Molecular screening in a translational large animal trial identifies a differential inflammatory response for MINOCA.

ABSTRACT: Myocardial infarction without obstructive coronary arteries (MINOCA) comprises up to 15% of all myocardial infarctions (MI) and could be caused by cardiac microembolization (CME) originating from plaque rupture and/or erosion. Early diagnosis remains a challenge due to limited early biomarkers, leading to high morbidity. Here, we have systematically characterized acute (up to 5 h) CME-induced MINOCA in comparison to MI using clinical markers, histology, multi-ELISAs, miRNA profiling, and proteomics in a translational porcine animal model. CME-induced MINOCA model was created by injecting autologous microthrombi, generated by carotid crush maneuver, into the coronary arteries, whereas MI was induced by LAD balloon occlusion/reperfusion. MINOCA animals exhibited low troponin (547.0 ± 489.2 n

SUBMITTER: Iske J 

PROVIDER: S-EPMC12325550 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature