Fuad A Abdu
Myocardial infarction with nonobstructive coronary arteries (MINOCA) is identified in approximately 5 to 10% of patients with myocardial infarction referred for coronary angiography, and it remains a working diagnosis rather than a final mechanistic one. The diagnostic challenge is greatest in young women during pregnancy and the early postpartum period. Pregnancy-related and pregnancy-amplified conditions are increasingly recognized contributors, yet direct MINOCA evidence is uneven. This review examines how hypertensive disorders of pregnancy (HDP), gestational diabetes mellitus (GDM), antiphospholipid syndrome (APS) and inherited thrombophilia, and spontaneous coronary artery dissection (SCAD) map onto distinct patterns of coronary and microvascular injury. The links between HDP or GDM and MINOCA are supported mainly by mechanistic and microvascular studies outside dedicated MINOCA cohorts. APS, by contrast, is supported by direct although limited MINOCA-specific data, and pregnancy-associated SCAD is better characterized as a cause of myocardial infarction, although only cases with less than 50% angiographic stenosis meet MINOCA criteria. Serial high-sensitivity cardiac troponin and standard acute coronary syndrome assessment remain the diagnostic foundation. Cardiac magnetic resonance, selective intracoronary imaging, and targeted antiphospholipid testing can refine mechanism assignment after stabilization. The ratio of soluble fms-like tyrosine kinase-1 to placental growth factor is established for the evaluation of suspected preeclampsia, but its relevance to coronary microvascular injury in MINOCA remains uncertain. Inherited thrombophilia testing should be individualized rather than applied routinely. The assigned mechanism should then guide antithrombotic treatment, revascularization decisions, and follow-up. Prospective phenotype-defined studies are needed before routine biomarker-driven strategies can be recommended.