Phenotype-oriented therapy in non-coronary myocardial ischemia and coronary microvascular dysfunction: from the OMI/NOMI paradigm to the prognostic role of ranolazine

October 13, 2026
40
УДК:  УДК 616.12-008.46-036.11
Resume

Modern emergency cardiology is currently undergoing a revision of diagnostic algorithms for acute coronary syndrome. The traditional classification into ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) possesses significant limitations, leaving up to one-third of patients with total arterial occlusion without urgent revascularization. Data from the European Society of Cardiology Congress (ESC Congress 2026) and clinical trials (specifically DIFOCCULT-3) have substantiated the transition to the pathomorphological OMI/NOMI concept (occlusive / non-occlusive myocardial infarction). Patients with MINOCA and INOCA phenotypes present a distinct clinical challenge; while lacking macrostructural epicardial vessel stenoses, they exhibit persistent ischemia driven by coronary microvascular dysfunction, immune mimics (Kounis syndrome), neurogenic crises (Takotsubo cardiomyopathy), or anatomical anomalies (myocardial bridging). This review analyzes the shared pathophysiological mechanisms of non-coronary ischemia, the molecular role of the late sodium current, and the clinical efficacy of its selective inhibitor, ranolazine. Integrated data from the large-scale TriNetX study (2026) demonstrate the long-term prognostic benefits of ranolazine in reducing heart failure hospitalization rates within this patient cohort.

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