A Tough ECG, But Learn From It!

I have to tell this story from my point of view because I don't want anyone to think that the recognition of LAD occlusion was made in retrospect.  I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG.

The Case:

I was reading dozens of leftover ECGs from over a weekend and saw this one:

There are symmetric T-waves and poor R-wave progression.  There is 1 mm of ST elevation at the J-point in leads V2 and V3.  This formerly met "criteria" for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific.  It is nonspecific because normal variant ST elevation can be even much greater.  However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke.  See image below:

Slow upstroke, fast downstroke.  Asymmetric.

This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion.  So I went to look at the chart and here is the history:

This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.

This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:  

His pain continued and his ECG was read as normal.  His first troponin was normal.  He was admitted to the hospital for a "rule out."  His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml.  His ECG was repeated at this point:

This shows a well developed anterior STEMI.

The cath lab was activated and an LAD occlusion was opened.  The peak troponin I was over 100.  On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.

I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4).  The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.

To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.  

It is not a missed STEMI, but it is a missed coronary occlusion.  As you can see, the subtle findings are apparent and, with a prepared mind, can be detected.  Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation.  This is because of subtle ECG findings.  These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.


This patient had continued and ongoing pain.  If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.  

Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB.  In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve. 


References

Continuous ST Segment Monitoring

Fesmire FM, Percy RF, Bardoner JB, Wharton DR, Calhoun FB. Usefulness of automated serial 12-lead ECG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998;31(1):3-11.

Occlusion in NonSTEMI

1.  Wang T, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography Am Heart J 2009;157(4):716-23.

2.   From AM, Best PJM, Lennon RJ, Rihal CS, Prasad A. Acute Myocardial Infarction Due to Left Circumflex Artery Occlusion and Significance of ST-Segment Elevation. Amercan Journal of Cardiology 2010;106(8):1081-5.

3.   Sorajja P, Gersh BJ, Cox DA, et al. Impact of delay to angioplasty in patients with acute coronary syndromes undergoing invasive management: analysis from the ACUITY (Acute Catheterization and Urgent Intervention Triage strategY) trial. J Am Coll Cardiol 2010;55(14):1416-24.

4.     Pride YB, Tung P, Mohanavelu S, et al. Angiographic and Clinical Outcomes Among Patients With Acute Coronary Syndromes Presenting With Isolated Anterior ST-Segment Depression: A TRITON–TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) Substudy Journal of the American College of Cardiology: Cardiovascular Interventions 2010;3(8):806-11.

37 yo with 1.5 hours of burning chest pain

A 37 year old with a history of DM on metformin complained of acute onset of burning chest pain.  He called 911. They did an ECG but it is not available.  However, the medics were very concerned and brought him to the critical care area with a high suspicion of STEMI.  Here is the initial ECG:


This shows sinus rhythm and abnormal septal Q-waves in V1 and V2, with what appear to be hyperacute T-waves in V2-V4.  The computer read ***Acute MI***.  Though the early repol vs. anterior STEMI formula, strictly speaking, should not be used because there are Q-waves, if you did, you would use STE60V3 = 3.5 mm, RAV4 = 8.5 mm, and computerized QTc = 413.  This gives a value of 25.8, indicating anterior STEMI.



So this ECG would seem to support anterior STEMI.  The cath lab was about to be activated.  However, there was a previous ECG from 3 months prior:

This is nearly identical, and establishes that the first ECG is not acute STEMI.

The patient ruled out for MI by serial troponins.

Is there an old MI present?  The best way to evaluate that would be an echocardiogram.  However, none was ever done. 

Whether this patient has coronary disease is unknown.  His ECG suggests it, but does not prove it. 

When the patient had presented the first time, he had chest pain, and they were unconcerned about the ECG and they got lucky as he simply ruled out by troponins.

Lesson:

Whenever the ECG is abnormal, look for a previous one before coming to conclusions!

Formula to differentiate Normal Variant ST Elevation (Early Repolarization) from Anterior STEMI

I should have made this a post a long time ago:

Here is a link to the full text of the article in Annals of EM

It is critical to use it only when the differential is subtle LAD occlusion vs. early repol. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI. ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PR segment, in millimeters.

(1.196 x STE at 60 ms after the J-point in V3 in mm) + (0.059 x computerized QTc) - (0.326 x R-wave Amplitude in V4 in mm).


Use the calculator below. A value greater than 23.4 is quite sensitive and specific for LAD occlusion.

A Tragic Case, related to the last post

5-10 years ago, a male  in his 70's presented with weakness.  There was no chest pain.  Here is his initial ECG:

There is sinus rhythm with first degree AV block.  There is ST elevation in II, III, and aVF and reciprocal ST depression in aVL.  The computer read inferior MI.  As for precordial leads: this is from my files and I don't have all the information, but it is clearly a right sided ECG (QRS in V5, V6 is inverted from QRS in I, aVL)  What else do you see?

The cath lab was activated for STEMI.  The patient had very poor IV access and bloods were only obtained just before leaving the ED for the cath lab.  A second ECG was recorded 35 minutes later, just before transfer to the cath lab:

This one is left sided.  There is still 1st degree AVB.  There is much more ST elevation and depression.

The potassium returned at 8.4 mEq/L.  Unfortunately, the patient had a cardiac arrest on arrival  to the cath lab, before return of the potassium.  In spite of therapy for hyperkalemia, he was not resuscitated.  He never underwent an angiogram.


A closer look at the ECGs reveals the hyperkalemia: In the first ECG, the T-waves are tented and the QRS is prolonged (the computer read it as 133 ms, which is also how I read it).

Until I saw the below ECG a couple days ago (see full post here), I assumed that the patient above had BOTH hyperkalemia and coronary occlusion. This one below proves to me that hyperkalemia alone can cause inferior-posterior pseudo-STEMI.  There was no MI.

Notice that in both cases, the ST elevation is downsloping and the T-wave is inverted.  After doing a literature search, I have found no formal studies of hyperkalemia causing pseudoSTEMI, though it is a well known phenomenon.  So I can't say if this morphology is typical, or universal, or is just anecdotal.

So, in retrospect, the first patient probably did not have STEMI at all.  A close  reading of the ECG would have revealed that it is diagnostic of hyperkalemia.

History obtained later from the wife indicated that the patient had felt ill and thought that he was low on potassium (I don't know why he thought this).  He took potassium pills and overdosed.

Lessons:

1. Always consider hyperkalemia.  It is the great imitator.  Especially when the patient comlains of weakness.
2. Hyperkalemia can result in ST elevation that imitates STEMI
3. A patient who does not present with chest pain should be particularly scrutinized for other causes of the ECG abnormalities. 

Hyperkalemia and ST Segment Elevation, Post 1

A male in his 60's presented with weakness.  Here is his initial ECG.  He had no chest pain:

Probable junctional rhythm, with wide QRS (162 ms) and peaked T-waves.  Obvious hyperkalemia.  But there is also ST elevation in III and aVF, with reciprocal ST depression in I and aVL, and ST depression in V2 and V3.  Is there also an infero-posterior STEMI?

The K returned at 9.4 mEq/L.  He was treated with 5 g of calcium gluconate, 20 units of insulin and 100 ml of 50% dextrose and 100 mL of 8.4% bicarbonate.  Here is the second ECG 60 minutes later, with a concurrent K of 7.4 mEq/L:

Sinus rhythm with a normal QRS at 94 ms, with hardly any change in the serum potassium.  All the difference is in calcium administration.  The ST elevation is gone.

The troponin was normal.  All ST elevation was due to hyperkalemia.




A woman in her 40's was found down:

Sinus rhythm with wide QRS at 133 ms and obvious Peaked T-waves with obvious hyperkalemia.  But there is also significant ST elevation in V1-V3.  Is there anterior STEMI?

The K = 8.1.

After treatment with 3 g of calcium gluconate, 10 units of insulin, and 50mL of 8.4% bicarbonate (at 100 minutes), the K was measured again and was 6.5 mEq/L and this ECG was recorded:

QRS = 88 ms and ST elevation is now normal, not excessive.   


 The troponin was normal.


Lesson:

Hyperkalemia can cause ST segment shifts that mimic STEMI.  Here is a post with two more cases.  



My next post will be a similar dramatic presentation in which the diagnosis is a mystery.

K. Wang Video: the Atrial Repolarization Wave (Ta Wave)

Ta Wave (Atrial Repolarization Wave) from HQMedEd on Vimeo.

 Here is an example of the atrial repolarization wave mimicking ST depression 

4 mm of ST elevation in lead V2 (at the J-point) relative to PQ junction

A male in his 30's male complained of chest pain  while having a dental procedure, then became syncopal.  The patient is young and healthy, and thin.  He had no past medical history.  In the ED, he felt and looked fine, with normal vital signs and no chest pain.


Sinus rhythm.  High voltage.  The computerized QTc is 390 ms.  There is 4 mm of ST elevation in lead V2, and 1.5 mm in V3 (at J-point, relative to PQ junction).  There are straight ST segments in V2 and V3, which suggest STEMI.  However, the voltage is very high and the QT is relatively short.  


In this case, the ST elevation does meet the standard STEMI  "criteria" (see below) because there is 1 mm in V1 and 4 mm in V2, even though there is only 1.5 mm in V2.

Strictly speaking, the early repol vs. anterior STEMI formula should not be used because the ST segments are non-concave (i.e., straight, though not upwardly convex).  Nevertheless, if it is used, the result is 17.4, which is very low.

From reference 1: At least 2 Consecutive Leads With ST elevation of:

V1, V4-V6: 1 mm
V2, V3: for men over 40 yo: 2 mm
for men under 40 yo: 2.5 mm
for women, any age: 1.5 mm


A repeat ECG 2 hours later was unchanged.  The patient was discharged.

Diagnosis: Early repolarization with high voltage in young healthy patient with a thin chest wall.  Syncope due to vasovagal event (neurocardiogenic syncope) in dentist's chair.



1. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized  Electrocardiology. J Am Coll Cardiol. 2009;53:1003-1011.

Activate the Cath Lab?

This 52 year old African American male presented with chest pain that was not clearly typical.  Here is his ED ECG:

There is ST elevation with "coving" (upward convexity) and T-wave inversion.  

The treating physicians were appropriately worried about STEMI and activated the cath lab.  I happened by and saw the ECG and was quite certain that it was Benign T-wave Inversion (BTWI), not STEMI.  The cath lab was de-activated.  A stat echo was done and showed no wall motion abnormality.  The patient was admitted and ruled out for MI.

I was unable to fully explain why I knew this was BTWI.  But below are some factors that I have noticed about BTWI:

First, Dr. K. Wang has shown that it is by far most common in African American males.

1. There is a relatively short QT interval (QTc < 425ms).  (It was 390 ms here.)
2. The leads with T-wave inversion often have very distinct J-waves (as in V4 and V5 here).
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which evolves).
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
6. Right precordial leads often have ST elevation typical of classic early repolarization (not in this case)
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves (as here)
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude (as here)
9. II, III, and aVF also frequently have T-wave inversion.


--In this case, the ST elevation in also not high (less than the "criteria" of 2 mm in V2 and V3 in men over age 40)
--The T-waves are not upright, so if this is MI as in Wellens' syndrome, the pain should be resolved.  Acute and ongoing occlusion should have an upright T-wave.

Recognizing this requires some experience and seeing many such cases.  Here is a post with several cases of BTWI.

This ECG is pathognomonic of a life threatening condition, and you must be able to immediately recognize it

What is wrong with this patient who complains of weakness?

PR is 224 ms, QRS 177 ms.  Answer below

Answer: HyperK.  You must be able to recognize this immediately if you take care of patients in EMS or the ED.

3 grams of Calcium gluconate, 100 mEq of bicarbonate, 10 units of regular insulin, and 50g of D50 were given immediately after reading the ECG. 

Then this ECG was recorded:

QRS is now 117 ms

30 minutes later, the lab reported a K of 7.2 mEq/L.

STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician

This is a male in his 50's who was lying face down on the pavement stating that his chest was "killing him."  He stated it felt like his previous MI.  H/o 2 prior stents.  Skin was cool and clammy.  He started to vomit.  He had this prehospital ECG recorded at time zero:

No QTc is available on this.  But in this case, you don't need to do any analysis to determine if the ST elevation is normal variant or not.  The PVC provides the diagnosis: it is an RBBB configuration (originating  in the left ventricle): it has a qS pattern (not rSR' because there is an initial Q-wave typical of old or new MI) and ST elevation.  In RBBB, the ST segment should never be in the same direction as the terminal part of the QRS, as it is here.  This is ST elevation of myocardial infarction.  

A follow up ECG about 15 minutes later was nearly identical except that there was no PVC:

I have estimated the QTc as 418ms.  If you do not recognize this as STEMI, you can use the formula (STE60V3 = 2.5, QT = 418, RAV4 = 5.5) and you get 25.85 which is pretty much diagnostic of STEMI.

The medic called in an anteroseptal STEMI and transmitted the EKG.  To the chagrin of the medic, the ED MD thought that it was not a STEMI and did not activate the cath lab. 

At  t = 4 hours 15 minutes (255 minutes), the troponin returned positive and the patient was becoming hypotensive.  He was taken for PCI of a 98% occluded LAD and 100% occluded circumflex.

The patient survived.  I don't have further info, but I suspect there was substantial myocardial loss.

Lessons:

1. Listen closely to the medics.  They often know more about EKGs than you do (this message is for all emergency physicians and cardiologists).
2. Take advantage of all information.  PVC's often give you a lot of information.  See also this case and this case.
3. Use the anterior STEMI formula.  I have found since my study that it is incredibly accurate.  I use it all the time to help confirm or refute my readings.

K. Wang Video Lecture: Misleading Ventricular Pre-excitation (WPW) Findings

This lecture is also great for those who don't have a full understanding of WPW.  And this post on "WPW mimicking and obscuring MI" is very complementary.  See these other posts on other aspects of WPW.

K. Wang, MD
Clinical Professor of Medicine
Cardiology Division
University of Minnesota

med.umn.edu/cardiology/faculty/wang/home.html

Woman in her 60's with 1 hour of chest pain

A woman in her 60's with h/o DM and HTN complains of 1 hour of sudden onset chest pain.  Here is her prehospital ECG:



Sinus rhythm.  Computerized QTc is 422.  What do you think?





There is ST segment elevation (STE) at the J-point, 1.0 mm in lead V2 and 1.5 mm in lead V3, relative to the PR segment (PQ junction).  This does not meet the most commonly used "criteria" for diagnosis of anterior ST elevation MI (see below).  So is this normal variant ST elevation?  Or is it abnormal?  Is it early repolarization?  Could it be anterior STEMI?

Remember that normal variant ST elevation is less common as age increases.

The standard "criteria" are (1): At least 2 Consecutive Leads With ST elevation of:
V1, V4-V6: 1 mm  

V2, V3:   for men over 40 yo: 2 mm
                for men under 40 yo: 2.5 mm
                for women, any age: 1.5 mm 

"The threshold value for abnormal J-point elevation in V2 and V3 recommended in that part is 0.2 mV for men 40 years of age and older and 0.25 mV for men less than 40 years of age. The recommended threshold value for adult women in V2 and V3 is 0.15 mV. The threshold recommended for abnormal J-point elevation for men and women in all other standard leads is 0.1 mV. These threshold values appear to be an appropriate compromise for practical clinical use in the evaluation of ST elevation."

We found these criteria to be very insensitive and nonspecific in differentiating subtle anterior STEMI from early repol.  However, if we use the formula for differentiating early repolarization from subtle LAD occlusion (see sidebar of this blog for excel applet), and use these numbers: 
1. STE at 60 ms after the J-point in lead V3 = 2.0 mm, 
2. QTc = 422 ms, and 
3. R-wave amplitude in lead V4 = 4mm, 
 --we get a value of  25.99 (greater than 23.4 correlates highly with LAD occlusion).  It is the relatively long QT interval and the low R-wave amplitude which make this likely to be STEMI.

Case continued:

The medics (and computer) interpreted the ECG as normal and brought the patient to the ED without alerting me.  By protocol, an ED ECG was recorded and this ECG was brought to me:

Now there is slightly more ST elevation, the QTc is slightly longer at 427ms, and lateral precordial T-waves are larger.

This is the first ECG that I saw and it is clearly diagnostic of LAD occlusion, with anterolateral STEMI.  I immediately activated the cath lab.  The formula value for this is now 27.2 (STE60V3=2.5, QTc=427, RAV4=3)

While waiting for the cath lab, we did a bedside echo and the anterior wall motion abnormality was very subtle and would not have helped with the diagnosis.

She went to the cath lab and had an ostial occlusion of a type III (wraparound) LAD to the inferior wall.  There was a large ramus intermedius (artery between the LAD and circ which functions like a large first diagnonal) which supplied the lateral wall.

Subsequent formal echo with Definity contrast showed an akinetic distal septum anterior and apex as well as akinetic distal inferior wall, so there was a dense MI.  The peak troponin was 257 ng/mL, so this was a large anterior MI.

The inferior wall involvement does not show on the ECG and I find this difficult to explain.

Here is the ECG 2 days later:

Interestingly, the T-wave inversion is consistent with only anterolateral (not antero-infero-lateral) MI.  And T inversions in I and aVL are present in spite of absence of clear evidence of injury on the previous ECGs.

Reference:


1. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized  Electrocardiology. J Am Coll Cardiol. 2009;53:1003-1011.

Brugada pattern induced by tricyclic antidepressant

A 31 year old male presented obtunded after a suspected intentional overdose with amitryptiline.  He was intubated, and this ECG was recorded:

Time zero: QRS duration = 162 ms, QRS axis = 147.  There is a wide QRS and large R-wave in lead aVR, typical of amitryptiline toxicity.  But the ECG also looks like classic type I Brugada pattern, in V1 and V2 but especially in V2: there is an rSR' with downsloping ST elevation.

After immediate intravenous bicarbonate, this ECG was recorded 14 minutes later:

Time 14 minutes: after 100 ml of 8.4% bicarbonate: QRS = 146 ms.  The QRS has narrowed slightly.  The Brugada pattern is still present


At 2 hours, after more bicarbonate, this was recorded:

Time = 2 hours, after more bicarbonate: QRS = 117 ms.  There is still a hint of Brugada pattern in V1.


Day 4 this was recorded:

Again, there is a hint of Brugada in V1, and even moreso in V2, with rSR' and downsloping ST elevation.

Day 5 this was recorded:

Still a hint of Brugada in V1

One month later:

Normalized

When the patient awoke, he and his family reported a family history of close relatives with cardiac arrest of uncertain etiology.  The patient himself had never had syncope or dysrhythmias.  Without Brugada pattern on the baseline ECG, there is no Brugada syndrome.  However, there is an uncertain history of sudden death as well as inducible Brugada pattern.

There is no clear management solution for such patients.  The electrophysiologist was of the strong opinion that an IVCD was not indicated without further information.  The management of inducible type I Brugada pattern is not at all clear.

The electrophysiologist felt that if the pattern was also inducible with procainamide, then genetic testing would be indicated.  If not, then avoidance of the TCA would be enough.  He proceeded also with an implantable loop recorder to detect subclinical dysrhythmias, and this was negative.

Drug-Induced Brugada Syndrome

Suffice it to say that this is a very complex topic and I know little more about it than can be read in this 2009 article from Europace, the most recent article I could find on the topic.  It is free full text.    http://europace.oxfordjournals.org/content/11/8/989.full.pdf+html

Here are a very few salient points from the article:

Brugada syndrome is due to a genetic defect in the gene (SCN5A) that codes for tha alpha unit of the sodium channel.  There appear to be many kinds of defects with variable manifestations and penetrance, and variable susceptibility to drugs, including TCAs (or also to other states such as fever).

TCAs even at therapeutic doses have been reported to unmask latent Brugada, and such reported cases have polymorphism of the gene. 

24 yo woman with chest pain: Is this STEMI? Pericarditis?

A 24 yo with no past medical history and no risk factors except for tobacco smoking presented with chest pain.  The pain started in her left chest at 6:20 AM and radiated up through her arms and into her back. She admitted to drinking heavily the previous night and returned home about 1:30 or 2 AM.  She had multiple episodes of vomiting overnight. She's never had chest pain like this before.  BP was 140/100 and pulse of 93.  There was no rub on exam.

Here is her prehospital ECG at 0720:

Sinus rhythm.  Inferior and lateral ST elevation with reciprocal ST depression in aVL.  There is no significant PR segment depression

She was given 2 sublingual NTG and her pain improved from 10/10 to 7/10, and continued to improve.  Here is her first ED ECG at 0748:

Not much change except for less STE in lateral leads.

Chest X-ray confirmed absence of Boerhaave's syndrome.

Some might suspect pericarditis in a young person with diffuse ST elevation.  However, you diagnose pericarditis at your peril!  I believe pericarditis is over diagnosed, even in the literature, and that many cases assumed to be pericarditis in the past would not be proved to be Acute MI.  This is conjecture based on many cases that I have seen, not based on peer-reviewed evidence.

Furthermore, in our study of benign inferior ST elevation vs. inferior STEMI, ST depression in aVL was nearly perfect in diagnosing MI.

I activated the cath lab immediately. A bedside echo performed by a world expert, Dr. Asinger, showed no effusion, and he could not discern a wall motion abnormality.  The patients pain was almost gone by this time.

While waiting for the team, we recorded another ECG at 0826:

Again, not much change.

And a right sided ECG at 0827:

This appears to show right sided ST elevation, though perhaps not a full mm.  This strongly suggests an RV infarct. 

At cath, the culprit was a proximal LAD lesion (open, with TIMI-3 fllow)!  It had embolized to the distal LAD, which was a "type III" or "wraparound" LAD supplying the inferor wall.  So this was an antero-infero-lateral MI.  The proximal lesion was stented and the distal was treated with antiplatelet and antithrombotic therapy.

The next day she has reperfusion T-waves in the anterior leads, as well as inferior and  lateral leads:

Looks like Wellens' syndrome in anterior leads, because it is analogous.

Formal Echo later showed moderate hypokinesis of the septum and dense hypokinesis of the apex and inferior wall.  Peak troponin I was 24 ng/ml.

We always look for explanations when young people have MI.  "They must have done cocaine."  "They must have high cholesterol."  But sometimes coronary atherosclerosis is accelerated, or there is one focal lesion, without good reason.  Her lipids were: LDL 139, VLDL 10, HDL 70, total cholesterol 219.

Lessons:

1) Myocardial Infarction does occur in young women!  They need not have a lot of risk factors or take cocaine.  In young women with STEMI, the diagnosis is more often missed or delayed than in any other demographic group, probably because of the bias that leads us to say, as my chief of EM always expresses it: "Nah, couldn't be."  MI is much more common in young people, including women, than previously recognized.  Many MI in very young women may be due to spontaneous coronary dissection, but this is not the most common etiology.  If the ECG is diagnostic, as in this case, believe it!  Do not try to convince yourself that it "couldn't be."

There was an important article published in fall of 2012 showing that young women with STEMI have longer Door to Balloon times and higher mortality.  There are a couple smaller studies with the same findings here and here.

2) You diagnose pericarditis at your peril

3) Absence of Wall motion abnormality may be misleading, especially if the pain and/or ECG abnormalities have resolved.  In this case, the difference between the informal and formal echo was the use of Definity contrast.

PVC or Aberrant Conduction? (Another Guest Post from Dr. Wang)!

Question: This tracing shows (choose one from the list below)

               a) atrial bigeminy with aberrant conduction

               b) ventricular bigeminy

 Annotated ECG:

Answer:   a) atrial bigeminy with aberrant conduction.

Discussion: Every other QRS is wide, different looking from the sinus beats and, at a quick glance, the tracing seems to show ventricular bigeminy. However, careful observation reveals a prematurely occuring P wave (↓) in front of these wide QRSs and this is an examle of atrial bigeminy with aberrant conduction. Why does aberrant conduction ever occur? It is simply because the two bundle branches (BBs) have different length of refractory periods. If an impulse occurs when one BB is still refractory while the other has recovered from the refractory period, the impulse will conduct thru the recovered BB, bypasssing the refractory BB: aberrant conduction results. Of course, if an impulse occurs at a time when both BBs have recovered from the refractory period, it will conduct normally, while if both BBs are refractory, it won't conduct at all (non-conducted PAC). This was well diagrammed and explained in the Medscape ECG of the week posted on 3/7/2012.