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

===================================

MY Comment, by KEN GRAUER, MD (12/6/2023): 

===================================

Even a decade ago — Dr. Smith was already convincingly diagnosing acute OMIs, as per his discussion above. The time for moving past the outdated STEMI paradigm has long since arrived ...

• For clarity in Figure-1 — I've labeled the initial ECG in this June 18, 2013 post.

Figure-1: I've labeled the initial ECG from this June 18, 2013 post. This is but one of many examples presented in the Webinar by Drs. Smith, Meyers & Herman on Diagnosing Acute OMI from the December 5, 2023 post.

ECG Findings in Figure-1 that Indicate Acute OMI:

I've combined Dr. Smith's 2013 description (above) — with some additional thoughts about ECG #1:

• The ECG in Figure-1 — “looks” like an acute OMI (ie, chest lead T waves just do not “look” normal) — because there are disproportionately large and symmetric T waves in multiple leads (outlined in RED) — with these T waves being “fatter”-at-their-peak and wider-at-their-base than they should be. Thus, there are multiple hyperacute T waves!
• Dr. Smith’s formula for LAD Occlusion vs Repolarization is satisfied (ie, value = 24.5, as he notes above).
• There is poor R wave progression — with “loss” of R wave between V2-to-V3 (GREEN arrows in these leads).
• T waves in  high-lateral leads I and aVL are also hyperacute (clearly “fatter”-at-their-peak than they should be).
• Leads III and aVF show reciprocal ST-T wave changes — including diagnostic down-up terminal T waves (RED arrows in these leads).
• There is that “magical” reciprocal relationship between the T wave in lead aVL and the ST-T wave in lead III (within the BLUE rectangles).
• In all — every lead except aVL is abnormal ( = 11/12 leads in this ECG). By the concept of “neighboring leads” — the disproportionately “fat” T wave peak in lead V5 is also hyperacute (outlined in RED) — and — the abnormally flat ST segments in leads II, V5 and 6 lack what should normally be at least slight upsloping (outlined in PURPLE).

NOTE: Any 1 or 2 of the above ECG findings in a patient with new CP would suffice to justify the need for prompt cath with PCI. That said — the better emergency providers become able to recognize multiple abnormal ECG findings — the more astute they will become at identifying non-STEMI criteria that indicate immediate need for cardiac cath and PCI.

• P.S. — With experience — it does not take long to recognize non-STEMI indicators of acute OMI (as demonstrated by Drs. Smith and Meyers in the December 5, 2023 Webinar post).