Background
MicroRNAs are small, endogenous, non-coding RNAs that regulate the expression of many
genes. It has recently been shown that circulating microRNAs may be biomarkers of
hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy (HCM).
Objective
To determine whether circulating levels of microRNAs involved in HCM are associated
with electrocardiographic and echocardiographic parameters.
Methods
This study enrolled 20 patients with familial HCM and 20 blood donors. Peripheral
serum levels of miR-29a-3p, miR-199a-5p and miR-451a were assessed by quantitative
real-time polymerase chain reaction and compared with levels in the control group.
Whether circulating levels of miRNAs in HCM patients correlated with electrocardiographic
and echocardiographic parameters was also assessed.
Results
Median circulating levels of miR-29a and miR-451a were significantly higher in HCM
than the control group. Median miR-199a levels did not differ between groups. However,
circulating levels of miR-199a negatively correlated with corrected QT duration (Bazett
formula). Median miR-29a levels positively correlated with QRS duration. In addition,
circulating levels of miR-29a correlated with maximal wall thickness, left ventricular
mass index and left atrial volume index.
Conclusions
The data suggested that serum levels of miR-29a and miR-451a were significantly increased
in HCM patients. As the circulating level of miR-29a correlated with QRS duration,
left ventricular hypertrophy and left atrial dilatation, the serum miR-199a level
negatively correlated with corrected QT duration. These miRNAs may be seen as potential
biomarkers for further research in HCM pathophysiology.
Keywords
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Article info
Publication history
Published online: June 01, 2021
Accepted:
April 25,
2021
Received in revised form:
December 31,
2020
Received:
August 18,
2020
Identification
Copyright
© 2021 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.