MINOCA (Myocardial Infarction With Non-obstructive Coronary Arteries) Due to Diffuse Coronary Microvascular Dysfunction in a Patient With Systemic Autoimmune Disease and Chronic Kidney Disease

TL;DR

A patient with autoimmune disease and kidney disease experienced a heart attack due to microvascular dysfunction, confirmed through advanced imaging and treated with targeted therapy.

Contribution

Demonstrates an inflammatory-triggered MINOCA case confirmed by multimodal imaging and highlights mechanism-directed therapy effectiveness.

Findings

Inflammatory flare-up caused diffuse coronary microvascular dysfunction confirmed by PET and invasive tests.

Optimized immunosuppressive therapy and tailored cardiovascular management stabilized the patient's condition.

Short-term antiplatelet therapy was sufficient due to absence of plaque rupture and high bleeding risk.

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. 13N-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.

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