Summary

1. The STEMI criteria significantly underestimate the incidence of acute coronary occlusion (ACO), missing approximately 25-30% of cases that would benefit from emergent reperfusion.
2. Occlusion Myocardial Infarction (OMI), defined by ECG and clinical findings suggestive of acute coronary occlusion, is the true indication for emergent reperfusion therapy, superseding the STEMI/NSTEMI paradigm.
3. ECG diagnosis of OMI requires a nuanced approach evaluating the entire ECG complex and pattern, not just isolated ST-segment elevation measurements.
4. Patients with unrecognized OMI (often labeled NSTEMI) suffer worse outcomes due to delayed reperfusion compared to NOMI patients or OMI patients who receive timely treatment.
5. Trials comparing early versus delayed intervention in broad NSTEMI populations have limited ability to inform the optimal management of OMI due to patient exclusion criteria and definitions of "early" intervention often being too late for maximal myocardial salvage.

Introduction

Timely reperfusion is the cornerstone of managing acute myocardial infarction (MI) to salvage myocardium and improve patient outcomes. However, the long-established ST-elevation myocardial infarction (STEMI) criteria have significant limitations, often failing to identify patients with acute coronary occlusion (ACO) who require emergent intervention. This diagnostic gap can lead to critical delays in care. Understanding the concept of Occlusion Myocardial Infarction (OMI) provides a more pathophysiologically sound approach, focusing on identifying true coronary occlusion regardless of whether traditional STEMI voltage criteria are met. This guide outlines key facts physicians need to know about the OMI paradigm versus the traditional STEMI/NSTEMI classification. This information is adapted from the OMI manifesto, linked below.

1) The STEMI criteria significantly underestimate the incidence of acute coronary occlusion (ACO), missing approximately 25-30% of cases that would benefit from emergent reperfusion.

The fundamental reason for emergent reperfusion therapy, whether percutaneous coronary intervention (PCI) or thrombolysis, is the presence of an ACO that threatens imminent transmural infarction. This physiological reality is not perfectly captured by merely measuring ST-segment elevation (STE) against specific voltage thresholds. Multiple studies, including post-hoc analyses like Wang et al. (PARAGON-B) and prospective studies such as Schmitt et al., have confirmed this gap, finding that approximately one-quarter to one-third of patients initially classified under the non-ST-elevation acute coronary syndrome (NSTE-ACS) umbrella actually had an occluded culprit artery identified during angiography.

Occlusions of the left circumflex (LCx) artery are particularly notorious for being missed by standard STEMI criteria. These often manifest without significant STE or present only with subtle posterior ECG changes, such as anterior ST depression. This failure to meet formal STEMI criteria despite having an OMI ("STEMI(-) OMI") results in critical delays to reperfusion. Consequently, these patients experience larger infarct sizes, lower resulting ejection fractions, and an increased long-term risk of heart failure and mortality. Conversely, the STEMI criteria are also known for triggering false-positive catheterization lab activations (rates reported between 10-40%). This occurs frequently due to various STE mimics, including benign early repolarization, left ventricular hypertrophy (LVH), pericarditis, or stable left ventricular aneurysms, highlighting the criteria's lack of specificity.

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2) Occlusion Myocardial Infarction (OMI), defined by ECG and clinical findings suggestive of acute coronary occlusion, is the true indication for emergent reperfusion therapy, superseding the STEMI/NSTEMI paradigm.

The primary objective of emergent reperfusion is the rapid restoration of blood flow in an acutely occluded coronary artery to salvage heart muscle at risk. This therapeutic benefit is specifically relevant to patients experiencing an OMI, regardless of whether their ECG meets the formal voltage criteria for STEMI. In contrast, Non-Occlusion MI (NOMI) includes myocardial infarctions resulting from non-occlusive thrombi, cases where spontaneous reperfusion occurred before presentation, type 2 MI stemming from supply-demand mismatch, or other causes lacking a persistent occlusion. Patients with NOMI typically do not benefit from emergent reperfusion (aiming for <2 hours), although urgent angiography (within 24-72 hours) is frequently indicated based on their overall risk profile.

Identifying OMI requires advanced ECG interpretation skills that go beyond simply measuring STE. Clinicians must recognize subtle patterns like hyperacute T-waves, STE that is disproportionately significant relative to the QRS amplitude, specific patterns indicating posterior MI, certain T-wave inversions (like Wellens' sign, which signifies critical LAD stenosis but isn't typically an OMI itself), and interpret findings in the context of underlying QRS morphology (e.g., applying modified Sgarbossa criteria in Left Bundle Branch Block or paced rhythms). The clinical context is also paramount. Persistent ischemic symptoms unresponsive to medical therapy, hemodynamic instability, or the presence of cardiogenic shock strongly point towards OMI and necessitate immediate intervention, sometimes even if the initial ECG is non-diagnostic. It's worth noting that the landmark Fibrinolytic Therapy Trialists' (FTT) meta-analysis, which established the benefit of reperfusion, included many patients who did not meet defined STE criteria, underscoring that STE was an early, though imperfect, surrogate for the actual condition benefiting from reperfusion: ACO/OMI.

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3) ECG diagnosis of OMI requires a nuanced approach evaluating the entire ECG complex and pattern, not just isolated ST-segment elevation measurements.

Recognizing OMI often involves identifying signs beyond standard STE criteria. Hyperacute T-waves, characterized by their broad base, prominence, and symmetry (often taller than the associated QRS complex in some leads), can represent the earliest ECG manifestation of OMI. They may precede significant STE or, in some cases, be the only sign present. The clinical significance of any measured STE amplitude must always be assessed relative to the amplitude of the preceding QRS complex. Seemingly minor STE (<1 mm) can be highly indicative of OMI if the corresponding QRS voltage is low, especially in leads I, aVL, or V5-V6. Conversely, substantial absolute STE might be a normal or expected finding in conditions like LBBB or LVH, reflecting appropriate discordance.

Suspicion for posterior OMI, frequently involving the LCx artery, should arise when ST depression is maximal in leads V1-V4, particularly if accompanied by upright T waves in those leads. Tall R waves in V1-V2 can also be suggestive. Obtaining posterior ECG leads (V7-V9) is crucial in these situations, as they may reveal diagnostic STE not visible on the standard 12-lead ECG. Furthermore, specific patterns like de Winter T-waves (characterized by upsloping ST depression in the precordial leads that merges into tall, peaked, symmetric T-waves) are considered OMI equivalents, strongly suggesting proximal LAD occlusion. The presence of reciprocal changes (ST depression in leads electrically opposite to those showing STE) significantly increases the specificity of STE for OMI. This helps differentiate true ischemic STE from mimics like pericarditis, which typically causes diffuse STE without clear reciprocal depression (except potentially in leads aVR and V1).

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4) Patients with unrecognized OMI (often labeled NSTEMI) suffer worse outcomes due to delayed reperfusion compared to NOMI patients or OMI patients who receive timely treatment.

When OMI is not promptly identified and treated, often because it doesn't meet formal STEMI criteria, the delay in reperfusion allows the infarct to progress. This leads to a greater extent of myocardial necrosis, which in turn increases the likelihood of developing left ventricular dysfunction, subsequent heart failure, life-threatening ventricular arrhythmias, and contributes to higher mortality rates both in the short and long term.

The post-hoc analysis of the PARAGON-B trial by Wang et al. provided clear evidence of this disparity. It showed that patients initially classified as NSTE-ACS but found to have an ACO on angiography had significantly higher 6-month mortality and larger infarct sizes (indicated by cardiac biomarkers) compared to NSTE-ACS patients without ACO, even though both groups had similar (delayed) times to angiography within the trial protocol. Failure to recognize subtle OMI patterns on the ECG can also lead to misclassification using standard risk stratification tools like TIMI or GRACE scores. This may result in inappropriately delayed invasive management for patients who actually require emergent reperfusion. Conversely, prompt recognition and emergent reperfusion of OMI, irrespective of meeting STEMI criteria, aims to limit infarct size and improve clinical outcomes, potentially bringing the prognosis closer to that observed in STEMI patients who receive treatment within guideline-recommended timeframes. Supporting this, the Koyama et al. study implemented an immediate invasive strategy for all suspected ACS, including NSTEMI (finding TIMI 0 flow in 47% of this group), and observed similar outcomes between the STEMI and NSTEMI groups. This suggests that eliminating the reperfusion delay for occult OMI mitigates the typically worse prognosis associated with this subgroup when managed conventionally.

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5) Trials comparing early versus delayed intervention in broad NSTEMI populations have limited ability to inform the optimal management of OMI due to patient exclusion criteria and definitions of "early" intervention often being too late for maximal myocardial salvage.

Interpreting the results of major trials that randomized NSTEMI patients to different invasive timing strategies (e.g., TIMACS, ICTUS, ELISA) requires acknowledging their limitations regarding the OMI population. Critically, many of these key trials explicitly excluded patients presenting with ongoing refractory ischemia, hemodynamic instability, or significant arrhythmias. These are precisely the patients most likely to harbor an underlying OMI requiring immediate attention.

Furthermore, the definition of "early" intervention within these trials often spanned from less than 12 hours to less than 24 hours (for instance, the median time in the early arm of TIMACS was 14 hours). This timeframe is considerably longer than the "golden hour" (generally considered <60-90 minutes) targeted for optimal reperfusion in OMI/STEMI to achieve the greatest degree of myocardial salvage. While some trials, like TIMACS, did demonstrate a benefit for an "earlier" (<24h) invasive strategy specifically in high-risk NSTEMI patients (defined by a GRACE score >140), this finding doesn't directly address the potential advantage of emergent reperfusion (within <2 hours) for the subset of patients within that high-risk group who actually have an OMI.

The RIDDLE-NSTEMI trial offers more direct insight. It specifically randomized higher-risk NSTEMI patients (those with STE or T-wave inversions) to either immediate (<2h) or delayed (median 61h) PCI. The results showed a significant reduction in the primary endpoint (a composite of death or new MI at 30 days) favoring the immediate intervention group. This benefit was largely attributed to preventing adverse events that occurred while patients were awaiting delayed catheterization, supporting the idea that prompt intervention is beneficial for a high-risk NSTEMI subgroup likely enriched with OMI cases. Therefore, it is crucial to understand that NSTEMI timing trials compare different strategies within the conventional NSTEMI paradigm; they do not directly compare an OMI-focused emergent strategy versus a delayed strategy for patients specifically identified using OMI criteria.

Conclusion

The traditional STEMI/NSTEMI paradigm, while historically useful, has inherent limitations, particularly its failure to identify a significant proportion of patients with acute coronary occlusion (OMI) who require immediate reperfusion. Recognizing OMI, based on a nuanced ECG interpretation beyond simple STE criteria and careful consideration of the clinical context, represents a more accurate approach to identifying patients who will benefit most from emergent intervention. Delays in reperfusion for unrecognized OMI lead to demonstrably worse outcomes. While large NSTEMI trials offer some insights, their design limitations prevent direct extrapolation to the OMI population. Embracing the OMI framework encourages clinicians to look beyond rigid criteria, apply advanced ECG skills, and prioritize rapid reperfusion for all patients with evidence of acute coronary occlusion, ultimately aiming to reduce infarct size and improve survival.

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Source

The OMI Manifesto

Authors: Dr. Stephen Smith, Dr. Pendell Meyers, Dr. Scott Weingart

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Other Resources

Acute Myocardial Infarction: A Shifting Paradigm

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