The role of miR1 and miR133a in new-onset atrial fibrillation after acute myocardial infarction

Abstract

Abstract Background: The development of new-onset atrial fibrillation (NOAF) after acute myocardial infarction (AMI) is a clinical complication that requires a better understanding of the causative risk factors. In this study, we aimed to explore risk factors and the expression and function of miR1 and miR133a in new atrial fibrillation after AMI. Methods: We collected clinical data from 172 patients with AMI treated with emergency percutaneous coronary intervention (PCI) from October 2021 to October 2022. Independent predictors of NOAF were determined using binary logistic univariate and multivariate regression analyses. The NOAF predictive value was evaluated using the area under the receiver operating characteristic (ROC) curve for related risk factors. In total, 172 venous blood samples were collected preoperatively and on the first day postoperatively; the expression levels of miR1 and miR133a were determined by polymerase chain reaction. The clinical significance of miR1 and miR133a expression levels was determined by Spearman correlation analysis. Results: The Glasgow prognosis score, left atrial diameter, and infarct area were significant, independent risk factors for NOAF after AMI. We observed that the expression levels of miR1 and miR133a were significantly higher in the NOAF group than in the non-NOAF group. On postoperative day 1, strong associations were found between miR133a expression levels and the neutrophil ratio and between miR1 expression levels and an increased left atrial diameter. Conclusions: Our findings indicate that the mechanism of NOAF after AMI may include an inflammatory response that is associated with an increased miR1-related mechanism. Conversely, miR133a could play a protective role in this clinical condition.