What is Occlusive Myocardial Infarction (OMI)?
Occlusive myocardial infarction (OMI) refers to acute myocardial infarction caused by complete or near-complete coronary artery occlusion with TIMI 0-2 flow (or TIMI 3 flow with highly elevated troponin >10.0 ng/mL), regardless of whether traditional STEMI criteria are present on ECG. 1
Key Distinction from Traditional STEMI Classification
The critical issue is that 40% of patients with acute coronary occlusion do not meet traditional STEMI criteria, yet they have the same pathophysiology—complete arterial blockage requiring immediate reperfusion. 1 This represents a major gap in the current classification system that delays treatment and worsens outcomes.
Traditional STEMI Criteria Miss Many OMIs
- Traditional STEMI requires ST elevation ≥0.25 mV in men <40 years, ≥0.2 mV in men ≥40 years, or ≥0.15 mV in women in leads V2-V3, and ≥0.1 mV in other leads 2
- However, patients with STEMI(-)OMI had only 11% receiving PCI within 12 hours compared to 77% of STEMI(+)OMI patients, despite having identical angiographic findings and complication rates 1
- The in-hospital mortality for STEMI(-)OMI was 0.9% compared to 4.2% for STEMI(+)OMI, but mechanical complications occurred at nearly identical rates (46.4% vs 46.8%) 1
Pathophysiology and Mechanisms
OMI most commonly results from Type 1 MI—atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus causing complete coronary occlusion. 3
Alternative Occlusive Mechanisms
- Coronary vasospasm can cause complete or near-complete epicardial artery occlusion, classified as Type 2 MI, where prolonged spasm is the critical determinant for progression to infarction 4
- Focal spasm causing transmural ischemia occurs when dysfunctional endothelium exposes smooth muscle to vasoconstrictors (catecholamines, thromboxane A2, serotonin) 4
- Syncope during chest pain suggests severe ischemia from acute occlusion due to focal spasm 4
Temporal Progression
- After coronary occlusion, histological cell death takes as little as 20 minutes to develop 2
- Complete necrosis of myocardial cells at risk requires 2-4 hours or longer, depending on collateral circulation, intermittent occlusion, and individual oxygen demand 2
- The entire healing process takes at least 5-6 weeks 2
Clinical Recognition Beyond STEMI Criteria
The American College of Cardiology recommends looking beyond traditional STEMI criteria for signs of OMI, including: 5
- ST depression in V1-V3 suggesting posterior OMI (requires checking V7-V9 leads) 5
- Ongoing chest pain despite medical therapy 5
- Hemodynamic instability or cardiogenic shock 5
- New or presumed new significant ST-segment changes or new LBBB 2
Diagnostic Approach
- Obtain 12-lead ECG within 10 minutes of first medical contact 5
- Machine learning algorithms show superior performance (AUC 0.953) for identifying OMI compared to traditional STEMI criteria, though not yet standard practice 5
- Angiographic definition: acute culprit lesion with TIMI 0-2 flow, or TIMI 3 flow with highly elevated troponin (cTnI >10.0 ng/mL or hs-cTnI >5000 ng/L) 1
Treatment Implications
All OMI patients require immediate reperfusion regardless of STEMI criteria, as they have complete coronary occlusion: 1
- Primary PCI is preferred when available within 120 minutes of diagnosis 3
- If PCI cannot be performed within 120 minutes, immediate fibrinolysis should be initiated within 10 minutes 3
- Antithrombotic therapy includes anticoagulants (unfractionated heparin) and dual antiplatelet therapy (aspirin plus prasugrel/ticagrelor) 3
Critical Pitfall
The most dangerous error is delaying catheterization in STEMI(-)OMI patients because they don't meet traditional STEMI criteria. These patients have identical rates of requiring PCI (89% vs 93%) and similar complication rates as STEMI(+)OMI patients. 1 The current STEMI/NSTEMI paradigm causes systematic delays in treatment for 40% of patients with complete coronary occlusion. 1