Purpose: The aim of this study was to investigate plasma miR-146a levels in hypertrophic cardiomyopathy patients and normal controls.
Materials and methods: miR-146a levels were analysed in plasma samples from 50 patients with hypertrophic cardiomyopathy and 30 normal controls using real time qPCR and specific TaqMan assays. cel-miR-39 was used as external spike-in control. Relative quantitation was performed using the 2-??Ct method. Patients were subjected to standard echocardiographic evaluation. Data regarding myocardial fibrosis assessed using late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) were retrieved from patients’ records. Serum Troponin I was used as a marker of myocardial damage. Statistical analysis was performed using SPSS (v25). This research was approved by the appropriate institutional review board, and a written informed consent was obtained from each participant.
Results: miR-146a plasma levels was significantly higher in HCM patients than in healthy controls (p=0.012). Interestingly miR-146a was not associated with maximal myocardial wall thickness (rs=0.098, p=0.595), the extent of myocardial fibrosis (LGE-CMR) (rs=-0.094, p= 0.760) and serum troponin I levels (rs=0.097, p=0.524).
Conclusion: Our study indicates that plasma miR-146a is increased in HCM patients. However, the potential role of miR-146a as a genetic modifier in HCM remains to be elucidated.