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Objective To investigate the expression of cardiac troponin-Ⅰ (cTnⅠ) levels in patients diagnosed with sepsis-associated myocardial dysfunction and explore the relationship between cTn Ⅰ and cardiac systolic and diastolic function.Additionally,we evaluated the prognostic value of cTn Ⅰ as a valuable biomarker.Methods We admitted 65 patients with sepsis.Using echocardiography,the ratio of early diastolic mitral inflow velocity to early diastolic mitral annulus velocity (E/e') and the left ventricular ejection fraction (LVEF) were measured as an evaluation index of left ventricular diastolic and systolic function,respectively.Patients were divided into a cardiac dysfunction and a normal cardiac function group.The cTn Ⅰ level was measured and compared between the two groups,and we determined the correlation between cTn Ⅰ levels and cardiac diastolic and systolic function.Based on assessment of 28-day mortality,cases were divided into a survivor and a death group.A receiver operating characteristic curve was constructed to predict the prognostic value of cTn Ⅰ.Results The cTn Ⅰ level in the cardiac dysfunction group was significantly higher than that observed in the normal cardiac function group (P ＜ 0.05) and showed a positive correlation with E/e'(r =0.421,P =0.008).However,there was no correlation noted between the cTn Ⅰ level and LVEF (P ＞ 0.05).Compared to the survivor group,the level of cTn]Ⅰ was significantly higher in the death group (P ＜ 0.05).The prognostic value of cTn Ⅰ area under the curve was 0.892,with a cut-off value of 0.82 ng/mL (sensitivity =88.0％ and specificity =82.5％).Conclusion The cTn Ⅰ level is noted to be significantly elevated in patients with sepsis-associated cardiac dysfunction and shows a positive correlation with left ventricular diastolic function.A cTn Ⅰ level ≥ 0.82 ng/mL can be used as a valuable predictor of mortality in patients with sepsis.
ABSTRACT
Objective To investigatethe clinical value of troponin-I(cTnI)in patientswith septic shocka-nd left ventricular diastolic dysfunction. Methods As a retrospective analysis ,38 patients with left ventricular di-astolic dysfunction and septic shock(Sa group),as well as 20 patients with normal cardiac function(Sn group) were enrolled in this study. Moreover ,20 patients with left ventricular diastolic dysfunction and without septic shock were used as control group(Ca group). The ratio of early diastolic mitral inflow velocity to early diastolic mi-tral annulus velocity(E/e′)was measured as the evaluation index of left ventricular diastolicfunction by echocar-diography within 72 hours after admission to ICU. Level of cTnI was detected in all cases and the relationship was evaluated by E/e′. Receiver operating characteristic curve(ROC)was constructed to indicate the predictable value of left ventricular diastolic dysfunction in patients with septic shock. Results The level of cTnI was significantly elevated in both Sa group and Sn group(P<0.05),while the level of cTnI and E/e′in Sa group were significantly higher than those in Sn group(P < 0.05). cTnI was positively correlated with E/e′(r = 0.367 ,P = 0.004). The area under the curve(AUC)of cTnI was 0.834,with the cut-off value of 0.49 ng/mL(sensibility=77.6,specificity=80.7). Conclusion The level of cTnI was significantly higher in patients with septic shock. cTnI was significantly correlated to left ventricular diastolic dysfunction in patients with septic shock. cTnI ≥ 0.49 ng/mL could be an available predictor for left ventricular diastolic dysfunction in patients with septic shock.
ABSTRACT
Objective To explore the effects of tumor necrosis factor-α (TNF-α) on ventricular arrhythmias resulted from acute myocardial infarction (AMI) in rats. Method Two hundred and forty male Wistar rats were randomized (random number) into sham operation group, AMI group and recombinant human tumor necrosis factor receptor (rhTNFR) fusion protein (Fc) group. Acute anterior wall myocardial infarction was produced in rats of AMI group with ligating the left anterior descending coronary artery (LAD) , and the rats were just operated without ligation of LAD in sham group. The rats of Fc group were treated with rhTNFR-Fc (10 mg/kg), a TNF-α antagonist, 24 hours before LAD ligation. The original ECG was recorded 10 min before ligation and the ECGs of ventricular arrhythmias occurred spontaneously or induced by programmed electrical stimulation were recorded 10 min, 20 min, 30 min, 60 min, 3 h, 6 h and 12 hours after ligation. The protein levels and mRNA expressions of TNF-α in rats in different groups were detected with histochemistry and real-time fluorescent quantitative PCR. Results The expressions of TNF-α mRNA and levels of TNF-α protein markedly increased 10 min after infarction, reached the climax 20-30 min later, and then gradually returned to the original level in AMI group and Fc group. The time-windows of spontaneous and induced ventricular arrhythmias were consistent with the time-window of expressions of TNF-α mRNA and levels of TNF-α protein. Compared with AMI group, there were lower levels of TNF-α protein and lower incidence of ventricular arrhythmias in Fc group ( P < 0.05) , but there was no significant difference in TNF-α mRNA between two groups. There was no obvious change in TNF-α in rats of sham operation group. Conclusions The expressions of TNF-α mRNA and levels of TNF-α protein induced by AMI could contribute the initiation of ventricular arrhythmias.