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Mir-146a plasma levels are increased in patients with hypertrophic cardiomyopathy

Session Poster Session 3

Speaker Dimitrios Ntelios

Event : Heart Failure 2019

  • Topic : arrhythmias and device therapy
  • Sub-topic : Hypertrophic Cardiomyopathy
  • Session type : Poster Session

Authors : D Ntelios (Thessaloniki,GR), GK Efthymiadis (Thessaloniki,GR), S Meditskou (Thessaloniki,GR), T Zegkos (Thessaloniki,GR), D Parcharidou (Thessaloniki,GR), H Karvounis (Thessaloniki,GR), G Tzimagiorgis (Thessaloniki,GR)

D Ntelios1 , GK Efthymiadis1 , S Meditskou2 , T Zegkos1 , D Parcharidou1 , H Karvounis1 , G Tzimagiorgis3 , 1Ahepa University Hospital - Thessaloniki - Greece , 2Aristotle University of Thessaloniki, Department of Histology, Medical School - Thessaloniki - Greece , 3Aristotle University of Thessaloniki, Department of Biological Chemistry, Medical School - Thessaloniki - Greece ,

Hypertrophic Cardiomyopathy

Introduction: Hypertrophic cardiomyopathy (HCM) is a genetic disease of the myocardium caused by mutations in sarcomeric genes and characterized by hypertrophy and fibrosis. MiRNAs are important posttranscriptional regulators of gene expression with an increasingly recognized role in cardiovascular disease. Among the miRNAs studied so far, miR-146a could be a promising biomarker or therapeutic target for HCM. Besides its role in the inflammatory response resolution, emerging evidence suggests that mir-146a also plays a significant role in cardiac hypertrophy, atherosclerosis and peripartum cardiomyopathy.

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.

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