Cardiac troponin I (cTn I) and cardiac troponin T (cTn T) are currently widely used as diagnostic biomarkers for myocardial injury caused by ischemic heart diseases in clinical and forensic medicine.
Alterations in myocardial ischemia and hypoxia were examined by hematoxylin-basic fuchsin-picric acid (HBFP) staining and the concentration of cardiac Troponin I (cTnl), a sensitive and specific marker for myocardial injury, was detected using immunochemiluminescence analysis.
Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process.
Perioperative cardiac damage was defined on the basis of postoperative elevation of the blood level of cardiac troponin I (0.05-0.5 ng/ml) in the absence of myocardial ischemia.
Serum cardiac troponin I (cTnI) levels and hematoxylin basic fuchsine picric acid (HBFP) staining were used to observe the degree of myocardial ischemia.
The cardiac troponin I level (cTnI) on postoperative day 1 (MD: -0.39, 95% CI: -0.45--0.34, P<0.00001) and the incidence of myocardial ischaemia (OR: 0.43, 95% CI: 0.27-0.68, P=0.0004) within 3 postoperative days were significantly lower after sevoflurane anesthesia than propofol anesthesia.
The combination, compared to G, R and S, could significantly reduce the concentration of serum CK-MB and cTn-I, and decrease myocardial infarct size, which demonstrated the advantages of this combination for myocardial ischemia.
What is New: • The observed positive results of cardiac troponin I and high values of galectin-3 in sickle cell children during vaso-occlusive crisis are strong indicator of myocardial ischemia and ongoing cardiac fibrosis respectively.