
The relationship between myocardial fibrosis and myocardial micro RNA s in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events
Author(s) -
Rubiś Paweł,
TotońŻurańska Justyna,
WiśniowskaŚmiałek Sylwia,
Dziewięcka Ewa,
KołtonWróż Maria,
Wołkow Paweł,
Pitera Ewelina,
RudnickaSosin Lucyna,
Garlitski Ann C.,
Gackowski Andrzej,
Podolec Piotr
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13535
Subject(s) - dilated cardiomyopathy , medicine , myocardial fibrosis , fibrosis , cardiology , biopsy , rna , heart failure , gene , biology , biochemistry
It is unknown whether fibrosis‐associated micro RNA s: miR‐21, miR‐26, miR‐29, miR‐30 and miR‐133a are linked to cardiovascular ( CV ) outcome. The study evaluated the levels of extracellular matrix ( ECM ) fibrosis and the prevalence of particular micro RNA s in patients with dilated cardiomyopathy ( DCM ) to investigate any correlation with CV events. Methods: Seventy DCM patients (48 ± 12 years, EF 24.4 ± 7.4%) underwent right ventricular biopsy. The control group was comprised of 7 patients with CAD who underwent CABG and intraoperative biopsy. Micro RNA s were measured in blood and myocardial tissue via qPCR . The end‐point was a combination of CV death and urgent HF hospitalization at the end of 12 months. There were differential levels of circulating and myocardial miR‐26 and miR‐29 as well as myocardial miR‐133a when the DCM and CABG groups were compared. Corresponding circulating and myocardial micro RNA s did not correlate with one another. There was no correlation between micro RNA and ECM fibrosis. By the end of the 12‐month period of the study, CV death had occurred in 6 patients, and a further 19 patients required urgent HF hospitalization. None of the circulating micro RNA s was a predictor of the combined end‐point; however, myocardial miR‐133a was an independent predictor in unadjusted models ( HR 1.53; 95% CI 1.14‐2.05; P < .004) and adjusted models ( HR 1.57; 95% CI 1.14‐2.17; P < .005). The best cut‐off value for the miR‐133a level for the prediction of the combined end‐point was 0.74 ΔCq, with an AUC of 0.67. The absence of a correlation between the corresponding circulating and myocardial micro RNA s calls into question their cellular source. This study sheds new light on the role of micro RNA s in ECM fibrosis in DCM , which warrants further exploration.