Tuesday, October 20, 2015

An Obvious LAD Occlusion that did not meet STEMI "Criteria"

This case was provided by Tom Bouthillet, who is Editor-in-Chief of EMS 12-Lead and Chief Content Architect of ECG Medical Training.

Case

An elderly male with a history of an RCA and mid-LAD stent started feeling ill with nausea and vomiting.  3 hours later he developed substernal chest pain.

Paramedics found him with a normal exam. Pain was 5/10 without radiation or diaphoresis.  This ECG was recorded:
 The computer algorithm read "nonspecific".  Computerized QTc is 439 ms. 
What do you think?  See below.  





















Sinus rhythm.  There is ST elevation which is very worrisome for STEMI, especially in this high risk patient.  However, there are not 2 mm of ST elevation at the J-point, relative to the PQ junction, in two consecutive right precordial leads, which is the ACC/AHA and Universal Definition of MI criteria for males over age 40 (2.5 mm are required for males under 40; 1.5 mm for women). 

This ECG is very worrisome for LAD occlusion [in fact, when Tom and I (Smith) saw it, we had no doubt that it represented LAD occlusion], partly because the T-waves appear so bulky and wide.  This is partly because of a slightly longer QT interval and smaller T-wave amplitude.  See below:

Here is V2 from a typical early repol ECG:
The STE is 4 mm at the J-point.  The T-wave is 13 mm tall.

Compare it with V2 in the above ECG.   
Here there is 2.5 mm STE at the J-point.  The T-wave is 10 mm tall.This looks wider and more "bulky," don't you think?

What should you do when you suspect that this may be LAD occlusion?

Features to look for to differentiate subtle LAD occlusion from normal variant ST elevation in V2-V4 ("early repolorization"):
1. Early repol must have upward concavity in all of leads V2-V6 (all are concave here)
2. Early repol must not have any Q-waves in V2-V4 (there are none here)
3. There must be no "inferior" or precordial ST depression (there is none here)
4. There must be no "terminal QRS distortion" in either V2 or V3 (this means neither an S-wave that goes below the level of the PQ junction, nor a J-wave).  This is explained very well here.
5.  There should be no T-wave inversion in precordial leads, unless it is "Benign T-wave Inversion," which can only be diagnosed by someone very familiar with it.


If an ECG has all these features that qualify it for early repolarization, then one should apply the early repol vs. LAD occlusion formula below.

The differential diagnosis must be only early repol vs. LAD occlusion: LVH is likely to result in a false positive.

Formula: (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).

STE 60 V3: ST elevation (STE) is measured at 60 milliseconds after the J-point, relative to the PQ junction, in millimeters.

 A value greater than 23.4 is quite sensitive and specific for LAD occlusion.  A value less than 22.0 is extremely unlikely in LAD occlusion.  There is an applet on the sidebar of the blog which I have reproduced here.  Just fill in the values and get the result:




A couple other findings may give a clue:

1. An upright T-wave in V1
2. Less upward concavity

In our study, we found that neither of these findings were independently associated with LAD occlusion.

The formula value is 27.2, which is clearly in the LAD occlusion range above 23.4.


Another ECG was recorded at t = 21 minutes, when the patient was feeling slightly better:
QTc is 442.  T-waves are slightly smaller, but the formula value is still over 27.

Another ECG was recorded at t = 26 minutes:
QTc is 448.  No significant change.


In spite of these ECGs, and the high pretest probability, the patient was only taken to the cath lab after a long delay and absence of improvement with medical therapy.

The exact delay is uncertain, and the exact reasoning uncertain, but physicians still are inappropriately dependent on millimeter criteria for diagnosing STEMI even if the diagnosis is obvious, even though these criteria are very insensitive for acute MI (less than 50%, and about 75% sensitive for occlusion

The patient was eventually taken to the cath lab and had a 100% in-stent thrombosis occlusion of the LAD.

Learning Point:

Millimeter criteria are dangerously insensitive for acute myocardial infarction (sensitivity 48%!), though better for acute coronary occlusion (around 70%).  If you rely on them, you will miss approximately 25-30% of acute occlusions.

7 comments:

  1. Would the (almost concave) straight ST segment in V1 and the lack of R wave progression make the diagnosis as well?

    ReplyDelete
    Replies
    1. Jos,
      V1 is normally convex. However, you are correct that the ST elevation in V1 would be unusual for early repol. And you are right on about R-wave progression. That should always progress in early repol, and it is the main reason that the formula works here: had there been normal R-wave progression, the R-wave in V4 might have been 20 mm and then the formula value would be less than 23.
      Steve

      Delete
  2. We are 2,000km from our cath lab. At what point would you have made the call to thrombolyse him?

    ReplyDelete
    Replies
    1. David,
      I would have thrombolysed him on arrival. After the first ECG.
      Assuming no absolute contraindications.
      Steve

      Delete
  3. Steve,
    I'm planning on having a talk about subtle ischemic findings and was wondering if you have a reference on the millimeter criteria sensitivity of 70-75 % for acute coronary occlusion?
    Peter

    ReplyDelete
    Replies
    1. 1. Diagnosis of Acute Myocardial Infarction in Angiographically Documented Occluded Infarct Vessel* Limitations of ST-Segment Elevation in Standard and Extended ECG Leads. CHEST 2001; 120:1540–1546

      2. Marti et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation
      myocardial infarction. Am Heart J 2014;168:884-90.

      3. Wang T et al. Am Heart J 2009;157(4):716-23.

      4. From AM, et al. Am J Cardiol 2010;106(8):1081-5.

      5. Pride YB et al. JACC: Cardiovasc Interventions 2010; 3(8):806-11.

      Delete

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