Abstract

BackgroundMyocardial infarction (MI) is defined as myocardial cell necrosis due to significant and sustained ischemia. TN-C is an extracellular matrix glycoprotein that is expressed in several important steps during the very early stage of cardiogenesis. TN-C is not normally expressed in the adult heart, but transiently appears during pathological conditions and plays important roles in tissue remodeling. AimTo study the role of TN-C in myocardial infarction patients and to evaluate its role as a predictor of HF in these patients. MethodsThis study was conducted on 45 cases uniformly divided into 3 closely matched (in age and sex) groups as follows: Group (I) includes 15 patients who were suffering from AMI; Group (II) includes 15 patients who were suffering from HF on top of MI; and Group (III) includes 15 healthy volunteers coming for regular annual checkup. 3–6ml venous blood was collected on the day of admission under complete aseptic conditions and stored at −70°C until assayed by ELISA. ResultsTN-C levels in the sera of patients with AMI Group (I) were significantly higher than those of healthy volunteers. Moreover, in Group I of AMI, a positive correlation between TN-C level on one side and CK, CK-MB and troponin T level on the other side was found. TN-C levels in the sera of patients with congestive heart failure on top of acute MI Group (II) were significantly higher than those of healthy volunteers. Pro-BNP levels in patients with heart failure Group (II) were significantly higher than those with AMI not complicated with heart failure Group (I). Levels of pro-BNP were also positively correlated with those of TN-C in patients with heart failure on top of AMI Group (II). ConclusionsSerum TN-C might be a novel marker reflecting active structural remodeling in the myocardium following infarction, with high TN-C levels at acute stages possibly predicting progression of LV remodeling. Also, the incorporation of a combination of serum TN-C and plasma BNP levels may improve risk stratification for congestive heart failure after AMI. Further studies on large scale are needed for more evaluation of TN-C role in HF.

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