Abstract
Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a heterogeneous entity requiring systematic exclusion of alternative diagnoses and identification of the underlying mechanism. Coronary microvascular dysfunction (CMD) is an important but often underdiagnosed cause. Systemic inflammatory flares may precipitate microvascular ischemia, yet direct multimodality confirmation remains limited. A 51-year-old woman with active perinuclear anti-neutrophil cytoplasmic antibody (P-ANCA) vasculitis, rheumatoid arthritis, and stage 3b chronic kidney disease presented with acute chest pain, dynamic ST-segment changes, and a rise in high-sensitivity troponin T (peak 2,526 pg/mL), fulfilling criteria for acute myocardial infarction. Coronary angiography demonstrated non-obstructive coronary arteries (<50% stenosis). Cardiac magnetic resonance imaging (including T1 mapping, T2 mapping, and LGE) excluded myocarditis, stress cardiomyopathy, and infiltrative disease. Invasive coronary physiology revealed impaired coronary flow reserve (CFR 1.7) and an elevated index of microvascular resistance (IMR 32). Acetylcholine provocation excluded epicardial vasospasm. (13)N-ammonia positron emission tomography (PET) confirmed reduced global stress myocardial blood flow and global myocardial flow reserve (1.8), consistent with diffuse CMD. The inflammatory surge (leukocytosis, raised ESR, raised CRP) temporally paralleled troponin elevation. A diagnosis of inflammatory-triggered MINOCA due to diffuse CMD was established. Immunosuppressive therapy was optimized alongside mechanism-directed antianginal therapy. Dual antiplatelet therapy was limited to a short course given the absence of plaque rupture and elevated bleeding risk. At the six-month follow-up, inflammatory markers and troponin normalized, and the patient remained symptom-free. This case demonstrates an inflammatory endotype of MINOCA, where acute autoimmune activation precipitated diffuse CMD. Multimodality confirmation with invasive physiology and PET imaging established the mechanism beyond exclusion. Mechanism-directed therapy targeting the inflammatory substrate, in addition to tailored cardiovascular management, resulted in clinical stabilization.