2001南京医科大学学报:英文版Requires access

Elevation of Cardiac Troponin I in Diagnosis and Progress of Viral Myocarditis

Xiang Chen

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Abstract

Objective To investigate whether measurement of serum cardiac troponin I (cTnI) could aid in the diagnosis and the evaluation of 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 monoclonal antibodies. 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[ 3H QNB] and frozen sliced human cardium. EVs RNA , mutation of mitochondrium DNA(mtDNA) in lymphocyte and cardiac biopsy specimen were assayed by the method of PCR. CVB IgM and neutralizing antibody titer were measured in part of patients. Results The level of serum cTnI in 157 of 282 patients was higher than the upper normal limit (7.1 μg/L), the positive rate being 55.7%. The rate of cTnI level returning to the normal range was 52.3% and 90 8%, in 3 months and 6 months respectively. The serum from the patients with sustained cTnI elevation inhibited the capacity and affinity of human cardiac M receptor, which resulted in downregulation and desensitization of the receptor; these reactions were similar to those of the serum from patient with dilated cardiomyopathy(DCM). The mutation frequency of mtDNA in lymphocyte and cardiac biopsy specimen in VMC cases were 15.8 and 2.5 times higher than that in normal subjects. The duration of CVB IgM present in serum was much longer and the rates of symptom improvement and arrhythmia disappearance were significantly lower in the patients with higher serum cTnI than in those with normal level cTnI. Conclusion Elevation of serum cTnI seemed to be a good marker for the presence of myocardial injury in VMC patients. Sustained high level of serum cTnI in VMC patients might suggest the development of autoimmune antibodies, cardiac receptor injury and the higher frequency of mtDNA mutation that possibly contributed to DCM process.

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Objective To investigate whether measurement of serum cardiac troponin I (cTnI) could aid in the diagnosis and the evaluation of 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 monoclonal antibodies. 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[ 3H QNB] and frozen sliced human cardium. EVs RNA , mutation of mitochondrium DNA(mtDNA) in lymphocyte and cardiac biopsy specimen were assayed by the method of PCR. CVB IgM and neutralizing antibody titer were measured in part of patients. Results The level of serum cTnI in 157 of 282 patients was higher than the upper normal limit (7.1 μg/L), the positive rate being 55.7%. The rate of cTnI level returning to the normal range was 52.3% and 90 8%, in 3 months and 6 months respectively. The serum from the patients with sustained cTnI elevation inhibited the capacity and affinity of human cardiac M receptor, which resulted in downregulation and desensitization of the receptor; these reactions were similar to those of the serum from patient with dilated cardiomyopathy(DCM). The mutation frequency of mtDNA in lymphocyte and cardiac biopsy specimen in VMC cases were 15.8 and 2.5 times higher than that in normal subjects. The duration of CVB IgM present in serum was much longer and the rates of symptom improvement and arrhythmia disappearance were significantly lower in the patients with higher serum cTnI than in those with normal level cTnI. Conclusion Elevation of serum cTnI seemed to be a good marker for the presence of myocardial injury in VMC patients. Sustained high level of serum cTnI in VMC patients might suggest the development of autoimmune antibodies, cardiac receptor injury and the higher frequency of mtDNA mutation that possibly contributed to DCM process.

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Available abstract

Objective To investigate whether measurement of serum cardiac troponin I (cTnI) could aid in the diagnosis and the evaluation of 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 monoclonal antibodies. 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[ 3H QNB] and frozen sliced human cardium. EVs RNA , mutation of mitochondrium DNA(mtDNA) in lymphocyte and cardiac biopsy specimen were assayed by the method of PCR. CVB IgM and neutralizing antibody titer were measured in part of patients. Results The level of serum cTnI in 157 of 282 patients was higher than the upper normal limit (7.1 μg/L), the positive rate being 55.7%. The rate of cTnI level returning to the normal range was 52.3% and 90 8%, in 3 months and 6 months respectively. The serum from the patients with sustained cTnI elevation inhibited the capacity and affinity of human cardiac M receptor, which resulted in downregulation and desensitization of the receptor; these reactions were similar to those of the serum from patient with dilated cardiomyopathy(DCM). The mutation frequency of mtDNA in lymphocyte and cardiac biopsy specimen in VMC cases were 15.8 and 2.5 times higher than that in normal subjects. The duration of CVB IgM present in serum was much longer and the rates of symptom improvement and arrhythmia disappearance were significantly lower in the patients with higher serum cTnI than in those with normal level cTnI. Conclusion Elevation of serum cTnI seemed to be a good marker for the presence of myocardial injury in VMC patients. Sustained high level of serum cTnI in VMC patients might suggest the development of autoimmune antibodies, cardiac receptor injury and the higher frequency of mtDNA mutation that possibly contributed to DCM process.

Key concepts: Medicine, Troponin I, Myocarditis, Internal medicine, Viral Myocarditis, Cardiology, Titer, Troponin

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