The main manifestations of these 51 patients with AMI were as follows: the serum levels of myocardial injury markers (creatine kinase-Mb [CK-Mb] and cardiac troponin I [cTnI]) and heart failure markers (N-terminal pro B-type natriuretic peptide [NT-pro BNP]) were significantly higher, when compared with the control group (P < .001), and the incidence of arrhythmia (FVPB, P = .02; RAA, P = .03; RVA, P = .02; ST-T changes, P = .01) and heart failure (P = .04) was also significantly higher when compared with the control group.
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.
Furthermore, in the Cox proportional hazard analysis, cTnI, but not ACE, IL2R or BNP, was a predictor of fatal arrhythmia in sarcoidosis patients (HR 2.418, P = 0.003).Higher ACE and sIL2-R are associated with systemic lesions, whereas BNP is a useful marker for detecting cardiac involvement in sarcoidosis patients. cTnI is a predictor of fatal arrhythmia in CS patients.
Moreover, the increased Ca2+ bound to myofilaments containing the mutant cTnIs may be an important factor in triggered arrhythmias associated with the cardiomyopathy.