The case:
A 68 year old male called 911 for "10/10" chest pain, and took aspirin before EMS arrival. Nitroglycerin was given by the medic, but it dropped the BP. Some normal saline took care of that, and transport was expedited.
The first ECG:
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| Computer interpretation: "Widespread ST-T abnormality suggests myocardial injury/ischemia" |
A repeat ECG then showed:
No further events enlivened transport to the tertiary-level, primary-PCI facility.
So what does the first ECG show?
This ECG suggests a proximal LAD occlusion in two different ways, and justifies cath-lab activation, in my view.
The first pattern is likely familiar to astute 12-lead ECG readers. There is widespread depression throughout the ECG (II, III, aVF, and V3-V6), and ST elevation in aVR. Such a pattern indicates either severe 3-vessel disease or severe occlusion of the left main artery.
The second indication of LAD occlusion is not as well-known. Note the upsloping pattern of ST depression in the precordial leads. This is distinct from the horizontal or downsloping pattern that you often find with a posterior AMI.
For example, this posterior MI demonstrates horizontal ST depression:
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| Source |
Another example of a posterior MI shows a downsloping pattern of the ST segment:
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| Source |
By contrast, in our ECG we have a sharply upsloping ST segment. Furthermore, it terminates in a tall, fairly sharp, T-wave.
DeWinter "waves"
Back in 2008, de Winter and a few other authors described a ECG pattern that they had seen in 2% of anterior AMIs. Interesting, all of the patients with this pattern had occlusions of the LAD in the proximal region - a very serious blockage that could infarct a good chunk of myocardium.
[T]he ST segment showed a 1- to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R-wave progression. In most patients there was a 1- to 2-mm ST-elevation in lead aVRThey offered 8 examples of the precordial ST-T pattern:
Interesting looking ST segments and T-waves! Comparing these examples to our patient, looking at a blow-up of the precordial leads:
So even without the 20/20 hindsight that blogging affords me, I'm anticipating a proximal LAD occlusion.Upsloping ST-segment depression? Check.
Tall, positive, symmetrical T waves? Check.
Loss of R-wave progression? Check.
Normal-width T-wave? Check.
ST-elevation in aVR? Check.
The final ECG
It appears the ST segments have normalized - both the ST elevation in aVR, and the ST depressions in multiple leads have returned to baseline. Even though this spontaneous reperfusion is an encouraging development, the patient still requires emergent angiography in my opinion, given the high likelihood of a dangerous, unstable lesion.
The Bottom Line
There - you know what I know now. Do you see anything that points to an alternative diagnosis, another concomitant problem, or different management?
I'll dig up the final results, and and them in the comments in a few days.
Nice case by BROOKS! - with excellent illustration of DeWinter T waves - which as emphasized produces a very different type of ST depression in ant. leads than does posterior MI.
ReplyDelete- The "burst of activity" on the 2nd tracing shows short runs of VT (looks like there is AV dissociation, though hard to make out given baseline artifact that is present).
I'll add a few point re DeWinter T waves:
i) Looks like acute MI is already in process at the time of the 1st tracing - as there is a highly suggestive Q-equivalent already formed in V2 - and a definite Q in lead aVL. Also - the QRS is in process of widening already, with S wave formed in V6. In the DeWinter series - a fair number of their patients DID go on to evolve actual infarction (GOAL is to pick up the DeWinter ST-T wave sign of impending prox LAD occlusion before the MI, but it doesn't always work that way ... ).
ii) I assume the "Final ECG" you are referring to is the "Repeat ECG" above. If so - additional findings to mention include more QRS widening into frank complete RBBB - with now an S also formed in lead I. There is a definite Q (QR pattern) in V1,V2 - indicating new RBBB with new anterior MI (which had been heralded in point i) above). Also - there is now actually bifascicular block = RBBB/LAHB (note the QRS in lead II is now more negative than positive, which is a change from the initial ECG.
iii) Although the ST segments have virtually returned to the baseline - the overly peaked T waves in multiple leads on the repeat ECG are ischemic and reflect the acute MI evolution that has just occurred.
For those interested in additional examples - I posted on my ECG Blog at: http://ecg-interpretation.blogspot.com/2012/11/ecg-interpretation-review-53-peaked-t.html
THANKS Brooks for your excellent post!
You have some great examples on your site!
DeleteI think you're spot-on with your reading of these tracings. I only wish that I could bring some cath data back to the discussion. Unfortunately, follow-up was lost due to the infamous "brought to the other hospital" problem.
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