-V4 is greater than 0.36 (let's say 0.33 for both convenience and for better sensitivity), then assume there is an acute component to the MI.

Here, in V2, the T/QRS ratio = T/S ratio = 7/15 = 0.48

Furthermore, the ST depression in II, III, and aVF strongly suggests acute MI.

The previous is here:

This one had less STE in V1 and a less tall T-wave in V1.
This one did not have ST depression in lead II, III, aVF

These confirm that today the patient is having an acute MI.

There was a fragmented QRS in V4, III, and aVF and a Q-wave in V5.  The fragmented QRS on the old ECG doubly confirms old MI.

The ECGs suggest new ischemia superimposed on old anterolateral MI.

But this patient has no history of MI or anything else!

I performed this bedside echo (only parasternal short axis is shown):

This shows a clear anterior wall motion abnormality. This does not prove that the MI is acute, but in a patient with no prior history, it must be assumed that it is acute until proven otherwise.

We activated the cath lab.

Coronary angiogram was performed and revealed severe 3-vessel CAD with presumably chronic, old occlusions: mid LAD occlusion, mid circumflex occlusion, OM1 90% stenosis, distal RCA 70% stenosis.  

There was no definite culprit to open and stent.  CABG was planned.

Formal echo revealed moderate LV dysfunction (EF 37%) and multiple regional WMA with elevated filling pressures.  

The initial trop returned at 0.058 ng/mL.

Here is the troponin profile:

So there was indeed acute on chronic MI

It was thought that this was ACS on chronic CAD, with a new insult involving OM or distal RCA.

Here is the next AM ECG:

T-waves are still tall, but the inferior ST depression is resolved.

T-waves are still tall, but the inferior ST depression is resolved.

Fragmented QRS is defined as:

The RSR′ pattern includes various morphologies of the QRS interval (QRS duration less than 120 ms) with or without the Q wave. It was defined by the presence of an additional R wave (R′) or notching in the nadir of the S wave, or the presence of 2 or more R′-waves (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory.(1) 

Functional MRI confirmed:
1) decreased LV function, with calculated ejection fraction of 29%.
2)  large, old, non-viable MI in:
      a) the mid to distal anteroseptal and apical area, with wall thinning (aneurysm), consistent with chronic myocardial infarction in the distal LAD territory, and 
      b) the circumflex territory, with absence of viability, old infarct
3) basal inferolateral wall with preserved wall thickness, compatible with acute myocardial infarction. 
4) The RCA distribution showed no old infarct and viable myocardium.

So this MRI helps to determine if there is myocardium that will recover its contractility with revascularization.  Unfortunately, a large part of the heart is chronically infarcted and, in fact, aneurysmal, and will not recover.

Learning Points:

1. Young people do get acute MI and can even have severe coronary disease.

2. If there is clear old MI on the ECG, especially QS-waves, then look at the size of the T-wave.  If it is proportionally large, then it is due to acute MI, or to acute MI superimposed on old MI.  The best measure of proportionally large is a T/QRS ratio is greater than 0.33 in any of leads V1-V4. 

3. The fragmented QRS on a 12-lead ECG is a marker of a prior MI, defined by regional perfusion abnormalities, which has a substantially higher sensitivity and negative predictive value compared with the Q wave.(1)

References

1.  Mithilesh K. Das, Bilal Khan, Sony Jacob, Awaneesh Kumar, Jo Mahenthiran.   

Significance of a Fragmented QRS Complex Versus a Q-wave in Patients with 

Coronary Artery Disease.  Circulation. 2006;113:2495-2501.
Full Text link

2.  Smith SW. T/QRS Amplitude Best Distinguishes Acute Anterior MI from Anterior Left Ventricular Aneurysm. American Journal of Emergency Medicine 2005; 23(3):279-287. 

3.  Klein LR. Shroff G. Beeman W. Smith SW. Electrocardiographic Criteria to Differentiate Acute Anterior ST Elevation Myocardial Infarction from Left Ventricular Aneurysm. The American Journal of Emergency Medicine 2015; 33(6):786-790.   

4.  Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, Klocke FJ, Bonow RO, Judd RM.  The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction.  N Engl J Med 2000;343(20):1445.