MiR-146a Contributes to Thromboinflammation and Recurrence in Young Patients with Acute Myocardial Infarction

Abstract: Studies on older patients have established notable conceptual changes in the etiopatho genesis of acute coronary syndrome (ACS), but little is known about this disease in young patients ( Q4 more frequently had a history of previous stroke (6.1% vs. 1.6%). In turn, rs2431697 did not confer...

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Detalles Bibliográficos
Autores: de los Reyes García, Ascensión M., Rivera Caravaca, José Miguel, Zapata Martínez, Laura, Águila, Sonia, Véliz Martínez, Andrea, García Barberá, Nuria, Gil Pérez, Pablo, Guijarro Carrillo, Pedro J., Orenes Piñero, Esteban, López García, Cecilia, Lozano, María L., Marín, Francisco, Martínez, Constantino, González Conejero, Rocío
Tipo de recurso: artículo
Fecha de publicación:2022
País:España
Institución:Universidad Católica San Antonio de Murcia (UCAM)
Repositorio:RIUCAM. Repositorio Institucional de la Universidad Católica San Antonio de Murcia
OAI Identifier:oai:repositorio.ucam.edu:10952/10706
Acceso en línea:http://hdl.handle.net/10952/10706
Access Level:acceso abierto
Palabra clave:miR-146a
Thromboinflammation
Acute Myocardial infarction
Recurrence
Young Patients
Descripción
Sumario:Abstract: Studies on older patients have established notable conceptual changes in the etiopatho genesis of acute coronary syndrome (ACS), but little is known about this disease in young patients ( Q4 more frequently had a history of previous stroke (6.1% vs. 1.6%). In turn, rs2431697 did not confer increased risk for the onset of ACS, but T carriers had significantly higher levels of NET markers. By groups, we found that cfDNA levels were similarly higher in all patients, but citH3–DNA was especially higher in G1, suggesting that in plasma, this marker may be attenuated over time. Finally, patients from G2 with the worst markers (cfDNA and citH3–DNA > Q2 and T allele) had a two-fold increased risk of a new ischemic event at 2-year follow-up. In conclusion, our data confirm that ACS is younger onset with thromboinflammatory disease. In addition, these data consolidate rs2431697 as a silent proinflammatory factor predisposing to NETosis, and to a higher rate of adverse events in different cardiovascular diseases