Circulating Small Extracellular Vesicles Reflect the Severity of Myocardial Damage in STEMI Patients
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Published:2023-09-29
Issue:10
Volume:13
Page:1470
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ISSN:2218-273X
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Container-title:Biomolecules
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language:en
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Short-container-title:Biomolecules
Author:
Zarà Marta1, Baggiano Andrea12ORCID, Amadio Patrizia1, Campodonico Jeness1, Gili Sebastiano1, Annoni Andrea1ORCID, De Dona Gianluca1, Carerj Maria Ludovica1, Cilia Francesco1, Formenti Alberto1, Fusini Laura13ORCID, Banfi Cristina1ORCID, Gripari Paola1, Tedesco Calogero Claudio1, Mancini Maria Elisabetta1, Chiesa Mattia1ORCID, Maragna Riccardo1, Marchetti Francesca1, Penso Marco1ORCID, Tassetti Luigi1, Volpe Alessandra1ORCID, Bonomi Alice1, Marenzi Giancarlo1, Pontone Gianluca14, Barbieri Silvia Stella1ORCID
Affiliation:
1. Centro Cardiologico Monzino IRCCS, 20138 Milan, Italy 2. Department of Clinical Sciences and Community Health, University of Milan, 20122 Milan, Italy 3. Department of Electronics, Information and Bioengineering, Politecnico di Milano, 20156 Milan, Italy 4. Department of Biomedical, Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy
Abstract
Circulating small extracellular vesicles (sEVs) contribute to inflammation, coagulation and vascular injury, and have great potential as diagnostic markers of disease. The ability of sEVs to reflect myocardial damage assessed by Cardiac Magnetic Resonance (CMR) in ST-segment elevation myocardial infarction (STEMI) is unknown. To fill this gap, plasma sEVs were isolated from 42 STEMI patients treated by primary percutaneous coronary intervention (pPCI) and evaluated by CMR between days 3 and 6. Nanoparticle tracking analysis showed that sEVs were greater in patients with anterior STEMI (p = 0.0001), with the culprit lesion located in LAD (p = 0.045), and in those who underwent late revascularization (p = 0.038). A smaller sEV size was observed in patients with a low myocardial salvage index (MSI, p = 0.014). Patients with microvascular obstruction (MVO) had smaller sEVs (p < 0.002) and lower expression of the platelet marker CD41–CD61 (p = 0.039). sEV size and CD41–CD61 expression were independent predictors of MVO/MSI (OR [95% CI]: 0.93 [0.87–0.98] and 0.04 [0–0.61], respectively). In conclusion, we provide evidence that the CD41–CD61 expression in sEVs reflects the CMR-assessed ischemic damage after STEMI. This finding paves the way for the development of a new strategy for the timely identification of high-risk patients and their treatment optimization.
Funder
Italian Ministry of Health, Rome, Italy
Subject
Molecular Biology,Biochemistry
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