Unraveling MINOCA: The hidden impact of inflammation on myocardial infarction without coronary obstruction

Abstract Myocardial infarction with non-obstructive coronary arteries (MINOCA) accounts for 5% to 15% of myocardial infarction (MI) cases; it presents with clinical signs of MI without significant coronary artery obstruction. Unlike MI with obstructive coronary artery disease (MICAD), which is primarily caused by atherosclerotic plaque rupture, MINOCA arises from mechanisms such as coronary vasospasm, coronary microvascular dysfunction (CMD), thromboembolism, plaque disruption, and spontaneous coronary artery dissection (SCAD). Inflammation plays a key role in both conditions, though its mechanisms differ; MICAD is driven by atherosclerosis-related inflammation, while MINOCA is associated with endothelial dysfunction, oxidative stress, and immune activation. Elevated biomarkers such as high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) highlight systemic inflammation in MINOCA, correlating with adverse outcomes. Despite the absence of significant coronary obstruction, MINOCA is not benign, and has a significant mortality rate and a high risk of recurrent cardiovascular events. Imaging modalities such as cardiac magnetic resonance (CMR) and intravascular ultrasound (IVUS) improve diagnosis, while emerging therapies targeting inflammation, including IL-1β inhibitors and colchicine, may offer benefits. Future research should focus on personalized treatment strategies addressing the inflammatory and microvascular components of MINOCA to enhance risk stratification and improve long-term outcomes.