EVALUATION OF CARDIAC SPECIFIC MARKER CARDIAC TROPONIN I AFTER CORONARY BYPASS SURGERY

Background: Cardiac troponin I (cTnI) is reported to be very specific formyocardial cell damage without cross reactivity with skeletal muscle isoform.Evaluation of cTnI after CABG will be useful as an early marker of excessivepost operative myocardial damage when a specific therapeutic intervention canstill be efficient and improve outcome.Methodology: The study comprised of 50 patients who undergo Coronary arterybypass surgery at V.S group of Hospital. Blood sample were taken after 12 hour (T12) and 24 hour ( T24 ) of post CABG. The sample were analysed for cTnI.Results: Our results show that Troponin I levels after 2 hours, 12 hours and 24hours in patients who had better outcome after CABG was 9.2 ng/ml, 13.9 ng/mland 10.9 ng/ml respectively. Whereas, Troponin I levels after 2 hours, 12 hoursand 24 hours in patients who had adverse outcome like death of patients afterCABG was 10.6 ng/ml, 38.7 ng/ml and 28.9 ng/ml respectively.Conclusion: Routine measurement of cardiac troponin levels after cardiactroponin can identify group of patients at increased risk of complications ordeath.

Optimization of Expression by Response Surface Methodology and Purification of Recombinant Human Cardiac Troponin-I(cTnI) in Escherichia coli / 中国生物工程杂志

To optimize the growth condition for the established gene engineer bacteria express cardiac troponin-I(cTnI) and to obtain purified cTnI as an antigen to produce clinical assay kits used in acute myocardial injury(AMI) diagnosis.Plackett Burman Design(PBD) was applied to select the factors which effect the expression of cTnI in Escherichial coli(E.coli) mostly.Induction time,pH and KCl were proved influenced expression of cTnI notably.Afterward,Response Surface Methodology(RSM) as second step to optimize the selected three factors,an equation was deduced to predict the percent of cTnI.In the most optimized condition,the percent of cTnI can reach to 26% of total cell protein.The procedures of purification included ammonium sulfate deposition and DEAE Cellulose ion exchange chromatography.SDS-PAGE shows that purified cTnI contain one band.cTnI could be used to immune animals as an antigen to produce monoclonal antibodies with high affinity and specificity.It maybe as calibrators to harmony the difference assays of cTnI measurement in clinical.

The clinical usefulness of cardiac troponin I as a marker for severity in patients with congestive heart failure

BACKGROUND AND OBJECTIVES: Spontaneous progression of severe congestive heart failure is structurally characterized by cellular degeneration and multiple foci of myocardial cell death. The cardiac troponin I (cTnI), one of the subunits of the troponin regulatory complex, binds to actin and inhibits interaction between actin and myosin. cTnI is uniquely expressed in the adult human myocardium, and an increase in its circulating levels is highly indicative of myocardial injury. In this study, we addressed the usefulness of cTnI as a sensitive and specific molecular marker for severity in patients with congestive heart failure. MethodscTnI, creatinin kinase-MB (CK-MB), and myoglobin were assessed in 59 patients with severe congestive heart failure diagnosed by the echo-cardiography and gated equilibrium blood pool heart scan. Also we assesed cTnI, creatinin kinase-MB (CK-MB), and myoglobin in 25 persons without cardiac disease in echocardiography. RESULTS: 1) The cTnI con-centration was 89.6+/-69.3 pg/mL in patients with congestive heart failure and its level was greater than that of the control group (22.4+/-17.1, p=0.001). 2) The cTnI level differed significantly according to left ventricular ejection fraction (EF), 117.3+/-73.8 pg/mL in patients with EF\ or =40% (31 patients), 22.4+/-17.1 pg/mL in the control group (25 persons) (p=0.001). CONCLUSION: cTnI was useful as a specific and sensitive serum molecular marker in patients of congestive heart failure. And its level reflected the severity of congestive heart failure.

The Significance of Serum Cardiac Troponin I Concentration in the Patients with Acute Myocardial Infarction

BACKGROUND: The cardiac troponin I (cTnI), one of the subunits of the troponin regulatory complex, binds to actin and inhibits interactions between actin and myosin. cTnI is highly sensitive and specific marker for myocardial injury and is useful in diagnosis and detection of reperfusion in acute myocardial infarction (AMI). In this study, we measured the serum concentration of cTnI according to serial time after chest pain in patients with AMI and compared serum concentration of cTnI with CK-MB and echocardiographic data to evaluate the significance of measuring serum concentration of cTnI in AMI. SUBJECTS AND METHODS: The study was carried out on 16 patients with first attack of AMI within 6 hours of chest pain. All patients were performed thrombolytic therapy and reperfusion was confirmed by coronary angiography. Blood samples for measuring of CK-MB and cTnI were collected at 4-h intervals during the first 24 h, 12-h intervals until 48 h, and 24-h intervals until fourth days after hospitalization. Echocardiography were performed before thrombolytic therapy in all patients. RESULTS: 1) The mean age of subjects was 63.6+/-11.5 years (range:44 - 84 years) and 11 patients were men and 5 patients were women. The site of infarction was anterior in 11 patients and inferior in 5 patients. 2) The peak concentrations of CK-MB and cTnI were reached from 4-h to 12-h after admission in all patients (7.3+/-2.6-h, and 9.0+/-3.1-h, respectively), but there was no significant difference in peak time. 3) Serum concentration of CK-MB was normalized at 72-h after admission, but cTnI was remained in increased state until 96-h after admission. The numbers of the patients with above cutoff value of CK-MB and cTnI at different time after admission were significantly different after 72-h (p<0.05). 4) The peak cTnI and sigma cTnI level were significantly correlated with peak CK-MB and sigma CK-MB level, respectively (r 2 =0.7955, p<0.0001 and r 2 =0.6378, p=0.0002, respectively). 5) The ejection fraction was not correlated with peak cTnI concentration (r 2 =0.0948, p=0.2461) and sigma cTnI (r 2 =0.1867, p=0.0946). 6) The wall motion score index was not correlated with peak cTnI concentration (r 2 =0.2135, p=0.0716), but significantly correlated with sigma cTnI (r 2 =0.2540, p=0.0465). CONCLUSION: The serum concentration of cTnI was useful in late diagnosis of AMI and cTnI release in patients with AMI was correlated with myocardial infarct size.