It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Aims
Heart failure describes a large and heterogeneous spectrum of underlying cardiac diseases. MicroRNAs (miRs) are small non‐coding RNAs that in recent years have been shown to play an important role in the pathogenesis of heart failure. Cardiac magnetic resonance imaging is a powerful imaging modality for the evaluation of cardiac characteristics in heart failure. In this study, we sought to compare heart failure patients with a diagnosis of either idiopathic dilated cardiomyopathy (DCM) or ischaemic heart disease (IHD), in the context of serum levels of certain miRs and also magnetic resonance imaging parameters of cardiac structure and function.
Methods and results
A total of 135 subjects were studied: 53 patients with DCM (age: 59 ± 12 years, mean ± SD), 34 patients with IHD (66 ± 9 years), and 48 controls (64 ± 5 years). The participants underwent baseline medical examination, blood sampling, and a cardiac magnetic resonance imaging examination at 3 Tesla (Philips Ingenia). The serum levels of seven different miRs were analysed and assessed: 16‐5p, 21‐5p, 29‐5p, 133a‐3p, 191‐5p, 320a, and 423‐5p, all of which have been demonstrated to play potential roles in the pathogenesis of heart failure.
The patients in the DCM and IHD groups had left ventricles that had larger end‐diastolic volume (P < 0.001), larger mass (P < 0.001), and lower ejection fraction (P < 0.001) compared with controls. Serum levels of miR‐29‐5p were increased in DCM compared with IHD (P < 0.005) and serum levels of miR‐320a were elevated in DCM compared with healthy controls (P < 0.05). There was no significant association between miR levels and magnetic resonance imaging parameters of left ventricular structure and function.
Conclusions
Circulating miR‐320a can add to the discrimination between patients with DCM and healthy controls and circulating miR‐29‐5p can add to the discrimination between DCM and IHD.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
; Wågsäter, Dick 2 ; Alehagen, Urban 3 ; Carlhäll, Carl‐Johan 4 1 Department of Clinical Physiology, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden
2 Division of Drug Research, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
3 Unit of Cardiovascular Sciences, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden
4 Department of Clinical Physiology, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden, Unit of Cardiovascular Sciences, Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden, Center for Medical Image Science and Visualization, Linköping University, Linköping, Sweden





