CONGRESS ABSTRACT

53-year-old man with a history of arterial hypertension, active smoking, and a family history of myocardial infarction (father with MI at approximately 50 years of age). The patient presented to the emergency department with intense, persistent, oppressive chest pain. Similar episodes of pain had occurred over the past 4–5 days, although these were less severe and lasted approximately 15 minutes, resolving spontaneously at rest. On ECG: sinus rhythm with a heart rate of 90 bpm, minimal isolated ST-segment elevation in lead DIII with a j-point upward slope in aVF, reciprocal ST-segment depression in aVL, and premature ventricular complexes with a right bundle branch block morphology. Echocardiography revealed globally borderline left ventricular function (LVEF 55%), with akinesia of the mid-basal inferior wall. Initial troponin levels were markedly elevated, approximately 6000 pg/ml. An urgent coronary angiography was performed, revealing a thrombotic stenosis in the mid-right coronary artery (RCA), treated with primary percutaneous coronary intervention (PCI). Additionally, a critical stenosis in the mid-proximal left anterior descending artery (LAD) was identified and treated with staged PCI. Dual antiplatelet therapy (DAPT) with aspirin and prasugrel was initiated, along with optimal medical therapy. This case can be categorized as STEMI-negative but OMI-positive, referring to an occlusive myocardial infarction (OMI) that does not meet the classic STEMI criteria yet requires urgent revascularization to improve prognosis and morbidity by preventing large areas of myocardial necrosis. In this patient, the ECG findings did not fulfill the STEMI criteria (ST-segment elevation was present exclusively in lead DIII). However, the angiographic findings and significantly elevated troponin levels (in the context of typical chest pain and risk factors) confirmed an infarction requiring immediate activation of the catheterization laboratory and urgent revascularization. This clinical case highlights the limitations of the current STEMI/NSTEMI paradigm, as described by Smith et al. in multiple observational studies. Importantly, no previously described OMI patterns by Smith et al. were present in this ECG, only a very early ischemic vector. Alongside the ST-segment elevation in lead DIII, the exact reciprocal changes in lead aVL (from a vectorial perspective) are noteworthy.