Thursday, December 22, 2022

See OMI vs. STEMI philosophy in action

by Emre Aslanger

Dr. Aslanger is our newest editorial member.  He is an interventional cardiologist in Turkey. 

Dr. Aslanger is also the author of the DIFFOCULT study:

Emre K. Aslanger,a, Özlem Yıldırımtürk,b Barış Şimşek,c Emrah Bozbeyoğlu,c Mustafa Aytek Şimşek,a Can Yücel Karabay,b Stephen W. Smith,d and Muzaffer Değertekina  

DIFOCCULT: DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardial infarction.  International Journal of Cardiology Heart & Vasculature


A 40-year-old man presents with excruciating back pain which has started 1 hour ago. His medical history is unremarkable except a similar pain occurred 4-5 times in the previous 3 months with less intensity, short duration, unrelated to exertion. He visited an outpatient clinic for it and an echocardiogram and exercise stress test was normal. He has 40 packs-year of smoking history. There was no premature cardiovascular diseases or sudden death in his family. He denies taking any medication.

On his physical examination, cardiac and pulmonary auscultation was completely normal. Peripheral pulses were all palpable. Blood pressure: 130/80 mmHg, heart rate: 45/min, respiratory rate: 18/min, SaO2: %98, body temperature: normal.

As he seemed very agitated, fentanyl and diazepam were given.   

His first electrocardiogram (ECG) is given below:

--Sinus bradycardia. 
--There are some ST-segment elevations (STE) in V2-5 and lead II, III, aVF. 
--No reciprocal ST-segment depression (STD). 
--QT is short, R wave amplitudes are preserved. 
--For subtle anterior OMI, Smith's 4-variable and Aslanger's simplified formulas both supports benign variant STE. 
--For subtle inferior OMI, there is no STD in aVL or lead I. 
--In summary, some subtle findings which do not fit into a pattern, therefore may be nonspecific ECG changes which are encountered everyday.    

As his pain was very severe, emergency physicians concerned of aortic dissection and ordered a thoracic CT scan. Bi-phasic scan showed no dissection or pulmonary embolism. Coronary arteries cannot be assessed because the scan was not gated, but proximal segments of the coronary arteries seem to be open with some contrast. 

His pain is now settled a bit, around 4/10 and first troponin turned out to be 12 ng/L (normal <14 ng/L).

A second ECG was taken:

Baseline is slightly wandering, therefore it cannot be reliably said that there is no dynamic change from the first ECG, but it seems so. 

Second troponin at 1h comes 20 ng/L. It is above normal limit and there is a significant change

A third ECG and troponin was planned. 

In the meantime, cardiology consultant sees the patient and performs a bedside echocardiogram which revealed no major wall motion abnormalities

Nevertheless, the back pain is still ongoing, he orders another ECG:

Still the same suspicious STEs, but they did not change from the previous ECGs and also do not easily fit into any coronary localization. 
But there is a suspicious new finding here: Is there a new Q wave in lead III ? Or it is due to a slight axis change? Again nothing diagnostic.  

With ongoing pain, without any clinical evidence of OMI, cardiologist thinks NSTEMI and admits the patient to the step 1 coronary care unit.

His ECG on arrival to the CCU:

This ECG was taken with a different machine but there seems to be one dynamic change: There is T wave inversion in lead III and Q wave is still there. This is a very subtle change but cannot be anything other than an acute coronary event. The pain is still ongoing, therefore cath lab is activated.

Cath lab was not activated because we diagnosed a "high risk" NSTEMI; rather, it was because we suspected, actively searched for, and could not refute an OMI that needs to be immediately reperfused. 

Here is the coronary angiogram:

A distal thrombotic right coronary artery (RCA) occlusion ! A significant amount of thrombotic material was aspirated by manual thrombectomy (see below for aspirated thrombi). 

Aspirated thrombotic material. 

The lesion was successfully stented. Here is the post-intervention angiogram and post-PCI ECG. The pain was completely resolved after coronary intervention. 

Take home messages:

1- In STEMI/NSTEMI paradigm you search for STE on ECG. In OMI/NOMI paradigm you search a clue for acute coronary occlusion (ACO). If this patient was managed according to the STEMI/NSTEMI paradigm (although he would be a candidate for early invasive treatment), he would probably be taken to the cath lab hours later. In these golden hours, a majority of the salvageable myocardium would be lost. With OMI/NOMI approach we actively search for an ACO and used conventional angiogram to prove our suspicion even if there was no striking diagnostic clues at hand.

2-A subtle ECG does not mean a subtle pathology. This is a complete coronary occlusion with a good vessel caliber. 


1. Aslanger EK, Meyers HP, Smith SW. Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab. Turk Kardiyol Dern Ars. 2021 Sep;49(6):488-500. doi: 10.5543/tkda.2021.21026.


Comment by KEN GRAUER, MD (12/22/2022):
Brilliant post by Dr. Aslanger — with emphatic illustration of "the difference in OMI vs STEMI philosophy" — in action! 
  • To highlight the subtle ECG change Dr. Aslanger points out in lead III in the 4th tracing — I thought it helpful to magnify and compare the limb leads from that tracing, with the tracing recorded before this ECG change (Figure-1).

As per Dr. Aslanger — there is a subtle, but very important change in lead III of ECG #4 — in that despite no change in the frontal plane axis, the T wave in lead III is now indisputably inverted
  • The same small (but significant) Q wave in lead III remains (as do small Q waves in the other 2 inferior leads) — and the ST segment in lead III manifests coving prior to ending with T wave inversion. 

But aren't there other new ST-T wave changes in
 ECG #4

Figure-1: I've magnified and compared the 3rd and 4th set of limb leads in today's case. How many leads show subtle differences?

Subtle Changes in Other Leads:
Dr. Aslanger emphasizes the importance of clinical context! In a patient with ongoing, severe chest pain — the subtle-but-real ST-T wave changes are "dynamic" indication of an ongoing acute cardiac event — therefore prompting the need for cardiac cath!
  • Often with serial ECG changes — there will be 1 or 2 leads that "stand out" for being definitely different! I look for those first. It becomes easier to recognize more subtle changes in other neighboring leads once you identify the leads that are definitely abnormal.
  • Isn't the "magic" mirror-image opposite relationship between lead III and lead aVL maintained when comparing the 2 tracings in Figure-1? Although assessment of lead aVL is challenging, given the tiny size of the QRS complex in this lead — I thought the flat ST segment with tiny positive T wave in ECG #3 — has been replaced in ECG #4 by a hyperacute ST-T wave that is the mirror-image opposite of the ST-T wave that is now seen in lead III.

  • There are subtle differences in the other 2 inferior leads — as the small-but-upright T wave in lead aVF is now ever-so-slightly inverted — and — the ST-T wave in lead II is now clearly more flattened.

  • Finally — the T wave in lead I is more voluminous than it was in ECG #3.

  • To EMPHASIZE: The changes I describe for leads I, II and aVF are so subtle — that by themselves, I would never be confident they were "real". But in the context of ongoing severe cardiac chest pain — in which a definite "dynamic" ST-T wave change can be seen in both leads III and aVL of ECG #4 — these more subtle findings in the remaining limb leads are doubtlessly real!

Our appreciation to Dr. Aslanger for his brilliant demonstration of how OMI philosophy differs in practice from the previous (and now outdated) STEMI paradigm.


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