Background: The evaluation of the long-term risk of major adverse cardiovascular events and cardiac death in patients after acute myocardial infarction (AMI) is an established clinical process. Laboratory markers may significantly help with the risk stratification of these patients. Our objective was to find the relation of selected microRNAs to the standard markers of AMI and determine if these microRNAs can be used to identify patients at increased risk.
Methods: Selected microRNAs (miR-1, miR-133a, and miR-499) were measured in a cohort of 122 patients from the PRAGUE-18 study (ticagrelor vs. prasugrel in AMI treated with primary percutaneous coronary intervention (pPCI)). The cohort was split into two subgroups: 116 patients who did not die (survivors) and 6 patients who died (nonsurvivors) during the 365-day period after AMI. Plasma levels of selected circulating miRNAs were then assessed in combination with high-sensitivity cardiac troponin T (hsTnT) and N-terminal probrain natriuretic peptide (NT-proBNP).
Results: miR-1, miR-133a, and miR-499 correlated positively with NT-proBNP and hsTnT 24 hours after admission and negatively with left ventricular ejection fraction (LVEF). Both miR-1 and miR-133a positively correlated with hsTnT at admission. Median relative levels of all selected miRNAs were higher in the subgroup of nonsurvivors ( = 6) in comparison with survivors ( = 116), but the difference did not reach statistical significance. All patients in the nonsurvivor subgroup had miR-499 and NT-proBNP levels above the cut-off values (891.5 ng/L for NT-proBNP and 0.088 for miR-499), whereas in the survivor subgroup, only 28.4% of patients were above the cut-off values ( = 0.001).
Conclusions: Statistically significant correlation was found between miR-1, miR-133a, and miR-499 and hsTnT, NT-proBNP, and LVEF. In addition, this analysis suggests that plasma levels of circulating miR-499 could contribute to the identification of patients at increased risk of death during the first year after AMI, especially when combined with NT-proBNP levels.
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http://dx.doi.org/10.1155/2019/2925019 | DOI Listing |
Rheumatology (Oxford)
January 2025
Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
Objectives: Objective of this work was to examine myomiR levels in plasma, skeletal muscle, and skeletal muscle cells of patients with idiopathic inflammatory myopathy (IIM), their interrelations with the disease-related clinical phenotypes and with the effects of the disease-modifying 6-month training-intervention.
Methods: Samples of vastus lateralis muscle (n = 12/13) and plasma (n = 20/21) were obtained from IIM patients and healthy controls, respectively. Muscle and plasma were obtained before and after a 6-month training-intervention in 7 patients.
Kardiol Pol
January 2025
Core Facilities, Medical University of Vienna, Vienna, Austria.
Micro-ribonucleic acids (miRs) are small, non-coding RNAs, which play an important role in atherosclerotic plaque formation, development, and stability. Plaque destabilization and rupture lead to acute coronary syndromes (ACS). Previous studies have implicated several different miRs in the pathogenesis of atherosclerosis.
View Article and Find Full Text PDFJ Clin Med
December 2024
Department of Cardiology, Medical University of Lodz, Kniaziewicza Street 1/5, 91-347 Lodz, Poland.
: Available data suggest the diagnostic potential of testing microRNAs (miRs) in myocardial infarction, but their prognostic value remains unclear. To evaluate the prognostic value of circulating miRs (miR-1, miR-21, miR-133a, miR-208 and miR-499) for predicting major adverse cardiac events (MACEs), including death, non-fatal myocardial infarction (MI) or cardiovascular rehospitalization, in patients with non-ST segment elevation acute coronary syndromes (NSTE-ACS). Our prospective, single-center, observational study included patients (pts) with NSTE-ACS admitted <24 h after symptoms onset and pts with confirmed stable coronary artery disease (SCAD) as controls.
View Article and Find Full Text PDFWellcome Open Res
November 2024
Department of Clinical Science and Services, Comparative Neuromuscular Diseases Laboratory, Royal Veterinary College, London, NW1 0TU, UK.
Biomedicines
October 2024
Institute of Biochemistry and Molecular Genetics, Faculty of Medicine, University of Ljubljana, SI-1000 Ljubljana, Slovenia.
Spinal muscular atrophy (SMA) is a severe neurodegenerative disease caused by the loss of the survival motor neuron (SMN) protein, leading to degeneration of anterior motor neurons and resulting in progressive muscle weakness and atrophy. Given that SMA has a single, well-defined genetic cause, gene-targeted therapies have been developed, aiming to increase SMN production in SMA patients. The SMN protein is likely involved in the synthesis of microRNAs (miRNAs), and dysregulated miRNA expression is increasingly associated with the pathophysiology of SMA.
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