Serial measure of cardiac troponin T levels for prediction of clinical events in decompensated heart failure

BACKGROUND: This study determined whether serial determinations of cardiac troponin T (cTnT) in decompensated heart failure (HF) are predictive of clinical events (death, need for readmission for new episode of HF decompensation, or both) during 1 year of follow-up. METHODS AND RESULTS: Sixty-two patients with decompensated HF were enrolled in this cohort. The first measurement of cTnT (cTnT1) was from a blood sample drawn within 4 days of hospital admission; the second measurement (cTnT2) was on blood obtained 7 days later. Forty-nine clinical events (16 deaths, 10 readmissions, 23 combined readmission and deaths) occurred during the follow-up. The independent predictors of clinical events were: cTnT1>.020 ng/mL (P<.050), cTnT2>.020 ng/mL (P<.050), and serum sodium<135 mEq/L (P<.050). Based on levels of cTnT1 and cTnT2>.020 ng/mL (+) or .020 ng/mL) are predictive of higher rates of death and hospital readmission for decompensated HF.     

Cardiac troponin I as prognostic marker in heart failure patients discharged from emergency department

Despite evidence that cardiac troponin I (cTnI) identifies patients with advanced heart failure (HF) at risk of death, data on heterogeneous HF populations are scarce. Our purpose was to verify and analyze the prognostic role of cTnI in acute HF patients admitted to the emergency department. This was an observational longitudinal prospective study carried out in an urban hospital. We studied 99 patients discharged from the department between March and December 2002 with a HF diagnosis and samples of cTnI. Patients with acute coronary syndromes, myocarditis or renal failure were excluded. The main outcome was death from any cause. The detection level of the cTnI assay was 0.05 ng/ml. cTnI was detected in 45.5% of HF patients. These patients had a higher NYHA class (P < 0.001) at initial presentation and longer hospitalization (P = 0.004) than cTnI-negative patients. Nineteen deaths occurred during the study: 17 for HF and 2 for acute coronary syndrome. Finally, detectable cTnI was associated with increased mortality risk (RR 4.7; 95% CI 1.3–17.1; P = 0.021) also after adjustment for other adverse prognosis factors (age, NYHA class and presence of relapses). Our HF cTnI-positive patients had a worse clinical presentation and longer hospitalization. cTnI is a significant independent predictor of death and of longer hospitalization. It could be used for the early identification of HF patients at an increased risk of death in the long term, and of longer hospitalization. Thus, cTnI can aid decision-making and clinical management in the emergency department. A short abstract of the paper was presented at the A.C.E.P. Scientific Assembly-Research Forum in Boston U.S.A. October 2003.     

A comparison of troponin T and troponin I as predictors of cardiac events in patients undergoing chronic dialysis at a Veteran's Hospital: a pilot study.

OBJECTIVE: The purpose of this study was to prospectively evaluate the usefulness of the cardiac troponins as predictors of subsequent cardiac events in patients with chronic renal failure undergoing dialysis. BACKGROUND: Cardiac troponin T (cTnT) and I (cTnI) are cardiac markers that are specific for cardiac muscle. They are also excellent prognostic indicators for patients presenting with chest pain. Although cardiac disease is the leading cause of death in dialysis patients, standard methods to diagnose acute coronary syndromes in patients with renal failure are often misleading. METHODS: A six-month prospective study was done in a university-affiliated Veterans Hospital's dialysis clinic. Forty-nine patients undergoing chronic dialysis with no complaints of chest pain were followed for cardiac events occurring in the six months after cardiac troponin measurements. These included unstable angina, acute myocardial infarction and cardiac death. An additional 83 patients with renal failure but who were not undergoing dialysis were also examined. RESULTS: Within six months all three dialysis patients with elevated cTnI at entry into the study suffered an adverse complication (specificity and positive predictive value = 100%). Twenty-five patients had cTnT elevated at >0.10 ng/ml (53%). Patients with diabetes were more likely to have elevated troponin T levels (64% vs. 25%, p = 0.01). All six patients developing cardiac events within three months had elevations of cTnT >0.1 ng/ml (sensitivity = 100%). Whereas the specificity of cTnT was only 56% for a near-term cardiac event, the negative predictive value of cTnT using a cutoff of < or = 0.1 ng/ml was 100%. On restratifying patients using a cutoff value of cTnT of >0.2 ng/ml, only nine of 49 dialysis patients (18%) had elevated levels. In patients with renal failure not undergoing dialysis, only three of 83 (4%) had elevated troponin I or T. None of these patients suffered a cardiac event in the next six months. CONCLUSIONS: This prospective pilot study clearly delineates the troponins as important prognosticators in asymptomatic otherwise "stable" patients on chronic dialysis, especially those with concomitant diabetes mellitus. It also appears that troponins are more likely to be elevated in dialysis patients than other patients with renal failure not on dialysis. The above suggests that the combination of cTnI and cTnT might be very effective in elucidating cardiac risks of patients with renal failure undergoing chronic dialysis.     

Cardiac troponin T and I and creatine kinase-MB as markers of myocardial injury and predictors of outcome following percutaneous coronary intervention

AIMS: This study was performed to determine the most sensitive biochemical marker for the detection of cardiac myocyte damage potentially sustained during percutaneous coronary intervention (PCI) and to assess whether such a marker can be used to identify patients at increased risk of poor subsequent clinical outcome. METHODS AND RESULTS: We studied 109 consecutive patients presenting with clinical stable and unstable angina and undergoing PCI at our institution. Blood was sampled for creatine kinase-MB (CK-MB), cardiac Troponin T (cTnT) and I (cTnI) immediately before and at 6, 14 and 24 h post-PCI. Five patients with raised cardiac markers pre-PCI were excluded from further analysis. The occurrence of major adverse cardiac events (MACE) was documented in-hospital, at 30 days and at long-term clinical follow up of up to 20 months. MACE occurred in 26/109 (24%) patients: death=1, QWMI=4, NQWMI=5, repeat PCI=16 (nine target vessel revascularisations and seven de-novo lesions), CABG=5. cTnI had the highest detection rate for myocardial damage, with 58 cTnI-positive patients, 38 cTnT-positive patients and 28 CK-MB-positive patients in the 24 h following PCI (Pearson's Chi square test, P<0.01). The type of interventional strategy per se was not significantly associated with post-procedural cardiac marker concentrations (Kruskal-Wallis ANOVA, P>0.05). There was a significant association between post-procedural cardiac marker concentrations of CK-MB, cTnT and cTnI and the occurrence of procedural angiographic complications (P=0.0003, 0.0002, 0.001, respectively). All three markers, at each sampling time point between 6 and 24 h post-PCI, showed a significant predictive relationship with MACE in-hospital and at long-term follow up (ROC curve AUC analysis, P<0.05). All three markers provided equally predictive information at each of the three post-procedural sampling time points between 6 and 24 h following PCI. All levels of cardiac marker elevation above the clinically discriminant cut-off values were significantly predictive of outcome at long-term follow up. CONCLUSIONS: cTnI proved to be the most sensitive marker in detecting myocardial necrosis following PCI. CK-MB, cTnT and cTnI all provided similarly reliable prognostic information, with cTnT and cTnI being marginally superior in predicting MACE at follow up.     

Leakage of cardiac troponin I in aortic valve stenosis

OBJECTIVE: Degeneration and death of cardiomyocytes contribute to the genesis of heart failure (HF) in aortic valve stenosis (AS). We studied whether the ongoing myocyte damage in AS can be detected from circulating cardiac troponin I (cTnI) concentrations. DESIGN AND SETTING: A cross-sectional cohort study in a university hospital. SUBJECTS AND METHODS: We examined 131 adult patients undergoing echocardiography and cardiac catheterization for isolated AS. Blood was sampled from the aortic root and, in a subset of 49 patients, also from the coronary sinus for the determination of cTnI using a sensitive immunoanalysis. RESULTS: Seventy-three patients (56%) had detectable aortic cTnI (> or =5 ng L(-1)) with 30 of them (23% of the total group) having cTnI above the reference limit in healthy subjects (>14 ng L(-1)). Patients with detectable cTnI had a higher prevalence of HF than those with undetectable cTnI (42% vs. 19%, P = 0.004). Plasma cTnI rose from the aorta to the coronary sinus by > or =5 ng L(-1) in 13 of 49 patients with AS (27%) versus in none of 12 control patients free of structural heart disease (P = 0.044). AS patients with transcardiac cTnI gradients > or =5 ng L(-1) had lower left ventricular (LV) ejection fractions than AS patients with gradients <5 ng L(-1) (mean +/- SD, 52 +/- 14% vs. 61 +/- 11%; P = 0.011). CONCLUSIONS: Detectable circulating cTnI is not uncommon in AS and shows a moderate association with the presence of HF. Leakage of cTnI into the coronary sinus associates with impairment of LV systolic function. Monitoring cTnI could provide a means to expose incipient clinical deterioration in AS.     

Prognostic value of troponins in patients with non-ST-segment elevation acute coronary syndromes and chronic kidney disease

BACKGROUND: The prognostic value of cardiac troponins (cTn) in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) and chronic kidney disease (CKD) is debated. HYPOTHESIS: We tested the performance of cTnI and cTnT for risk stratification in patients with CKD and evaluated the prognostic significance of cTnI and cTnT elevations by their magnitude across the range of CKD severity. METHODS: We examined correlations among cTn elevation, CKD, and in-hospital mortality in 31,586 high-risk patients with NSTE ACS included in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress ADverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines initiative (CRUSADE). Cardiac tropinins I and T levels were categorized as ratios of each site's upper limit of normal (ULN) for myocardial necrosis: normal (cTn ratio < or =1 x ULN), mild (cTn ratio > 1-3 x ULN), and major (cTn ratio > 3 x ULN) elevation. Estimated glomerular filtration rate (eGFR) was calculated using the abbreviated Modification of Diet in Renal Disease equation. Stages of CKD were categorized as normal to mild (eGFR > 60 mL/min), moderate (eGFR 30-60 mL/min), or severe (eGFR < 30 mL/min). RESULTS: Mortality increased more steeply across CKD stages (2.0%-12.9%) than across cTn ratio categories (2.7%-5.4%). In normal or mild CKD, mortality was low regardless of cTn elevations. In moderate CKD, mortality increased incrementally with cTnI (3.3% versus 5.4% versus 7.4%) and cTnT (3.7% versus 5.3% versus 7.3%) elevation. Among severe CKD patients, only major cTn elevations further distinguished risk (cTnI: 10.1% versus 9.7% versus 14.6%; cTnT: 7.0% versus 5.7% versus 14.0%). CONCLUSIONS: In patients with CKD, cTnI and cTnT perform equally in differentiating short-term prognosis following NSTE ACS; however, the prognostic impact of cTn is dependent upon the degree of CKD severity.     

Cardiac troponins T and I in patients with end-stage renal disease: the relation with left ventricular mass and their prognostic value

BACKGROUND: Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial. HYPOTHESIS: The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and left ventricular mass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively. METHODS: We included 129 patients with ESRD (71 men, age 44 +/- 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, and transthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years. RESULTS: The cTnT concentration was > 0.03-0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p = 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were 25 (19.4%) deaths during follow-up. Multivariable analysis showed that elevation of cTnT and cTnI did not emerge as an independent predictor for death. Serum albumin level (p < 0.001) was the strongest predictor of mortality, followed by age (p = 0.002) and LVMI (p = 0.005). CONCLUSIONS: Cardiac troponin T and I related significantly to the LVMI. The increased serum concentration of cardiac troponins probably originates from the heart; however, they are not independent predictors for prognosis.     

Cardiac troponin T and I, echocardiographic [correction of electrocardiographic] wall motion analyses, and ejection fractions in athletes participating in the Hawaii Ironman Triathlon

Cardiac troponin T (cTnT) and troponin I (cTnI) are highly sensitive and specific for detecting myocardial damage even in the presence of skeletal muscle injury. In this study, we assessed whether ultraendurance exercise induced cardiomyocyte injury using plasma cTnT and cTnI measurements, quantitative echocardiographic wall-motion analysis, and ejection fraction measurement in athletes who participated in the Hawaii Ironman Triathlon. Twenty-three athletes (11 men) who completed the triathlon (3.9 km swim, 180.2 km bike, and 42.2 km run) participated in this study. Blood samples were obtained 2 days before and immediately after the triathlon for the determination of cTnT (Enzymun, Roche Diagnostics) and cTnI (Dade Behring) concentrations. Quantitative echocardiographic wall motion analysis and ejection fraction were obtained on 12 of the 23 participants before and immediately after the race. No subject had detectable cTnT or cTnI or abnormal echo score before the race. Following the race, 2 subjects (9%) had marked increases in both cTnT (0.15 and 0.33 microg/L) and cTnI (2.09 and 4.44 microg/L). Four additional subjects (17%) had moderate increases in cTnT (0.04 to 0.05 microg/L) but no detectable cTnI. Race time correlated inversely with cTnT (r = -0.65, p <0.01). Mean change in the number of abnormal echo segments after the race was 6.5 in those with a marked increase in cTnT and cTnI, 2.3 in those with a moderate increase in cTnT, and 1.7 in those with no increase. Ejection fraction decreased by an average of 24% after the race (p <0.002). Thus, ultraendurance exercise may cause myocardial damage as indicated by biochemical cardiac-specific markers and echocardiography. The cellular nature of this damage and whether it is transient or permanent is unclear at present.     

Vascular surgery patients: perioperative and long-term risk according to the ACC/AHA guidelines, the additive role of post-operative troponin elevation.

AIMS: The objectives of this study are to evaluate the prognostic role of pre-operative stratification in patients undergoing elective major vascular surgery, the timing of adverse outcomes, and the predictive role of troponin (cTn). METHODS AND RESULTS: Consecutive vascular surgery candidates (n=391) were prospectively stratified and treated according to the ACC/AHA guidelines. The patients were categorized into three groups: (1) with coronary revascularization in the past 5 years, (2) with intermediate clinical risk predictors, and (3) with minor or no clinical risk predictors. cTnI was measured post-operatively. By 18 months, 18.7% of subjects had experienced death or acute myocardial infarction (MI) (by the ACC/ESC criteria). The hazard ratio (HR) was 5.21 (95% CI=2.60-10.43; P<0.0001) in group 1 and 2.58 (95% CI=1.27-4.38; P=0.004) in group 2 when compared with group 3. Most events occurred within 30 days. Elevations of cTnI were associated with adverse outcomes even after multivariable adjustment at long-term (adjusted overall HR=4.73, 95% CI=2.92-7.65; P<0.0001) and at 30 days (adjusted HR=5.52, 95% CI=3.23-9.42; P<0.0001). CONCLUSION: After pre-operative stratification, patients undergoing elective major vascular surgery remain at high risk of MI and death. Events occur mainly early after surgery. cTnI elevations are frequent and independently associated with increased risk. These findings suggest the need for a major re-evaluation of our approach to these patients.     

心脏肌钙蛋白T对扩张性心肌病患者的预测价值

目的探讨心脏肌钙蛋白T(cTnT)对扩张性心肌病(DCM)的预测价值。方法用酶联免疫法测定60例DCM患者的血清cTnT水平并将患者分为cTnT升高组和cTnT正常组;观察其两组恶性心律失常,心源性死亡和因心衰再入院的发生率。结果在60例DCM患者中,cTnT升高26例(43.3%),cTnT升高组恶性心律失常,因心衰再入院的发生率显著高于cTnT正常组(P<0.01)。cTnT升高对因心衰再入院的阳性预测值为30.7%,阴性预测值为96%。结论cTnT对扩张性心肌病的预后相关。     

Cardiac troponin T levels are associated with poor short- and long-term prognosis in patients with acute cardiogenic pulmonary edema

Background The clinical determinants of increased cardiac troponin T (cTnT) in patients with acute cardiogenic pulmonary edema are not well defined, and the ability of this marker to predict long-term mortality has not yet been documented. Methods Eighty-four patients with acute cardiogenic pulmonary edema without acute myocardial infarction were prospectively enrolled. cTnT was measured in samples obtained 6 and 12 hours after admission. Results cTnT levels of 0.1 ng/mL or greater were found in 46 patients (55%). Thirty-two patients (38%) died during follow-up. The area under the receiver operating characteristic curve for cTnT was 0.70 and 0.69 at 6 and 12 hours (P = .47), and the cTnT cutoff value of 0.1 ng/mL was 66% and 69% sensitive and 63% and 71% specific, respectively, in predicting subsequent mortality. Patients were assigned to group 1 if they had cTnT lower than 0.1 ng/mL and to group 2 if they had cTnT levels of 0.1 ng/mL or greater. A history of coronary artery disease was present in 72% of group 2 versus 50% of group 1 patients (P = .04). Patients in group 2 were also older than those in group 1 (mean age, 68 years vs 61 years; P = .021). The 3-year survival in group 1 was 76% compared with 29% in group 2 (log-rank test, P < .001). In a Cox proportional hazards model, elevated cTnT emerged as the only prognostic marker of long-term mortality (risk ratio [RR] = 2.31; 95% CI, 1.011-5.280; P = .047). Conclusions A cTnT level of 0.1 ng/mL or greater was associated with poor long-term survival and emerged as a powerful independent predictor of mortality in patients with acute cardiogenic pulmonary edema. (Am Heart J 2002;143:814-20.)     

Combined measurements of cardiac troponin T and N-terminal pro-brain natriuretic peptide in patients with heart failure.

BACKGROUND: To examine the prognostic contribution of combined cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with heart failure (CHF) in the absence of acute coronary syndrome. METHODS AND RESULTS: Between July 2001 and March 2002, 71 consecutive patients (mean age = 68.4+/-1.4 years, 37 men), hospitalised for heart failure, were studied during hospitalisation and follow up until December 2002. Serum cTnT and NT-proBNP were measured on admission. Actuarial rates of adverse cardiac events, including sudden or CHF death, or rehospitalisation for CHF during follow up were compared with patients grouped according to initial serum cTnT and/or NT-proBNP concentrations. The adverse cardiac event-free rate among the 20 patients with cTnT > or 0.01 ng/ml was significantly lower than the 51 patients with cTnT <0.01 ng/ml (P<0.05). Similarly, the adverse cardiac event-free rate among the 36 patients with NT-proBNP > or =1,357 pg/ml (median) was significantly lower than the 35 patients with NT-proBNP <1,357 pg/ml (P<0.01). The 16 patients with high concentrations of both cTnT and NT-proBNP had a lower adverse cardiac event-free rate than the 31 patients with low cTnT and low NT-proBNP upon commencement of the study (P<0.005). CONCLUSION: Measurements of serum cTnT and NT-proBNP were reliable prognostic markers of adverse cardiac event in patients with CHF.     

Baseline troponin level: key to understanding the importance of post-PCI troponin elevations.

AIMS: The adverse prognostic significance of biomarker elevations after percutaneous coronary intervention (PCI) is well established. However, often baseline troponin values are not included in the analysis or sensitive criteria are not employed. Accordingly, we assessed the timing and magnitude of post-PCI troponin T (cTnT) levels and their relationships to outcomes in patients with and without pre-PCI baseline cTnT elevations using a sensitive assay and sensitive cut-off values. METHODS AND RESULTS: cTnT was measured at baseline (pre-PCI), 8 and 16 h post-PCI in 2352 patients. A cTnT elevation was defined as > or =0.03 ng/mL. No baseline cTnT elevations were detected in 1619 patients undergoing mostly (97%) non-urgent procedures (cTnT = 0.01 +/- 0.002 ng/mL; mean +/- SD). 733 patients had baseline cTnT elevations. Only the baseline troponin value had prognostic importance. Patients with elevated cTnT baseline levels had a higher overall cumulative 12-month death/MI rate of 11.1% compared with those without elevated baseline levels of 4.7% (P < 0.05). Neither the timing nor the magnitude of the post-procedure cTnT elevations was predictive of long-term death/MI rates when baseline elevations were included in the analysis. Similar findings were observed for baseline creatine kinase-MB (CK-MB) levels. Late increases in cTnT levels (16 h post-PCI) presaged in-hospital events only. CONCLUSION: Long-term prognosis is most often related to the baseline pre-PCI troponin value and not the biomarker response to the PCI. These results support a re-evaluation of the use of biomarker data in relation to PCI.     

Patterns and diagnostic value of cardiac troponin I vs. troponin T and CKMB after OPCAB surgery.

BACKGROUND: Cardiac troponin I (cTnI) has been shown to be a specific marker for myocardial injury in cardiac surgery. The object of this prospective study was to determine the patterns and kinetic and diagnostic value of cTnI, cardiac troponin T (cTnT), and creatine kinase MB (CKMB) activity after minimally invasive coronary revascularization using an octopus device on the beating heart (OPCAB). METHODS: 48 patients (33 male/15 female, mean age 68.3 +/- 8.7 years) underwent their first elective OPCAB surgery with median sternotomy without mortality. The mean number of grafts was 2.0 +/- 0.8 per patient. Preoperative mean ejection fraction was 56.6 % +/- 14.9%. CTnI and T levels, total creatine kinase (CK) and CK-MB activity in the serum were measured before operation, at arrival at the ICU, and 6, 12, 24, 48 and 120 hours afterward. Serial 12-lead ECGs were recorded preoperatively and at days 1, 2 and 5. The relationship between perioperative data and postoperative cTnI and cTnT levels and CKMB were statistically identified for all variables. RESULTS: The best cutoff value for cTnI was 8.35 micrograms/l. The patients were grouped by the ECG findings and maximal slopes of cTnI postoperatively (group I: unchanged ECG and cTnI < 8.35 micrograms/l, n = 38; group II: unchanged ECG and cTnI > 8.35 micrograms/l n = 6; group III: Q-wave in ECG and cTnI > 8.35 micrograms/l, n = 4). Baseline serum concentrations of cTnI were in the normal range, and significantly increased after surgery with a peak 24h after the operation. Maximal slopes of cTnI ranged in group II between 9.1 and 18.0 micrograms/l, and in group III between 35.9 and 88.8 micrograms/l. There was strong concordance between maximum cTnI, cTnT (p < 0.0001) and CK-MB levels (p = 0.003). First cTnI levels immediately post-op correlated with the maximum cTnI levels during the postoperative course (p = 0.009). CONCLUSIONS: CTnI after minimal invasive surgery shows a characteristic pattern with a maximum at 24h after the operation. The measurement of postoperative biochemical marker concentrations, specially cTnI, reflects myocardial injury incurred during the procedure. It is an accurate method for confirming or excluding a perioperative myocardial injury diagnosis after OPCAB surgery.     

Elevated troponin T on discharge predicts poor outcome of decompensated heart failure

Persistent elevation of cardiac troponin T (cTnT) predicts an adverse clinical outcome in patients with chronic heart failure (HF), but the underlying mechanisms remain to be determined. We investigated the association between predischarge cTnT elevation and coexistent pathophysiology in patients with decompensated HF. Plasma cTnT levels were determined before discharge in 170 patients with decompensated HF. We divided the patients into a group that was positive for cTnT [cTnT(+) group, n = 40] and a group that was negative for cTnT [cTnT(−) group, n = 130]. Multivariate analysis showed that use of β-blocker therapy (odds ratio [OR] = 0.236, P = 0.003), an elevated high-sensitivity C-reactive protein (hsCRP) level (OR = 3.731, P = 0.006), a high brain natriuretic peptide (BNP) level (OR = 3.570, P = 0.007), diabetes (OR = 3.090, P = 0.018), and anemia (OR = 2.330, P = 0.047) were independently associated with cTnT positivity. During a mean follow-up period of 441 days after discharge, total mortality (P < 0.001), cardiac death (P < 0.001), and exacerbation of HF requiring hospitalization (P = 0.007) were all more common in the cTnT(+) group than in the cTnT(−) group. Cox proportional hazards analysis showed that cTnT positivity was an independent predictor of total mortality (hazard ratio = 5.008, P = 0.004) in an age- and gender-matched model. Elevation of cTnT during convalescence was associated with lack of β-blocker therapy, a high hsCRP level at discharge, a high BNP level at discharge, diabetes, and anemia, and a worse clinical outcome in patients with decompensated HF.     

肌钙蛋白T联合血清氨基末端脑钠肽诊断儿童心衰的价值

目的：研究血浆肌钙蛋白T （cTnT）与 N 末端 B型利钠肽原（NT-proBNP）联合检测诊断儿童心力衰竭（HF）的价值。方法：选择我院73例儿童 HF患者为心衰组,另选儿童保健门诊75例健康儿童为健康对照组。检测两组的 cTnT、NT-proBNP浓度及左室射血分数（LVEF）,并比较。应用受试者工作特性曲线（ROC）分析 cT-nT和 NT-proBNP联用的诊断敏感度和特异度。结果：与健康对照组相比,心衰组 NT-proBNP [（2486.7±87.5） pmol/L比（3573.8±98.2）pmol/L]、cTnT [（0.03±0.01）ng/ml 比（0.35±0.09）ng/ml]浓度显著升高, LVEF [（70.8±5.2）％比（42.6±3.8）％]显著降低,P 均＜0.05;多元 Logistic回归分析显示,NT-proBNP为HF患童 LVEF的独立相关因素（OR＝1.006,P＝0.012）;NT-proBNP取值3200pmol/L、cTnT取值0.08ng/ml联合诊断儿童 HF的敏感性为89.5％,特异性为85.7％,ROC曲线下面积为0.795。结论：N末端 B型利钠肽原与心肌肌钙蛋白T联合检测对于儿童心力衰竭有较高的诊断价值。     

Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes

OBJECTIVES

We prospectively evaluated the relation between cardiac troponin T (cTnT) level, the presence and severity of coronary artery disease (CAD) and long-term prognosis in patients with chest pain but no ischemic electrocardiographic (ECG) changes who had short-term observation.

BACKGROUND

Cardiac TnT is a powerful predictor of future myocardial infarction (MI) and death in patients with ECG evidence of an acute coronary syndrome. However, for patients with chest pain with normal ECGs, it has not been determined whether cTnT elevation is predictive of CAD and a poor long-term prognosis.

METHODS

In 414 consecutive patients with no ischemic ECG changes who were triaged to a chest pain unit, cTnT and creatine kinase, MB fraction (CK-MB) were evaluated ≥10 h after symptom onset. Patients with adverse cardiac events, including death, MI, unstable angina and heart failure were followed for as long as one year.

RESULTS

A positive (>0.1 ng/ml) cTnT test was detected in 37 patients (8.9%). Coronary artery disease was found in 90% of 30 cTnT-positive patients versus 23% of 144 cTnT-negative patients who underwent angiography (p < 0.001), with multivessel disease in 63% versus 13% (p < 0.001). The cTnT-positive patients had a significantly (p < 0.05) higher percent diameter stenosis and a greater frequency of calcified, complex and occlusive lesions. Follow-up was available in 405 patients (98%). By one year, 59 patients (14.6%) had adverse cardiac events. The cumulative adverse event rate was 32.4% in cTnT-positive patients versus 12.8% in cTnT-negative patients (p = 0.001). After adjustment for baseline clinical characteristics, positive cTnT was a stronger predictor of events (chi-square = 23.56, p = 0.0003) than positive CK-MB (>5 ng/ml) (chi-square = 21.08, p = 0.0008). In a model including both biochemical markers, CK-MB added no predictive information as compared with cTnT alone (chi-square = 23.57, p = 0.0006).

CONCLUSIONS

In a group of patients with chest pain anticipated to have a low prevalence of CAD and a good prognosis, cTnT identifies a subgroup with a high prevalence of extensive and complex CAD and increased risk for long-term adverse outcomes.     

血肌钙蛋白Ⅰ、C-反应蛋白和D-二聚体水平与急性胸痛患者预后关系的评价

目的：前瞻性研究血清肌钙蛋白Ｉ（ｃＴｎＩ）、Ｃ－反应蛋白（ＣＲＰ）和血浆Ｄ－二聚体水平对急性胸痛患预后的评估作用。方法：９０例急性胸痛患，分别测定ｃＴｎＩ、ＣＲＰ和Ｄ－二聚体水平后，随诊３个月。随诊终点为心脏事件。结果：随诊期间１４例患发生心脏事件，其中８６％患ｃＴｎＩ水平升高，５０％ＣＲＰ升高，７９％Ｄ－二聚体升高，５０％患３项均升高。９０例患中，ｃＴｎＩ升高和正常组心脏事件发生率分别为２５％和５％（Ｐ〈０．０１），ＣＲＰ升高和正常组为３２％和１０％（Ｐ〈０．０１），Ｄ－二聚体升高和正常组为３３％和５％（Ｐ〈０．００１）。结论：急性胸痛患就诊时的ｃＴｎＩ、ＣＲＰ和Ｄ－二聚体水平分别与预后相关。     

Brain natriuretic peptide correlates with troponin T in patients with renal failure

OBJECTIVES: In patients with chronic renal failure, the main cause of mortality is cardiovascular disease. Cardiac troponin T (cTnT) and brain natriuretic peptide (BNP) are found to be related with decreased survival in both the normal population and in patients with chronic renal failure in different studies. Our aim is to investigate the relationship between cTnT and BNP in patients with chronic renal failure. METHODS AND RESULTS: 58 chronic haemodialysis patients were enrolled prospectively for the study. Blood samples for measurement of cTnT and BNP were collected after the haemodialysis. The patients are divided into 3 groups according to cTnT measurements. Group I included the patients with cTnT < 0.05 ng/ml, Group II included the patients with cTnT between 0.05 and 0.1 ng/ml and group III included the patients with cTnT > 0. 1 ng/ml.We performed echocardiography in all patients to measure the left ventricular ejection fraction and thickness of septum and posterior wall. When BNP levels were compared among the 3 groups, we found that the BNP level was lowest in group I and highest in group III (165.13 +/- 125.44 pg/dl; 236.0 +/- 107.83 pg/dl; 280.71 +/- 153.25 pg/dl, respectively) (P = 0.01).The difference in BNP levels among groups was statistically significant and independent from left ventricular hypertrophy, left ventricular ejection fraction and volume overload in multiple regression analysis.We also searched the relationship between plasma cTnT and BNP levels and found a positive correlation (r = 0.3; P = 0.023). CONCLUSION: cTnT and BNP levels were related to each other in patients with chronic renal failure.These parameters can help to identify the patients with a high risk for cardiovascular diseases.     

Cardiac troponin I threonine 144: role in myofilament length dependent activation

Myofilament length-dependent activation is the main cellular mechanism responsible for the Frank-Starling law of the heart. All striated muscle display length-dependent activation properties, but it is most pronounced in cardiac muscle and least in slow skeletal muscle. Cardiac muscle expressing slow skeletal troponin (ssTn)I instead of cardiac troponin (cTn)I displays reduced myofilament length-dependent activation. The inhibitory region of troponin (Tn)I differs by a single residue, proline at position 112 in ssTnI versus threonine at position 144 in cTnI. Here we tested whether this substitution was important for myofilament length-dependent activation; using recombinant techniques, we prepared wild-type cTnI, ssTnI, and 2 mutants: cTnI(Thr>Pro) and ssTnI(Pro>Thr). Purified proteins were complexed with recombinant cardiac TnT/TnC and exchanged into skinned rat cardiac trabeculae. Force-Ca2+ relationships were determined to derive myofilament Ca2+ sensitivity (EC50) at 2 sarcomere lengths: 2.0 and 2.2 microm (n=7). Myofilament length-dependent activation was indexed as deltaEC50, the difference in EC50 between sarcomere lengths of 2.0 and 2.2 microm. Incorporation of ssTnI compared with cTnI into the cardiac sarcomere reduced deltaEC50 from 1.26+/-0.30 to 0.19+/-0.04 micromol/L. A similar reduction also could be observed when Tn contained cTnI(Thr>Pro) (deltaEC50=0.24+/-0.04 micromol/L), whereas the presence of ssTnI(Pro>Thr) increased deltaEC50 to 0.94+/-0.12 micromol/L. These results suggest that Thr144 in cardiac TnI modulates cardiac myofilament length-dependent activation.