J Vis Exp. 2026 Oct 27;(236). doi: 10.3791/74890.
ABSTRACT
Primary percutaneous coronary intervention (pPCI) restores epicardial coronary flow in ST-segment elevation myocardial infarction (STEMI), but microvascular and tissue-level reperfusion may remain impaired. Cardiovascular magnetic resonance (CMR)-defined microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH) both mark severe reperfusion injury but reflect distinct tissue processes. This structured narrative review synthesizes evidence on MVO mechanisms, multimodal phenotypes, and interventions. Available evidence implicates interacting contributions from distal embolization, endothelial barrier and vasomotor dysfunction, pericyte-mediated capillary constriction, immunothrombosis, and tissue edema. IMH reflects more extensive microvascular destruction with erythrocyte extravasation. Angiography, electrocardiography, invasive physiology, angiography-derived indices, echocardiography, and CMR assess different pathophysiologic levels. Discordance between modalities is therefore not necessarily contradictory. Across trials, improvements in surrogate endpoints have often not translated into long-term clinical benefit, partly because of mechanistic heterogeneity and misaligned treatment timing and endpoints. A conceptual, reperfusion-centered T- to T5 research framework is proposed for serial within-patient assessment. It links early physiology, inflammatory and thrombotic biomarkers, acute-phase CMR, and long-term remodeling. Future trials should align mechanistic enrichment, intervention timing, and endpoint selection to establish a continuous evidence chain from target engagement to clinical outcomes.
PMID:42949117 | DOI:10.3791/74890