Total amount: € 0,00
Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Online ISSN 1827-1618
STRATEGIES FOR CARDIOVASCULAR REPAIR: STEM CELLS AND BEYOND
Nabiałek E. 1, Wańha W. 1, Kula D. 2, Jadczyk T. 1, Krajewska M. 2, Kowalówka A. 3, Dworowy S. 1, Hrycek E. 1, Włudarczyk W. 1, Parma Z. 6, Michalewska-Włudarczyk A. 1, Pawłowski T. 1, Ochała B. 1, Jarząb B. 2, Tendera M. 1, Wojakowski W. 1
1 Third Division of Cardiology Medical University of Silesia, Katowice, Poland;
2 Department of Nuclear Medicine and Endocrine Oncology Maria Sklodowska‑Curie Memorial Cancer Center and Institute of Oncology Gliwice Branch, Katowice, Poland;
3 Department of Cardiac Surgery Medical University of Silesia, Katowice, Poland;
4 First Division of Cardiology Medical University of Silesia, Katowice, Poland
Aim: The microRNAs (miRs) are small non-coding RNAs which regulate expression of multiple genes involved in atherogenesis. MicroRNA are also present in circulation. The aims of this study were: 1) assessment of expression level of miR-1, miR-208a and miR-423-5p in plasma in patients with STEMI, stable CAD and healthy individuals; 2) evaluation of correlation between plasma miRs and left ventricle ejection fraction, end- systolic and end-diastolic diameters and troponin release in patients with STEMI.
Methods: Study group consisted of 26 patients: 1) acute MI group (N.=17); 2) stable CAD group (N.=4); and 3) subjects with no history of CAD (control group, N.=5). Expression of miR-423-5p, miR-208 and miR-1 was measured in plasma before PCI, 6, 12 and 24 hours later. Expression level ofmiRs was measured using TaqMan® MicroRNA Assays. Expression was assessed by Pfaffl method, and miR-39 was used for normalization of the results.
Results: In stable CAD in comparison to control group the expression level of miR-1, miR-208a and miR-423-5p did not show significant differences. Also there was no significant increase of number of miR copies at 6, 12 and 24 hours after PCI. There was a significantly higher number of miR-423-5p copies in patients with acute MI before the pPCI. After 6, 12 and 24 hours post-procedure the expression level was similar to the control group and significantly lower than the baseline level. Conversely, the expression level of miR-1 and miR-208a were not significantly different than in the control group. In patients with acute MI there were no significant correlations between the expression level of miRs and any of the echocardiographic parameters of LV as well as level of troponin I at any time-point of the follow-up.
Conclusion: Early in acute myocardial infarction the expression of miR-423-5p in plasma is significantly increased with subsequent normalization within 6 hours. Potentially it is an early marker of myocardial necrosis.