Diagnostic Potential of MicroRNA-1, MicroRNA-21, and MicroRNA-29 as Novel Biomarkers for Early Development of Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction

Abstract

Abstract Background: Currently, there is an unmet need for a minimally invasive diagnostic tool with less radiation for the early development of myocardial fibrosis and targeted treatment for preserved ejection fraction (HFpEF). This study aimed to investigate the diagnostic potential of circulating microRNAs (miRNAs) for detecting early myocardial fibrosis development in HFpEF patients. Methods: This observational study used a case-control research design. Peripheral blood samples were isolated from 25 HFpEF patients and 25 normal patients. They were measured for complete laboratory testing, NTproBNP levels using ELISA, as well as MicroRNA-1, 21, and 29 levels using RT-PCR. All patients also underwent echocardiography for global longitudinal strain (GLS) to measure the myocardial fibrosis progression. Data were analyzed using SPSS 25.0. Results: HFpEF patients had significantly higher GLS compared to the normal patients (-13±2.4% vs -19±3.2%; p < 0.05), suggesting HFpEF patients tended to have myocardial fibrosis. HFpEF patients also had significantly higher microRNA-1 and microRNA-21 compared to the normal patients (p < 0.05), but they had lower microRNA-1 (p < 0.05). There was a positive correlation between microRNA-1 (r = 0.753; p < 0.05) and microRNA-21 (r = 0.675; p < 0.05) and an inverse correlation with microRNA-29 (r = -0.653; p < 0.05) based on the GLS findings. By using a GLS cutoff of -15% for myocardial fibrosis, microRNA-1, microRNA-21, and microRNA-29 were found to be able to predict myocardial fibrosis based on GLS with a specificity of 78% and sensitivity of 75%. Conclusion: Increasing microRNA-1 and microRNA-21 followed by decreasing microRNA-29 in HFpEF patients suggest early myocardial fibrosis. Detection of those biomarkers can be beneficial for early myocardial fibrosis diagnosis, early aggressive HFpEF treatment, and targeted miRNA silencing therapy to prevent worsening HFpEF.