Friday, July 19, 2019

A man in his 40s with chest pain and syncope after cocaine use

Written by Pendell Meyers, with edits by Steve Smith

A man in his early 40s with history of MI s/p PCI presented with bilateral anterior chest pain described as burning and belching with no radiation since last night starting around 11pm (roughly 11 hours ago). He also described a syncopal episode just prior to onset of symptoms. He had used cocaine approximately 20 minutes prior to onset of symptoms.

He still had active pain on arrival to the ED.

Here is his triage ECG:
What do you think?

His baseline ECG was on file:

--Sinus rhythm
--Subtle STE in V1-V5, II, III, and aVF
--Q-waves in V1-V5, as well as II, III, and aVF which must be assumed new until proven otherwise
--Possibly large area under the T-wave (concern for hyperacute T-waves) in V4, II, III, and aVF, with reciprocal negative T-wave in aVL
--These Q-waves are so fully developed that it appears to be a nearly completed MI, at a stage when it is likely that all ST elevation is resolved. STE occurs primarily in viable ischemic myocardium; persistent STE after completed infarction is ominous and portends development of an aneurysm.
--There is also an interesting Brugada-like morphology in V1 (also similar to hyperkalemia, which sometimes mimics brugada). This morphology can be cause by or associated with cocaine:

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***

This is OMI of the anterior, lateral, and inferior walls until proven otherwise. This distribution is classic for a type III "wraparound" LAD Occlusion.

But it does not meet STEMI criteria and it was not initially recognized. Whereas most STEMI(-) OMI is acute, this one might have had STE at its onset, or earlier in its course. We'll simply never know without ECGs from that time period.

The first troponin T was delayed for several hours for an unknown reason in the lab, and returned at 1.50 ng/mL (very elevated).

This prompted a repeat ECG (we do not have documentation from that time to tell us whether he had persistent, recurrent, or absent pain):  

Progression of anterior OMI to full Q-wave MI with large pathologic Q-waves in V2-V4 with persistent STE which now meets STEMI criteria (after full thickness infarction/stunning).

The cath lab was now activated.

He was found to have 100% mid LAD occlusion. Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow.



In this view you can see the extent of the "wraparound" distal LAD:

Peak troponin T was 35.70 (massive MI, rarely survivors at this level in my 3 years here).

Echo showed EF 30% with anterior, septal, apical, and inferior wall motion abnormalities.

ECG after cath:

Continued STE with anterior wall Q waves (LV aneurysm morphology), combined with extremely high troponin are likely indicative of full thickness irreversible MI (rather than stunning), and are high risk features for resulting LV aneursym. The extremely high troponin and ECG evidence of LVA morphology are very worrisome long term features for resultant morbidity and mortality.

Amazingly, he did not suffer any serious complication in hospital. He recovered and was discharged several days later. Long term follow up is unknown at this point.

Learning Points:

Even if NSTEMI Occlusions (STEMI- OMIs), overall prove to have slightly lower morbidity and mortality than STEMI Occlusions (STEMI+ OMI), there are many cases like this one showing that some of the worst, largest OMIs may not manifest STEMI criteria until far too late, if ever. Again, it is possible that this patient would have had obvious STE earlier in the time course of this MI, but we do not know. What we can say is that his initial ECG was certainly diagnostic and the delay of many hours could have been improved.

Wraparound type 3 LAD Occlusion causes STE in many leads including anterior, lateral, and inferior distributions. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Always keep in mind the possibility of diffuse STE (and other OMI findings) as being due to a type 3 LAD.

Comment by KEN GRAUER, MD (7/19/2019):
I was intrigued by the challenge of clinical correlation posed by the ECGs in this case. The patient is a man in his 40s with a history of prior MI (s/p PCI— who presented to the ED with new chest pain that had begun ~11 hours earlier. His initial ECG in the ED ( = ECG #1) is shown in Figure-1. The patient was still with ongoing chest pain at the time ECG #1 was done.
  • baseline tracing was found on this patient ( = ECG #2).
  • Several hours later a follow-up ECG was obtained in the ED, because the 1st troponin came back significantly elevated ( ECG #3).
Figure-1: The first 3 ECGs that were shown in this case (See text).

CHALLENGE: How did YOU interpret ECG #1 before you looked at ECG #2?
  • As we soon learned in this case — this patient has had a new STEMI. Cardiac cath (which was done soon after ECG #3) told us that this STEMI was the result of 100% mid-LAD occlusion (LAD with wraparound). But the BEST way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was new chest pain that began 11 hours earlier).
  • Strive to interpret this initial ECG before you look at additional information. THEN look for previous tracings in the patient’s chart, repeat ECGs, troponin and Echo results the patient’s clinical course. This sequence of assessment will not slow you down — and it is the BEST way to optimally “grow” as an astute ECG interpreter.
MTHOUGHTS on ECG #(determined BEFORE I looked at ECG #2):
Remember the History a man in his 40s with known prior MI (s/p PCI— who presented to the ED with new chest pain that had begun ~11 hours before ECG #1 was done.

Descriptive Analysis of ECG #1:
  • The rhythm is sinus at a fairly regular rate of ~80-85/minute. The PR, QRS and QTc intervals are all normal. The frontal plane axis appears to be normal — though the axis is difficult to calculate because of nearly isoelectric complexes in 4 of the 6 limb leads (leads I, III, aVL and aVF). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There are multiple Q wavesin ECG #1. Although small in size — the inferior Q waves are likely to be significant (ie, indicative of inferior MI at some point in time) — because relative to QRS dimensions, inferior Q waves are both large and relatively widened. There are large Q waves (relative to QRS complex size) in leads V1, V2 and V3. There is marked fragmentation of the Qcomplex in lead V3.
  • PEARL: Although Q waves in leads V4, V5 and V6 become much smaller and narrower — the fact that the wave in lead Vis decidedly larger than the Q waves in leads V5 and V6, tells us that the Q in V4 is significant (ie, part of the infarction process suggested by the Q waves in V1-V3). With normal “septal” q waves — the opposite progression occurs (ie, Septal q waves are uncommon in lead V4 — and when present, a septal Q in V4 should be smaller than the septal Q in V5 and V6).
  • The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed in ECG #1 (ie, it occurs between leads V4-to-V5).
Regarding — ST-T wave Changes:
  • As noted by Drs. Meyers and Smith — there is an interesting Brugada-like morphology to the ST-T wave in leads V1 and V2 (convex down RED line in V1,V2 of ECG #1). There is not enough ST elevation to qualify this as a Brugada-1 pattern — but, the clinical significance of recognizing this pattern is that the slight ST elevation in these leads is more likely to reflect a Brugada “phenotype” rather than acute septal infarction.
(For more on assessment of Brugada ECG patterns — CLICK HERE for a link to my 29-minute video on the subject. If you click on SHOW MORE under the video on the YouTube page — you’ll see a linked Contents to all in the video).
  • Back to ECG #1: As per Drs. Meyers and Smith — there is subtle-but-real Selevation in multiple leads. That said — the almost horizontal elevated ST segments in the inferior leads look less acute than one might have expected. These elevated ST segments are associated with prominent inferior T waves — and, reciprocal (albeit shallow) T wave inversion in lead aVL.
  • Similarly the subtle-but-real ST elevation in leads V3, V4 and V5 has a shape that looks less acute than one might have expected (gently upward concave, as suggested by curved BLUE lines in V3 and V4 of ECG #1).
  • NOTE: The different shape of the slightly elevated ST segments in leads V1,V2 of ECG #1 (curved-down RED lines) — vs the upward concavity ST segments in leads V3-thru-V6 (curved-UP BLUE lines) — in my opinion, adds further support that these are 2 different processes (ie, Brugada-like phenotype for the ST-T waves in leads V1,V2— vs recent acute injury for the elevated ST segments in leads V3-thru-V6).

Clinical IMPRESSION: Before finding this patient’s baseline tracing — I would have been hard pressed to know how much of what I was seeing in ECG #1 might have been due to the prior MI that this patient had — vs what might have developed since the onset of chest pain 11 hours earlier. This is the CHALLENGE I put forth to you earlier! Realizing there is NO way to be certain — these were my thoughts:
  • What we see in ECG #1 probably did not just happen. Although possible to develop new Q waves in as little as 1-2 hours after acute infarction — I thought the size and number of Q waves seen here the fragmentation in lead V3 suggested that at least some of these Q waves were the result of this patient’s prior MI. I would have guessed from the prominent T waves and subtle ST elevation that this patient manifests in ECG #1 — that he had suffered an acute event at the onset of symptoms (ie, ~11 hours earlier).
  • That said — because there is still ST elevation in ECG #1, with inferior T waves that look like they may still be hyperacute ongoing chest pain — cardiac cath sooner-rather-than-later seems indicated to clarify the clinical picture.

At this point in time — Finding a Baseline Tracing on this patient ( = ECG #2) proved invaluable! My thoughts on comparing ECG #2 with ECG #1:
  • I was wrong about my hunch that at least some of the Q waves in ECG #1 were old. Other than lead V1 — there are no Q waves at all in ECG #2! Instead, R wave progression in this earlier baseline tracing was normal — with development of a fairly tall R wave already by lead V3. This means that the extensive Q waves in ECG #1 (including the fragmentation in lead V3) are new since the baseline ECG #2 was done. We have to presume (until proven otherwise) that these ECG findings are new since the onset of symptoms 11 hours earlier.
  • There is virtually no ST elevation in ECG #2. Overall, I don’t see much difference in T wave appearance between ECG #1 and ECG #2. This left me with uncertainty regarding how acute the subtle-but-real ST elevation now present in ECG #1 might be. Did it develop days or weeks earlier? — or, sometime after the onset of symptoms within the 11-hour period prior to presentation in the ED? That said — persistence of chest pain the ECG changes that developed between ECGs #1 and 2 would be indication for acute cath to clarify the clinical picture.

Apparently — the new ST elevation that developed in ECG #1 (compared to the baseline ECG) was not recognized. Several hours later, when the 1st troponin came back elevated — ECG #3 was obtained.
  • I see no significant change in ST-T wave appearance in the limb leads between ECG #1 and ECG #3 done several hours later.
  • However – there has been marked change in ST-T wave appearance in the chest leads in ECG #3! Even accounting for slight change in QRS morphology and amplitude in the mid-chest leads (suggesting some variation in precordial lead placement) — there clearly is now straightening of the ST segment takeoff (slanted BLUE lines in ECG #3with more ST elevation in leads V3 and V4.
  • Beyond-the-Core: The Brugada-like morphology in lead V1 of ECG #3 looks the same as it did in ECG #1 (curved-down RED line). It is interesting that the shape of the elevated ST segment in lead V2 of ECG #3 now manifests a flattened (BLUE-RED line) morphology that is intermediate between the curved RED line in lead V1 — and the upward slanting BLUE line in lead V3. I suspect the reason for this is a “fusion” between the Brugada-like ST segment effect being exerted on lead V2 — with what is now acute ST straightening and elevation in leads V2, V3 and V4 from the actively evolving anterior STEMI.
  • Putting IAll Together  Despite the history of a prior MI (with PCI) — the baseline tracing ( = ECG #2) shows no evidence of prior infarction. From the information available — it’s impossible to know if a 2nd event occurred sometime after ECG #2 was done — but before the onset of symptoms associated with this admission. What can be said — is that regardless of whether this marks a 2nd or 3rd cardiac event, that there is definite ECG and troponin evidence of an acute STEMI that is actively evolving between the time that ECGs #1 and #3 were done.

Our THANKS to Drs. Meyers and Smith for this challenging case!

Wednesday, July 17, 2019

A Text Message in the Middle of the night. Do you give thrombolytics?

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.

I continued:

"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.

Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardial infarction

Pendell and I wrote an Editorial on this, but we cannot reproduce it here:
H. Pendell Meyers.  Stephen W. Smith.  Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)

Comment by KEN GRAUER, MD (7/18/2019):
This case was made especially challenging by small size of QRS complexes, baseline artifact in a number of leads, and continued use of the outdated “stemi” paradigm for defining acute coronary.
  • I focus my attention on interpretation of the ECG that was texted to Dr. Smith ( = ECG #1 in Figure-1).
  • NOTE: There is low voltage in all 12 leads. In my attempt to facilitate interpretation — I’ve relabeled this tracing, and have removed some of the excess spacing in between lead groups. I believe doing so makes it easier to appreciate the acute ST-T wave changes.
Figure-1: The ECG that was texted to Dr. Smith in this case (See text).

MTHOUGHTS on ECG #1: The patient in question was a 60yo woman with typical new-onset chest pain. As per Dr. Smith — the ECG in Figure-1 that was texted to him is diagnostic of acute OMI.

Descriptive Analysis of ECG #1:
  • Low voltage! There is baseline artifact in several limb leads. The rhythm is sinus at ~80/minute. The PR interval is normal. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is slightly leftward (ie, more negative than positive in lead aVF) — but not negative enough to qualify as LAHB (left anterior hemiblock), because the QRS is not predominantly negative in lead II. I estimate the axis to be about -15 degrees. There is no chamber enlargement.
Regarding Q-R-S-TChanges:
  • There are small, narrow Q waves in leads aVL, V5 and V6. These Q waves are of uncertain significance.
  • The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed (ie, it occurs between leads V4-to-V5). More importantly — the R wave remains tiny until lead V5This most probably is related to the acute ongoing process.
As has already been noted — ST-T wave Changes are diagnostic:
  • Considering the tiny size of QRS complex — there is significant Selevation in leads V3-thru-V6. This is associated with hyperacute waves (that are disproportionately taller and fatter-then-they-should-be-at-their-peakin leads V3V4V5, and probably also V6.
  • In the limb leads — there is ST elevation in lead aVL reciprocal ST-T wave changes in each of the inferior leads. While more difficult to appreciate because of artifact and small QRS complex size — the ST segment is conspicuously straightened in leads II and aVF; slightly depressed in lead III; and, associated with disproportionate T wave size in all 3 inferior leads.
  • Personal Observation: Doesn’t doubling the size of the QRST complex in certain leads of ECG #1 facilitate appreciation of a definite acute OMI(See Figure-2).
Figure-2: I’ve doubled the size of 1 complex in leads III, aVL, aVF, and V3-thru-V6. I have not changed proportions of the ECG grid within the RED rectangles. Doesn’t this facilitate diagnosis of acute OMI? (See text).

COMMENT: Regardless of whether the millimeter definition of acute “STEMI” is or is not met — the ECG in Figure-1 is diagnostic of acute OMI in this patient with new onset typical chest pain. Acute reperfusion is indicated.
  • The ECG in Figure-1 is consistent with acute mid- or distal-LAD occlusion — since ST elevation does not really begin until lead V3, and is maximal in leads V4 and V5 (ie, ST elevation typically begins sooner with proximal LAD occlusion).
  • From an ECG terminology standpoint — preservation of the initial r wave in leads V1 and V2 suggests that this is not anteroseptal infarction, but rather anterior infarction (ie, from a terminology standpoint — the initial r wave should be lost in lead V1 when there is “septal” infarction).
  • That said, persistence of no more than a tiny r wave until lead V5, and then no more than relatively small R waves in leads V5 and V6 — is consistent with the extensive area of jeopardized myocardium suggested by the number of leads in ECG #1 that show acute ST-T wave deviation.
  • P.S.: Taking another look at the magnified complexes within the RED rectangles in Figure-2 — perhaps the definition of acute “STEMI” is met after all in this case?

Our THANKS to Dr. Smith for presenting this case!

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