Background: Cardiac troponin I (CTnI ) is an essential component of the troponin complex and plays a central role in regulation of contraction in cardiac myocytes. With its high specificity and sensitivity, CTnI has been used as a serum marker of myocardial injury since 1990s, and has showed important value in diagnosing and assessing prognosis of cardiac disease. Up till now, the method of echocardiography or radionuclide inspection etc. may indicate the degree of cardiac function and assess prognosis in patient with heart failure, but these methods can not reflect the myocardium cell injury in micorcosmic field. With the progress of study on molecular mechanism in heart failure, the myocardium cell injury has been found in the evolution of chronic heart failure, so that myocardium cell injury has been concerned in chronic heart failure, as a specific and sensitive marker of cardiac muscle injury, and an increase in circulating levels of CTnI is highly indicative of myocardial injury , so CTnI may be used as the standard of heart failure evaluating. But there less relevant special reports that CTnI can be used as the standard in assessing cardiac muscle injury in the chronic congested heart failure . Objective: To study serum concentration changing of CTnI in patients with chronic heart failure and indicate the realationship between the serum concentration changing of CTnI and the heart fuction of chronic heart failure. Results: The serum concentration of CTnI in moderate heart failure was significantly higher than that in light group (heart function class II , III ) , the serum concentration of CTnI is parallel with the the degree of heart failure, the serum concentration of CTnI had significant differences between before and after treatment (p<0.05). Conclusion: The serum concentration of CTnI relates to the degree of heart failure, the different concentration of CTnI in patients with heart failure has different response to the treatment.and CTnI can be used as the standard of heart failure evaluating and therapy . |