Osteopontin (OPN), a bone-related protein, is present within the atherosclerotic plaques, most strikingly in calcified plaques. Valvular calcifications are accepted as a part of the spectrum of atherosclerosis and are associated with atherosclerotic calcification in the coronary arteries. The study aimed to evaluate the association of plasma OPN with the presence and extent of coronary stenosis, mitral annular calcification (MAC), and aortic valve sclerosis in stable angina patients. We studied 120 subjects who underwent coronary angiography because of ischemic chest pain. Coronary artery disease (CAD) was defined as > or = 50% stenosis in > or = 1 coronary artery. MAC and aortic valve sclerosis were detected by echocardiography. Lipid profile, high sensitive C-reactive protein (hsCRP), and OPN were measured in all studied subjects. Patients with CAD had increased plasma OPN when compared with those without CAD (P < 0.001). Plasma OPN levels were significantly positively correlated with atherogenic lipid profile, hsCRP, MAC grading, aortic valve sclerosis grading, and the number of stenosed coronary vessels in CAD patients. In multivariate analysis, OPN was an independent predictor of CAD (P = 0.01), MAC (P = 0.01), and aortic valve sclerosis (P = 0.04). In conclusion, OPN is an independent predictor of MAC and aortic valve sclerosis. Plasma OPN levels reflect the extent of coronary stenosis and can be used as a biomarker to identify patients with coronary atherosclerosis.
Background:
Biomarkers are the corner stone for diagnosis of myocardial infarction (MI). MicroRNA-208a (miR-208a) is known to be heart specific. So, this study was designed to explore its role as a marker for diagnosis of MI as well as a predictor of outcome of primary percutaneuos coronary angiography especially no-reflow phenomenon.
Methods:
This study was carried out between January 2018 and August 2019 in Cardiology Department, Zagazig University Hospitals, Egypt. Approval was obtained from institutional review board adhering to the guidelines of the Declaration of Helsinki. Patients (n=75) presented by chest pain were recruited into two groups. Group 1 (n=40) had STEMI and underwent primary PCI: 21 patients with sufficient reperfusion and 19 with no-reflow. Group 2 (n= 35) had negative troponin T (cTnT). Plasma miR-208a expression was assessed using quantitative polymerase chain reaction and patients were followed for occurrence of in-hospital (3 days average) major adverse cardiac events (MACE).
Results:
Analysis of relative expression values shows that miR-208a has reasonable sensitivity and specificity for MI diagnosis (AUC= 0.92, sensitivity = 92.5, Specificity = 80) which is comparable to the routine cardiac biomarkers; creatine kinase-MB (CK-MB) (area difference 0.0439, P= 0.235) and cTnT (area difference 0.0614, P= 0.06). The no-reflow group (b) had higher expression compared to subgroup (a). ROC analysis shows it to be a good predictor of no-reflow (AUC= 0.88, sensitivity = 73.7, Specificity = 95.2) which is significantly superior to cTnT (AUC difference of 0.231, P= 0.0233). As well, it was superior to cTnT as a predictor of in-hospital MACE (AUC difference of 0.367, P= 0.0053).
Conclusion:
This study highlights the value of miR-208a as a diagnostic and prognostic marker in STEMI context. To the best of our knowledge, this is the first study to investigate the value of miR-208a in no-reflow and almost the second to investigate the role of any known miRNA in no-reflow. Although still far from clinical application due to long time needed for the assay, the future introduction of new fast nucleic acids assays could support its clinical application. The study points to a possible mechanism for no-reflow development that needs to be thoroughly investigated.
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