Echocardiographic parameters combined with miR-660-3p for the assessment of acute myocardial infarction: clinical utility and in vitro functional validation

Acute myocardial infarction (AMI) strikes suddenly and progresses rapidly, yet early recognition remains difficult. This study explores combining miR-660-3p with echocardiography for noninvasive assessment of AMI, plus cell experiments to clarify its role in cardiomyocyte damage. A total of 105 non-cardiogenic chest pain cases and 127 AMI cases were enrolled, with clinical data, echocardiographic parameters, and serum miR-660-3p levels collected from all participants. Multivariate logistic regression identified independent factors associated with AMI, and ROC curves assessed the diagnostic value of individual and combined indicators. In vitro, H₂O₂ was used to induce injury in H9c2 cardiomyocytes, followed by transfection with a miR-660-3p inhibitor to evaluate changes in cell viability (CCK-8) and inflammatory cytokines (ELISA). Compared with controls, the AMI group exhibited markedly lower left ventricular ejection fraction and fractional shortening, along with a larger left ventricular end-diastolic diameter and significantly elevated serum miR-660-3p levels. Multivariate logistic regression identified miR-660-3p as an independent risk factor. ROC analysis showed an AUC of 0.815 for miR-660-3p alone, which increased to 0.944 when combined with echocardiographic parameters. In vitro, suppressing miR-660-3p alleviated H₂O₂-induced cardiomyocyte injury, improved cell viability, and reduced inflammatory cytokine release. miR-660-3p levels are significantly correlated with AMI, and incorporating this marker into echocardiography may enhance noninvasive diagnostic accuracy. The molecule may mediate cardiomyocyte injury via inflammatory pathways, suggesting its potential clinical value.