Elevation of cardiac troponin I and its association with diagnosis and progress of viral myocarditis
Zhang Ji-nan, Enben Su, Weilin Jin
Abstract
Zhang Ji-nan, Enben Su, Weilin Jin
Abstract
Objective To investigate whether measurement of serum cardiac troponin I (cTnI) could aid in the diagnosis and progress of viral myocarditis (VMC). Methods The cTnI of serum samples from 282 patients with clinical diagnosis of VMC were determined with ELISA using 2B1.9 and 2F6.6. The effect of the serum from 25 patients who had sustained high level of cTnI on the capacity and affinity of cardiac muscarinic receptor was evaluated with [ 3HQNB] and frozen sliced human cardium. EVs RNA as well as mutation of mitochondrium DNA (mtDNA) in lymphocyte and cardiac cell were assayed by the method of PCR. CVB IgM and neutralizing antibody titration were measured in part of patients. Results The level of serum cTnI in 157 of 282 patients was high over up limitation (7.1 ng/ml), positive rate was 55.7%. At the point of 3 months, the rate of cTnI turning to be in normal range was 52.3% and 90.8% at 6 months. The serum from the patients who had high cTnI level lasted for a long time that inhibited the capacity and affinity of human cardiac M receptor, which resulted in downregulation and desensitization of the receptor; those reactions were similar to those of the serum from patient with dilated cardiomyopathy (DCM). Frequency of mutation of mt DNA in lymphocyte and cardiac cell in VMC cases were 15.8 and 2.5 times higher than in normal subjects. Period of CVB IgM presented in serum was much longer and the rates of symptoms improved and arrhythmia stopped were lower significantly in the patients with higher serum cTnI than in whom had normal level of cTnI respectively. Conclusion Elevation of serum cTnI would be a good marker for the presence of myocardium injury in VMC patients. Sustained high level of serum cTnI in VMC cases may be related to the development of autoimmunoantibodies, damage of the cardiac receptors and to the higher frequency of mtDNA mutation that possibly contribute to DCM process.
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Objective To investigate whether measurement of serum cardiac troponin I (cTnI) could aid in the diagnosis and progress of viral myocarditis (VMC). Methods The cTnI of serum samples from 282 patients with clinical diagnosis of VMC were determined with ELISA using 2B1.9 and 2F6.6. The effect of the serum from 25 patients who had sustained high level of cTnI on the capacity and affinity of cardiac muscarinic receptor was evaluated with [ 3HQNB] and frozen sliced human cardium. EVs RNA as well as mutation of mitochondrium DNA (mtDNA) in lymphocyte and cardiac cell were assayed by the method of PCR. CVB IgM and neutralizing antibody titration were measured in part of patients. Results The level of serum cTnI in 157 of 282 patients was high over up limitation (7.1 ng/ml), positive rate was 55.7%. At the point of 3 months, the rate of cTnI turning to be in normal range was 52.3% and 90.8% at 6 months. The serum from the patients who had high cTnI level lasted for a long time that inhibited the capacity and affinity of human cardiac M receptor, which resulted in downregulation and desensitization of the receptor; those reactions were similar to those of the serum from patient with dilated cardiomyopathy (DCM). Frequency of mutation of mt DNA in lymphocyte and cardiac cell in VMC cases were 15.8 and 2.5 times higher than in normal subjects. Period of CVB IgM presented in serum was much longer and the rates of symptoms improved and arrhythmia stopped were lower significantly in the patients with higher serum cTnI than in whom had normal level of cTnI respectively. Conclusion Elevation of serum cTnI would be a good marker for the presence of myocardium injury in VMC patients. Sustained high level of serum cTnI in VMC cases may be related to the development of autoimmunoantibodies, damage of the cardiac receptors and to the higher frequency of mtDNA mutation that possibly contribute to DCM process.
Key concepts: Troponin I, Medicine, Viral Myocarditis, Myocarditis, Internal medicine, Cardiology, Receptor, Gastroenterology