OMI Facts and References

This page is used to reference important facts and figures regarding OMI. What were those new "STEMI equivalents" per the ACC in 2022? How do we know that missed NSTEMIs with OMI have double mortality compared to NSTEMIs without OMI again? What is the reference for that? See below!


2022 ACC Added "STEMI Equivalents"

Kontos et al. 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department. JACC 2022.

25-35% of NSTEMIs are found to have missed OMI (acute coronary occlusion) on their delayed cath, even in optimal RCT conditions:

Avdikos, Michas, Smith. From Q/Non-Q myocardial infarction to STEMI/NSTEMI: Why it's time to consider another simplified dichotomy; a Narrative Literature Review. Archives of Academic Emergency Medicine, 2022.

20% of consecutive OHCA (unconscious after ROSC) who underwent cath had acute coronary artery occlusion without STE

Defined as thrombotic culprit with TIMI 0 or 1 flow.

30-60% of anterior OMIs do NOT have reciprocal STD in inferior leads:

Forty to seventy percent of anterior AMI will manifest reciprocal ST depression in at least one of leads II, III, and aVF; this ST depression correlates strongly with a proximal LAD occlusion (see figures 1 and 19).103-106

103.     Birnbaum Y, Sclarovsky S, Solodky A, et al. Prediction of the level of left anterior descending coronary artery obstruction during anterior wall acute myocardial infarction by the admission electrocardiogram. Am J Cardiol 1993; 72:823-826.

104.     Engelen DJ, Gorgens AP, Cheriex EC, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute myocardial infarction. J Am Coll Cardiol 1999; 34:389-395.

105.     Tamura A, Kataoka H, Mikuriya Y, Nasu M. Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction. Eur Heart J 1995b; 16:1795-1799.

106.     Kosuge M, Kimura K, Toshiyuki I, et al. Electrocardiographic criteria for predicting total occlusion of the proximal left anterior descending coronary artery in anterior wall acute myocardial infarction. Clin Cardiol 2001; 24:33-38.

TIMI Flow at time of cath for STEMI(+) OMI:

Outcomes used to ascertain the presence of OMI on the ECG cannot be based solely on TIMI flow of the lesion at the time of the angiogram because the state of the artery frequently differs between the time of the ECG and the time of the angiogram. Proven STEMI has an open artery in 19% to 36% of cases, depending on whether it is TIMI −1, −2, or −3 flow. Karwowski et al showed that only 64% of 4581 STEMIs had TIMI 0 flow on angiogram. [25] Stone et al found that 72% have TIMI 0 or 1 flow. [26] Finally, Cox et al found that 80% had TIMI 0, 1, or 2.27 Thus, approximately 20% of true, obvious STEMIs have TIMI 3 flow at immediate angiogram. [27]

25. Karwowski J, Gierlotka M, Gasior M, Polonski L, Ciszewski J, Beckowski M, Kowalik I, Szwed H. Relationship between an in-farct related artery, acute total coronary occlusion, and mortality in patients with ST-segment and non-ST-segment myocardial infarction. Pol Arch Intern Med. 2017;127:401–411.

26. Stone GW, Cox D, Garcia E, Brodie BR, Morice MC, Griffin J, Mattos L, Lansky AJ, O’Neill WW, Grines CL. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation. 2001;104:636–641. doi: 10.1161/ hc3101.093701

27. Cox DA, Stone GW, Grines CL, Stuckey T, Zimetbaum PJ, Tcheng JE, Turco M, Garcia E, Guagliumi G, Iwaoka RS, et al. Comparative early and late outcomes after primary percutaneous coronary intervention in ST-segment elevation and non–ST-segment elevation acute myocardial infarction (from the CADILLAC Trial). Am J Cardiol. 2006;98:331–337. doi: 10.1016/j.amjcard.2006.01.102

Learning Points:

TIMI 3 flow at the time of cath does not mean a patient didn't have OMI or STEMI.

Many patient with obvious STEMI(+) OMI have TIMI 3 flow at the time of angiogram.

TIMI flow alone cannot be used as an outcome definition for OMI or STEMI.

Rates of initial negative high sensitivity troponin in STEMI(+) OMI:

HS Troponin I

Wereski et al. High-Sensitivity Cardiac Troponin Concentrations at Presentation in Patients With ST-Segment Elevation Myocardial Infarction JAMA Cardiology 2020.

We studied 925 STEMI(+) OMI, and showed that the median initial hs troponin I (Abbott Architect) was 196 ng/L.  20 of 925 (2%) had a level less than 5 ng/L. 133 patients (14.4%) had initial troponin less than the sex-specific 99th percentile upper reference.  26.8% had a level below the European Society "Rule-In" level of 52 ng/L.  Patients presenting less than 2 hours (216 of 809) were more likely to have the initial value below the 99th percentile (26.4%, or 57 of 216)[16 ng/L for women; 34 ng/L for men], compared to those presenting later (14.1%, or 95 of 674)

This shows that whether the patient presents at less than, or greater than, 2 hours, the initial hs troponin I below 5 ng/L does not rule out STEMI, and it certainly does not rule out OMI.  This is even more true for the 99th percentile (16 ng/L for women, and 34 ng/L for men).  And it is even more true for the Rule in level of 52 ng/L.

HS Troponin T

25% of STEMI(+) OMI have negative (less than European Society of Cardiology "rule-in" level of 52 ng/L) initial high sensitivity troponin T (personal communication from Christian Mueller).

Learning Points:

An undetectable or very low troponin does not rule out active Occlusion MI (even STEMI).

14% of patients with STEMI(+) OMI have initial hs troponin I less than the sex-specific 99% upper reference limit.

The lower the initial troponin in OMI, the more myocardium there is left to salvage.

See this case of complete acute LAD occlusion with undetectable hs troponin I: 

Cardiac arrest with anterior-inferior STEMI: Guess the value of the initial ED high sensitivity Abbott troponin I

2014 ACC AHA NSTEMI Guidelines - when is an immediate invasive (within 2 hours) strategy warranted in our current guidelines?

Amsterdam et al. 2014 AHA/ACC NSTE-ACS Guideline. JACC 2014.

4.4.4. Early Invasive and Ischemia-Guided Strategies: Recommendations CLASS I 1. An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures) (42,44,138,338). (Level of Evidence: A)

The Guidelines are Simply Not Followed: 

Lupu et al. Clincial Cardiology. 2022;1-11. Immediate and early percutaneous coronary intervention in very high risk and high risk non-ST segment elevation myocardial infarction patients.

Only 6.4% of very high risk NSTEMI patients underwent less than 2 hr angiography despite guideline indications. Only 44% of high risk patients underwent less than 24 hr angiography despite guideline indications.

"Conclusions: Despite guidelines recommendations for immediate and early PCI in very high-risk and high-risk NSTEMI patients, respectively, most patients do not undergo immediate or early PCI according to contemporary guidelines. Further studies are needed to better understand the reasons for guidelines' nonadherence in those high-risk patients."

Q Waves, Hyperacute T waves, ECG Acuity, and timing of OMI on ECG

(mostly from our EMRAP corependium chapter)

ECG-based timing assessment of OMI
  • High acuity on ECG is a significantly better indicator of a salvageable myocardium than the pain duration.
  • ECG indicators of acuity in general include:
    • The absence of Q waves
    • High ST segments
    • Large/hyperacute T waves
    • The absence of T-wave inversion
  • Anderson-Wilkins acuity score
    • High acuity according to the Anderson-Wilkins acuity score is demonstrated by tall T waves, whereas lower acuity is indicated by Q waves or T-wave inversion.1
    • This score correlates with salvageable myocardium better than the duration of symptoms based on ECG criteria and myocardial perfusion imaging.2-4
  • Hyperacute/tall T waves
    • “Tall” T waves are an independent marker of benefit from thrombolytics, such that STEMI patients who received thrombolytics with tall T waves had a lower 30-d mortality than patients who did not (5.2% vs. 8.6%, = .001), and were less likely to develop heart failure (15% vs. 24%, < .001) and cardiogenic shock (6.1% vs. 8.6%, = .023).5
    • The mortality after thrombolytics in patients with positive T waves is the same for those who have >2 vs. <2 h of symptoms.6
    • These data, combined with common sense and the ECG progression of occlusion MI (above), leads to the logical conclusion that the benefit would be even greater in the presence of hyperacute T waves before the stage of ST segment elevation, when the ratio of salvageable to infarcted myocardium is maximum, although this has never been studied.
    • Unfortunately, hyperacute T waves have never been formally defined.
  • Q-waves
    • Although Q waves may be indicative of lower acuity, it is important to note that QR waves are present in 50% of anterior MI within the first hour of symptom onset, representing ischemia of the conduction system rather than completed infarction. Despite the fact that patients with Q waves on initial ECG had larger final infarct size than those without, "the presence of abnormal Q waves on the admission ECG did not eliminate the effect of thrombolytic therapy on reducing the final infarct size." "Abnormal Q waves are a common finding early in the course of acute myocardial infarction. However, there is no evidence that abnormal Q waves are associated with less benefit in terms of reduction of infarct size after thrombolytic therapy." 7, 8
    • Patients with pathologic Q waves already present within the first hour have a larger final infarct size but benefit equally from thrombolytic therapy.
    • Armstrong et al. more recently showed that Q waves on the “baseline” ECG (first ECG recorded during the event) were an independent marker of a worse outcome, and “after multivariable adjustment, baseline Q-wave but not time from symptom onset was significantly associated with a 78% relative increase in the hazard of 90-d mortality and a 90% relative increase in the hazard of death, shock, and CHF.” 9
    • Therefore, QR waves alone should never be used as a reason to withhold immediate reperfusion therapy.
  • Despite our knowledge of the ECG characteristics of acuity, no randomized thrombolytic trials have been carried out based on these characteristics.

1. Wilkins ML, Pryor AD, Maynard C, et al. An electrocardiographic acuteness score for quantifying the timing of a myocardial infarction to guide decisions regarding reperfusion therapy. Am J Cardiol. 1995;75(8):617-620. doi:10.1016/s0002-9149(99)80629-8 More Info

2. Sejersten M, Ripa RS, Maynard C, et al. Timing of ischemic onset estimated from the electrocardiogram is better than historical timing for predicting outcome after reperfusion therapy for acute anterior myocardial infarction: a DANish trial in Acute Myocardial Infarction 2 (DANAMI-2) substudy. Am Heart J. 2007;154(1):61.e1-61.e618. doi:10.1016/j.ahj.2007.04.003 More Info

3. Engblom H, Strauss DG, Heden B, et al. The evaluation of an electrocardiographic myocardial ischemia acuteness score to predict the amount of myocardial salvage achieved by early percutaneous coronary intervention Clinical validation with myocardial perfusion single photon emission computed tomography and cardiac magnetic resonance. J Electrocardiol. 2011;44(5):525-532. doi:10.1016/j.jelectrocard.2011.03.008 More Info

4. Fakhri Y, Busk M, Schoos MM, et al. Evaluation of acute ischemia in pre-procedure ECG predicts myocardial salvage after primary PCI in STEMI patients with symptoms >12hours. J Electrocardiol. 2016;49(3):278-283. doi:10.1016/j.jelectrocard.2016.02.009 More Info

5. Hochrein J, Sun F, Pieper KS, et al. Higher T-wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for acute myocardial infarction (a GUSTO-I substudy). Global Utilization of Streptokinase and Tissue plasminogen Activator for Occluded Coronary Arteries. Am J Cardiol. 1998;81(9):1078-1084. doi:10.1016/s0002-9149(98)00112-x More Info

6. Herz I, Birnbaum Y, Zlotikamien B, et al. The prognostic implications of negative T waves in the leads with ST segment elevation on admission in acute myocardial infarction. Cardiology. 1999;92(2):121-127. doi:10.1159/000006959 More Info

7. Raitt MH, Maynard C, Wagner GS, Cerqueira MD, Selvester RH, Weaver WD. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol. 1995;25(5):1084-1088. doi:10.1016/0735-1097(94)00514-q More Info

8. Paventi S, Pelliccioni PR, Rossi F, et al. Correlazione tra efficacia della terapia trombolitica e comparsa di onde Q patologiche nella fase precoce dell'infarto miocardico acuto [Correlations between the efficacy of thrombolytic therapy and appearance of abnormal Q waves in the early stages of acute myocardial infarction]. Minerva Cardioangiol. 1997;45(11):559-565. More Info

9. Armstrong PW, Fu Y, Westerhout CM, et al. Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention. J Am Coll Cardiol. 2009;53(17):1503-1509. doi:10.1016/j.jacc.2009.01.046 More Info

Timing of Reperfusion by the ACC/AHA STEMI Guidelines:


The ACC/AHA guidelines state that

"Immediate PCI is recommended if available for STEMI patients with ischemic symptoms for <12 h in duration (class I, level A) and those with ongoing ischemia at 12-24 h after the onset of symptoms (class IIa, level B)."

ACC/AHA 2013 STEMI guidelines say this:

Primary PCI is reasonable in patients with STEMI if there is clinical and/or ECG evidence of ongoing ischemia between 12 and 24 hours after symptom onset (94,95). (Level of Evidence: B). 

But the ACC/AHA guidelines do NOT address the timing (emergent vs. urgent) and they reference two studies, one of which is the Schomig article above, and the other of which also does not address emergent vs. urgent PCI.  

94. Schömig A, Mehilli J, Antoniucci D, et al. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. JAMA. 2005;293: 2865–72.

95. Gierlotka M, Gasior M, Wilczek K, et al. Reperfusion by primarypercutaneous coronary intervention in patients with ST-segment elevationmyocardial infarction within 12 to 24 hours of the onset ofsymptoms (from a prospective national observational study [PL-ACS]). Am J Cardiol. 2011;107:501–8.

There are 2 excellent articles addressing whether a patient with completed MI should undergo PCI at all (vs. medical therapy alone), but none addressing this situation.

Schomig et al. published this in JAMA in 2005:  
Data presented shows benefit of PCI (vs. medical therapy alone) for patients who present between 12-48 hours after STEMI if there was persistent STE, or simply new Q-waveseven in the absence of pain.  But they did not assess the urgency of PCI.
"Conclusion: An invasive strategy based on coronary stenting with adjunctive use of
abciximab reduces infarct size in patients with acute STEMI without persistent symptoms
In this article, they assessed arteries occluded for 3 days or more, and found that PCI resulted in worse outcomes than medical therapy.


Time window for thrombolytics: The GISSI and the LATE trial both established that late thrombolysis, up to 12 hours after onset of chest pain, is beneficial for STEMI.  The FTT collaborative group meta-analysis confirmed this, and the benefit at various time points after pain onset is best described in the paper by Boersma (see Table below).  There are many STEMI, however, which will benefit beyond 12 hours of chest pain: the time onset of chest pain is not necessarily the time of onset of irreversible ischemia.  Many MIs have dynamic occlusion and reperfusion of the infarct-related artery and the pain can go on for days without any significnat necrosis.

Table 33-1 (from my book: The ECG in Acute MI): Time to thrombolysis and mortality reduction.  From: Boersma et al., Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. Lancet October 21, 1996, 348:771-775.  (This applies to all MI: anterior, inferior, lateral)

Time Window
Lives saved per 1000 patients treated (confidence intervals)
0-1 hour
65 (38-93)
1-2 hours
37 (20-55)
2-3 hours
26 (14-37)
3-6 hours
29 (19-40)
6-12 hours
18 (7-29)
12-24 hours
9 (-5-22) (not statistically significant)

NSTEMI Trials: "Early" vs. Late PCI in NSTEMI

Here is a table summarizing all trials:

Here is a quick summary:

Individual Trials

TIMACS (Timing of Intervention in ACS) 

Mehta, et al., New England Journal


•N= 3,000 NonSTEMI randomized to early or routine PCI

•Results: No difference in death/MI/stroke

•GRACE score > 140: better outcome with early PCI

•“Early” intervention was not early

–Median 16 vs. 52 hours

•Methods: no mention of refractory ischemia

•Personal communication with Dr. Mehta

–“I doubt investigators would have enrolled patients with ongoing chest pain in this Non-STE-ACS trial.”

VERDICT Trial (Early Versus Standard Care Invasive Examination and Treatment of Patients with Non-ST-Segment Elevation Acute Coronary Syndrome)

Kofoed et al, Circulation 2018

N=2147 NSTEMI pts (exclusions below), randomized to "very early" (4.7 hrs) vs. "standard" (62 hrs) angiography

88% vs. 84% in each group underwent coronary revascularization

median follow-up time 4.3 years

Primary endpoint: combination of all-cause death, nonfatal recurrent MI, admission for refractory myocardial ischemia, admission for heart failure

- All pts: 27.5% in very early group, 29.5% standard care, no difference

 - Pts with GRACE>140:

GRACE score > 140 confirmed in VERDICT trial

4.7 vs. 62 hours, persistent symptoms excluded. 

Kofoed KF, Kelbæk H, Hansen PR, Torp-Pedersen C. Correction to: Early Versus Standard Care Invasive Examination and Treatment of Patients With Non-ST-Segment Elevation Acute Coronary Syndrome: VERDICT Randomized Controlled Trial. Circulation [Internet] 2018;138(24):e750. Available from:

Exclusion criteria were pregnancy, patient inability to understand trial information, an indication for acute ICA (very high-risk NSTE-ACS,12 including ongoing ischemia despite intravenous nitroglycerin infusion, hemodynamic or electric instability, acute heart failure, mechanical complication, or cardiac arrest), expected survival 

ABOARD* trial (n=360), Montalescot, JAMA 302:947; 2009

       1 vs. 20 hours, no diff., LMWH mostly, No sophisticated ECG analysis

       Refractory symptoms excluded

TIMACS,* Mehta, NEJM 360:2165; 2009, 3000 patients

       No diff except for patients with in-hospital GRACE score > 140 (Early is better)

       Early was not very early (16 vs. 50 hours)

       Excluded refractory ischemia (personal communication, Mehta)

ISAR-COOL,* JAMA 290:1593, 2003; n = 410

       Better early (but 2.4 hours vs. 86 hours); included tirofiban and clopidogrel 600

       Death or Large MI: 11.6% vs. 5.9%;

       Before PCI: 3 death and 10 large MI vs. 0 deaths and 1 small MI; After PCI: 11 MI in both groups

LIPSIA-NSTEMI, Thiele, Eur Ht. Journal 2011, n = 400

       1.1 vs 18.6 hours.  Death or MI: 21% (delayed) vs. 16% (Immediate), p = 0.17, low power

       Excluded refractory ischemia

ELISA PCI, van’t Hof, Eur Ht J 24:1401; 2003.  N= 220. Delayed always got tirofiban. All LMWH.

       6 vs. 50 hours.  Patent vessel: 66% (late) vs. 82% (p = 0.05)

Sisca trial: Reuter P.  Int J Cardiol 182:414; 2015 Did not exclude persistent symptoms

       Early invasive far better. Median 2.8 hrs (1.4-4.7)

Verdict trial (2018): Early 4.7 hrs median. Ongoing symptoms were an exclusion

Optima: within 24 hours vs. 24-72 hours.  Early better.  Multiple studies show 24 hours is better than 72.

Meta-analysis.  Katritsis Eur Ht. J 32:32; 2011 (excludes LIPSIA-NSTEMI)

       In non-urgent cases, early PCI reduces recurrent ischemia and shortens length of stay

Summary: Rapid/Urgent Cath for high risk, unstable, or refractory ischemia.

OMI due to Aortic Dissection is Extremely Rare

Overall, there is likely more harm done by delaying routine OMI care than by missing dissection

STEMI or OMI secondary to dissection is very rare (, so looking for it in the absence of compelling reasons (eg focal neuro or pulse deficit) will just delay reperfusion (

Mortality of acute RBBB and LAFB in anterolateral OMI

Some of the most severe LAD or left main occlusions present with acute RBBB and LAFB, and these findings carry the highest risk for acute ventricular fibrillation, acute cardiogenic shock, and highest in-hospital mortality when studied by Widimsky et al. (in-hospital mortality was 18.8% for AMI with new RBBB alone). Additionally, the RBBB and LAFB make the recognition of the J-point and STE more difficult and more likely to be misinterpreted. Upon successful and timely reperfusion, the patient may regain function of the previously ischemic or stunned fascicles.

Widimsky PW, Rohác F, Stásek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86–95.


Key questions about culprits and TIMI flow

Smith asked Timothy Henry these questions:

In what % of NSTEMI with TIMI-3 flow is there a culprit found, vs. none?  

What percent have TIMI-3 flow AND stenosis < 50% (MINOCA)

What percent of MINOCA have a culprit?

Here is Dr. Henry's answer:

Complicated question! 

Key issue is the definition of “culprit”

We just went thru this is great detail for the Angiographic Core lab for NACMI- the largest COVID + STEMI registry and it would be a great cohort to test- STEMI in covid is very different because they get microvascular thrombi and more frequently have “no culprit” and more frequently have “multiple culprit”

NSTEMI more often have multivessel dz, cabg in 6-12% , I would say easy to tell culprit in 60%, frequently unable to tell and many + trop may not be due to ruptured plaque

5% of STEMI have MINOCA 10% of NSTEMI

MINOCA is  heterogenic with many etiologies: different for STEMI/NSTEMI

MRI with 72 hrs is able  to distinguish 80% into 3 categories: Takysubo/myocarditis/coronary distribution (could be spasm/unrecognized SCAD/emboli/thrombus with resolution)

OCT at the time of the cath in all 3 arteries able to pick up erosion and plaque rupture better but very few STEMI pts have had OCT

As always a major issue is the EKG and angio are not done simultaneous!!

In particular with our STEMI systems we have focused on Pretreatment with IV hep/asa/ticagrelor and this improves the number of pts w TIMI 2/3 flow at the time of angiography



Timothy D. Henry, MD, FACC, MSCAI

Medical Director, The Carl and Edyth Lindner Center for Research and Education

The Carl and Edyth Lindner Family Distinguished Chair in Clinical Research

Director of Programmatic and Network Development

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