Key result
OMI misclassification occurs at similar rates across all culprit vessel territories.
Why the study?
The study aimed to assess whether the culprit vessel influenced Occlusion Myocardial Infarction (OMI) reclassification patterns in acute coronary syndromes.
Does the culprit vessel influence OMI reclassification patterns in patients with acute coronary syndromes?
Observational (n=330)
Does the culprit vessel influence OMI reclassification patterns in patients with acute coronary syndromes?
Coronary occlusion (OMI) can remain unrecognized by traditional STEMI criteria across all vascular territories, independently of the specific culprit vessel.
Answers are grounded in this paper and cite their sources.
No significant vessel-specific OMI misclassification differences; confirms uniform reclassification accuracy across culprit arteries.
Introduction The Occlusion Myocardial Infarction (OMI) paradigm challenges the traditional STEMI paradigm, emphasizing the identification of coronary occlusion beyond classical ECG criteria. In this study, patients were initially classified as STEMI or NSTEMI and subsequently reclassified into STEMI, NSTEMI-OMI, and NSTEMI-non-OMI groups based on the OMI framework. We aimed to assess whether the culprit vessel influenced OMI reclassification patterns. Methods We retrospectively analyzed 330 patients admitted with ACS. Patients were initially classified as STEMI or NSTEMI. OMI was defined by angiographic occlusion (TIMI flow ≤ 2) and/or markedly elevated troponin levels (Troponin T > 1000 ng/L or Troponin I > 5000 ng/L) in the presence of regional wall motion abnormalities. Patients were thus stratified into STEMI, NSTEMI-OMI, and NSTEMI-non-OMI groups. Culprit vessels were categorized as left main (LM), left anterior descending (LAD), left circumflex (LCx), and right coronary artery (RCA). Results A total of 327 patients had complete data on OMI classification and culprit vessel. Among patients with STEMI (n = 193; 59.0%), the culprit vessel was the LAD in 91 cases (47.2%), the RCA in 60 (31.1%), the LCx in 39 (20.2%), and the LM in 3 (1.6%). Within the NSTEMI cohort (n = 134), reclassification according to the OMI framework identified 52 NSTEMI-OMI and 82 NSTEMI-non-OMI cases. In patients with NSTEMI-OMI the culprit vessel was the RCA in 23 cases (44.2%), the LAD in 18 (34.6%), and the LCx in 9 (17.3%). Among NSTEMI-non-OMI patients, the culprit was the LAD in 38 cases (46.3%), the RCA in 27 (32.9%), and the LCx in 16 (19.5%). When analyzed by vessel, LAD lesions (n = 147; 45.0%) corresponded to 91 STEMI (61.9%), 18 NSTEMI-OMI (12.2%), and 38 NSTEMI-non-OMI (25.9%). Among RCA lesions (n = 110; 33.6%), 60 (54.5%) were STEMI, 23 (20.9%) NSTEMI-OMI, and 27 (24.5%) NSTEMI-non-OMI. For LCx lesions (n = 64; 19.6%), 39 (60.9%) were STEMI, 9 (14.1%) NSTEMI-OMI, and 16 (25.0%) NSTEMI-non-OMI. Although the RCA showed a trend toward a higher proportion of misclassification, no statistically significant differences were observed between groups (p = 0.522). Discussion Our findings indicate that OMI misclassification occurs across all vascular territories and is not confined to a specific culprit vessel. The absence of a significant relationship between OMI reclassification and infarct-related artery suggests that anatomical distribution alone does not explain diagnostic under-recognition. Conclusion OMI can occur in any coronary territory, independently of the culprit vessel, highlighting that coronary occlusion may remain unrecognized regardless of infarct location.
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Lobo et al. (2026) conducted an observational in Acute coronary syndromes (ACS) (n=330). Occlusion Myocardial Infarction (OMI) reclassification was evaluated on Differences in OMI reclassification patterns by culprit vessel (p=0.522). Occlusion Myocardial Infarction (OMI) misclassification occurred across all vascular territories without statistically significant differences between culprit vessels (p = 0.522).
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