Do cardiac troponins provide prognostic insight in hemodialysis patients?

BACKGROUND: The diagnosis of myocardial necrosis in patients with chronic renal failure is often difficult because biochemical markers of cardiac damage such as creatine kinase MB (CKMB) and cardiac troponin T (cTnT) may be spuriously elevated. Recent small studies also report unexplained elevations in cardiac troponin I (cTnI) in chronic renal failure patients undergoing hemodialysis. The relative incidence of elevated cardiac troponins in this population and their relationship to clinical events remain unknown. OBJECTIVE: To determine the incidence and prognostic significance of asymptomatic elevations of cTnT and cTnI in patients undergoing hemodialysis for chronic renal failure. DESIGN: Prospective cohort study. SETTING: University tertiary care teaching hospital. PATIENTS: One hundred thirteen patients over 21 years of age undergoing onsite hemodialysis were enrolled between December 1997 and February 1998. MEASUREMENTS: All-cause and cardiovascular mortality, hospitalization for acute myocardial infarction, unstable angina or congestive heart failure, new onset sustained arrhythmia or need for unscheduled emergency hemodialysis due to volume overload at 30 days and six months. RESULTS: The incidence of abnormal results for cTnT, cTnI and CKMB were 42%, 15% and 4%, respectively. Independent predictors of mortality at six months were median age greater than 63 years (odds ratio 14.3, 95% CI 1.5 to 130.3, P=0.019) and positive cTnT (odds ratio 13.6, 95% CI 2.5 to 73.2, P=0.002). Diabetics were more likely to have positive cTnI and cTnT results than nondiabetics (P<0.001 and P=0.023, respectively). CONCLUSIONS: cTnT is commonly elevated in patients with chronic renal failure even in the absence of acute coronary syndromes. cTnT may be an important independent prognostic marker in patients on hemodialysis for chronic renal failure. While less common, elevations of cTnI are more frequent than CKMB elevations. The basis of these cardiac troponin elevations is unclear. These findings may represent, in part, a subclinical myocardial injury, an inflammatory response to chronic renal failure or a chronically volume overloaded state.     

Prognostic use of cardiac troponin T and troponin I in patients with heart failure

BACKGROUND: Troponin T (cTnT) and troponin I (cTnI) are present in the sera of some heart failure (HF) patients and have potential importance as prognostic markers. OBJECTIVE: To prospectively evaluate the prognostic value of cTnT and cTnI in well-characterized HF patients and clarify their relationship to other clinical markers of HF severity. METHODS: cTnT and cTnI were measured in 78 HF patients (45 inpatients, 33 outpatients) who were followed up prospectively for 12 months. RESULTS: Plasma cTnT (> or =0.02 ng/mL) and cTnI (> or =0.3 ng/mL) were detected in 51% and 46% of patients, respectively. These patients were more likely to be inpatients (70% versus 45% for cTnT, 75% versus 43% for cTnI, P<0.05 for both), have a higher plasma creatinine (153 versus 119 micromol/L for cTnT; 157 versus 118 micromol/L for cTnI, P<0.05) and lower plasma sodium (134 versus 138 mmol/L for both, P<0.05). At 12 months, they were more likely to have died or undergone cardiac transplantation (41% versus 14%, P=0.01 for cTnT; 43% versus 15%, P=0.004 for cTnI). After adjustment for New York Heart Association class, plasma sodium and inpatient status, a significant association with events was still evident for both troponins. CONCLUSIONS: Both cTnT and cTnI are strongly associated with other clinical indicators of HF severity and remain independent predictors of prognosis after adjustment for these factors. These results indicate a potential role for cTnT and cTnI in the clinical management of HF patients.     

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.     

Prognostic value of serum cardiac troponin I in ambulatory patients with chronic renal failure undergoing long-term hemodialysis: a two-year outcome analysis

OBJECTIVES: We sought to evaluate the prognostic value of cardiac troponin I (cTnI) in asymptomatic, ambulatory patients with chronic renal failure treated with long-term hemodialysis. BACKGROUND: Smaller, short-term follow-up studies on this subject have given conflicting results. METHODS: A total of 126 ambulatory patients with chronic renal failure treated with long-term hemodialysis were followed for two years for all-cause mortality, cardiac mortality, all-cause hospital admissions and cardiac hospital admissions. Serum cTnI was measured before dialysis at the time of study entry. RESULTS: One hundred two patients had normal serum levels of cTnI (< or =0.03 ng/ml) and 24 patients had elevated levels (0.015 +/- 0.007 vs. 0.053 +/- 0.029 ng/ml, p < 0.0001). No significant difference in all-cause mortality (20 vs. 4 deaths), cardiac mortality (4 vs. 1 death), all-cause hospital admissions (1.74 +/- 1.72 vs. 1.25 +/- 1.19 admissions/patient) or cardiac admissions (0.52 +/- 0.89 vs. 0.33 +/- 0.76 admissions/patient) was present between the patients with normal cTnI levels and those with elevated cTnI levels. Serum cTnI was not significantly different between patients who died versus those who survived (0.022 +/- 0.019 vs. 0.022 +/- 0.021 ng/ml). Serum cTnI was not an independent predictor of all-cause mortality, cardiac mortality, all-cause admissions or cardiac admissions. Age (older) and serum albumin (lower) were independent predictors of all-cause mortality, whereas a history of myocardial infarction was an independent predictor of cardiac mortality. Serum sodium (lower) was an independent predictor of all-cause hospital admissions, whereas hypertension and previous myocardial infarction were independent predictors of cardiac admissions. The best predictors of the time to death were age (older) and serum sodium level (lower), irrespective of the serum cTnI levels. CONCLUSIONS: Cardiac troponin I has a limited role in predicting mortality and hospital admissions in asymptomatic patients with chronic renal failure treated with long-term hemodialysis.     

Cardiac troponin T in patients with kidney disease

Atherosclerosis is accelerated in dialysis patients and cardiovascular mortality is up to 20 times higher than in the general population. Cardiac troponin T (cTnT) is a sensitive marker of myocardial necrosis and studies have confirmed the superiority of this marker over traditional cardiac enzymes. Elevated cTnT has been observed in patients with various degrees of renal failure and treatment modalities in the absence of an acute coronary event. The possibility that increased troponins reflect decreased clearance or analytical interference from uremic serum is unlikely. It is accepted that cTnT detected in serum from patients with end-stage renal failure is derived from myocytes and this effect could be caused by subclinical myocardial ischemic release of troponin, myocardial remodeling, or from uremic pericarditis or myocarditis. The significance of cTnT in patients with different degrees of renal failure and different treatment modalities is presented in this review.     

Serial analysis of troponin I levels in patients with ischemic and nonischemic dilated cardiomyopathy

BACKGROUND: Ongoing myocardial cell damage forms the basis for progression of chronic heart failure. Evidence is accumulating that progressive loss of cardiac myocytes is associated with the release of cardiac troponin I (cTnI). HYPOTHESIS: This study sought to determine whether levels of cTnI are of prognostic value for risk stratification of patients with chronic heart failure. METHODS: Release of cTnI was measured by conventional enzyme immunoassay following serum ultrafiltration in 58 consecutive patients hospitalized for chronic heart failure and 31 healthy volunteers serving as control group. Determination of serum levels was performed every 2 weeks over a time interval of 3 months. According to the results of coronary angiography, patients were divided into Group D showing normal coronary arteries (n=33, ejection fraction 27 +/- 6.1%) and Group I showing severe coronary heart disease (n=25, ejection fraction 28.8 +/- 7.8%). Survival of patients was evaluated after a mean time interval of 3 years. RESULTS: The mean cTnI serum level over all measurements was 0.66 +/- 1.8 ng/ml in patients versus 0.11 +/- 0.48 ng/ml in volunteers. At all six points of analysis, the mean cTnI serum level was significantly different (p < 0.001) between patients and volunteers. There was no significant difference between patients with and without coronary heart disease following hospital discharge, however, troponin release was significantly different between survivors and nonsurvivors (n=27) (0.56 ng/ml vs. 0.84 ng/ml; p < 0.05). CONCLUSION: Permanent cTnI release is a common finding in patients with chronic heart failure and a strong prognosticator. In this setting, coronary morphology seems to play a minor role for disease progression.     

Diversity of the elevation of serum cardiac troponin I levels in patients during their first visit to the emergency room.

BACKGROUND: Although measurement of serum creatine kinase levels, as well as myoglobin levels, has been used for screening patients with acute coronary syndrome (ACS), the specificity of both is low. Measurement of cardiac troponin levels is now extensively used for the diagnosis of ACS because of their superior cardiac specificity. However, troponin levels are reportedly elevated not only in patients with ACS but also in those with other diseases. METHODS AND RESULTS: The clinical characteristics of 1,023 patients (mean age: 63.5+/-16.3 years; males: 665, females: 358) whose serum cardiac troponin I (cTnI) levels had been measured at the initial visit to the emergency room of Toyota Memorial Hospital between April 2004 and March 2005 were retrospectively analyzed. A positive elevation of cTnI was defined as cTnI > or =0.03 ng/ml. There were 432 patients (42.2%) with positive cTnI levels. The cTnI levels (8.48+/-2.64 ng/ml) in patients with acute myocardial infarction (AMI) were greater than those (0.25+/-0.07 ng/ml) in patients with unstable angina pectoris (AP), as well as those (0.04+/-0.01 ng/ml) in patients with stable AP. In terms of the diagnosis of AMI, the sensitivity was high enough (94.6%), but its specificity was relatively low (61.9%). Furthermore, the differentiation between AMI and unstable AP by the cTnI value alone was impossible. The cTnI levels were elevated in patients with a variety of diseases other than ACS, including heart failure, cardiomyopathies, myocarditis, renal failure, tachyarrhythmias, and pulmonary embolism. CONCLUSIONS: Elevation of the cTnI level is frequently observed in patients in the emergency room with common diseases other than ACS.     

Troponin I and T levels in renal failure patients without acute coronary syndrome: a systematic review of the literature

BACKGROUND: Debate surrounds the interpretation of troponin assays for the diagnosis and prognosis of cardiac disease in patients with renal failure. OBJECTIVES: To systematically review the diagnostic and prognostic test characteristics of quantitative serum cardiac troponin I (cTnI) and T (cTnT) in renal failure patients without acute coronary syndrome (ACS) symptoms. METHODS: English-language literature was identified through searching MEDLINE from 1966 to August 2003 and reviewing reference lists. Studies were excluded if they did not meet research objectives, had fewer than 10 patients or focused primarily on nonrenal patients. Of 119 potential studies, 39 articles with over 349 patients with chronic kidney disease (CKD) and 3899 hemodialysis patients were selected for abstraction. RESULTS: Among CKD and hemodialysis patients without ACS symptoms, cTnI had a mean specificity of 97% (95% CI 93% to 99%) and 96% (95% CI 94% to 98%), respectively, using the myocardial infarction cut-off threshold. The mean specificity of cTnT compared less favourably at 85% (95% CI 75% to 93%) and 71% (95% CI 64% to 77%) for CKD and hemodialysis patients, respectively. In hemodialysis patients without ACS symptoms, positive and negative likelihood ratios for all-cause mortality over 12 to 24 months for cTnT were 4.5 (95% CI 2.9 to 7.1) and 0.6 (95% CI 0.4 to 0.8), and for cTnI were 1.6 (95% CI 0.9 to 2.9) and 1.0 (95% CI 0.9 to 1.1), respectively. CONCLUSIONS: In CKD and hemodialysis patients without ACS symptoms, troponin I, at the myocardial infarction cut-off threshold, is unlikely to be falsely elevated. Among hemodialysis patients without ACS symptoms, a positive troponin T helps predict all-cause mortality.     

Effect on outcome of an increase of serum cardiac troponin T in patients with healing or healed ST-elevation myocardial infarction

Recently, an association between minimally elevated cardiac troponin levels and cardiovascular risk in the general population has been reported. However, the prevalence and clinical importance of elevated cardiac troponin T (cTnT) levels remain unclear in patients with histories of myocardial infarction (MI). In this study, 1,807 consecutive patients with ST-segment elevation MIs were prospectively studied (77.1% men; mean age 64.4 years). Venous blood samples were obtained in the chronic stage of MI (28 +/- 7 days after onset), and serum cTnT levels were determined. During the average follow-up of 1,042 days, 84 patients died and 83 had nonfatal reinfarctions. Patients with cTnT levels in the highest quartile (> or = 0.040 ng/ml [n = 353]) had a higher incidence of all-cause death (8.2% vs 5.2%, p = 0.049) and nonfatal reinfarction (8.3% vs 5.1%, p = 0.048) than patients with cTnT levels from the lower 3 quartiles (<0.040 ng/ml [n = 1,064]). Multivariate Cox regression analysis revealed that a minimally elevated cTnT level (> or =0.040 ng/ml) was a significant predictor of all-cause mortality (hazard ratio 1.79, 95% confidence interval 1.10 to 2.90, p <0.02) and nonfatal reinfarction (hazard ratio 1.50, 95% confidence interval 1.13 to 2.20, p <0.03). Subgroup analysis showed that an elevated cTnT level was also a predictor of all-cause mortality and nonfatal reinfarction in patients without heart failure. In conclusion, minimally elevated cTnT levels in the chronic stage of MI predicted long-term adverse clinical outcomes.     

Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers

OBJECTIVES: The objectives of this study were: (1) to evaluate the specificity of cardiac troponin I and creatine kinase-MB isoenzyme in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis, and (2) to evaluate the effect of hemodialysis on the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme. METHODS: One hundred and forty-four consecutive ambulatory asymptomatic chronic renal failure patients on hemodialysis for a minimum of 1 year were evaluated clinically. Serum cardiac troponin I and creatine kinase-MB isoenzyme levels were measured with specific monoclonal antibodies before and after dialysis using ACCESS Troponin I and ACCESS CK-MB assays. RESULTS: The specificity of serum cardiac troponin I was 83% with a cutoff level of 0.03 ng/ml, which is an expected level for healthy population, but it rose to 100% with a cutoff level of 0.15 ng/ml, which is a reference level for patients with acute myocardial infarction. Twenty-four (17%) patients had borderline elevation in cardiac troponin I (>0.03 to <0.15 ng/ml). A history of angina pectoris was more common in the borderline-elevated cardiac troponin I subgroup. In 28% of the patients, serum creatine kinase-MB isoenzyme levels were increased with a specificity of 72% at a cutoff level of 4 ng/ml, which is the upper limit of normal, but the specificity rose to 98% by increasing the cutoff level value to 10 ng/ml. There were no statistically significant differences in serum levels of cardiac troponin I and creatine kinase-MB isoenzyme before and after dialysis. CONCLUSIONS: Cardiac troponin I is highly specific in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis; borderline elevations in cardiac troponin I may represent microinjury to the myocardium. A serum level of creatine kinase-MB isoenzyme >2.5 times of the normal upper limit may be highly specific in this patient population. Hemodialysis per se does not significantly change the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme.     

Elevated cardiac troponin levels in patients with submassive pulmonary embolism.

BACKGROUND: Cardiac troponins are reliable markers of myocardial injury that are being used increasingly in patients presenting with undifferentiated chest pain or dyspnea to diagnose an acute coronary syndrome. If elevated cardiac troponin levels also occur in patients with pulmonary embolism because of right ventricular dilation and myocardial injury, such patients could be misdiagnosed. We performed a prospective cohort study to determine the prevalence of elevated cardiac troponin I (cTnI) levels in patients with submassive pulmonary embolism. METHODS: Consecutive patients with objectively confirmed submassive pulmonary embolism and no previous history of ischemic heart disease, other cardiac disease, or renal insufficiency were included. Creatine kinase and cTnI levels were measured within 24 hours of clinical presentation on 2 occasions 8 to 12 hours apart. RESULTS: Of 24 patients with submassive pulmonary embolism, 5 (20.8%) had elevated cTnI levels of 0.4 microg/L or higher (95% confidence interval, 7.1-42.2%). One of these patients had a cTnI level higher than 2.3 microg/L that was suggestive of myocardial infarction. CONCLUSION: Pulmonary embolism should be considered in the differential diagnosis of patients presenting with undifferentiated chest pain or dyspnea and an elevated cardiac troponin level.     

Elevated cardiac troponin T predicts adverse outcomes in hypertensive patients

Ongoing myocardial damage detected as elevated serum cardiac troponin T (cTnT) indicates increased risk for future cardiac events in patients with chronic heart failure. Whether elevated cTnT is associated with adverse outcomes in patients with hypertension (HT) without left ventricular (LV) systolic dysfunction is unknown.We measured cTnT levels in 176 patients with essential HT without LV systolic dysfunction (LV ejection fraction ≤ 55%), renal failure, and prior cardiovascular or cerebrovascular diseases and 39 normal controls. Levels of cTnT were elevated (≥ 0.02 ng/mL) in 15 (9%) of the 176 patients and in 0 (0%) of the 39 normal controls (P = 0.04). The rate of diabetes mellitus (DM), the cardiothoracic ratio, plasma B-type natriuretic peptide (BNP) value, and LV mass index were significantly higher in patients with than without elevated cTnT (DM, 8/15 versus 29/161, P = 0.004; cardiothoracic ratio, 54.5 ± 4.5 versus 51.6 ± 5.2%, P = 0.04; BNP, 103.3 ± 142.3 versus 36.9 ± 50.7 pg/mL, P = 0.04; LV mass index, 227 ± 87 versus 152 ± 57 g/m(2), P = 0.0001). Kaplan-Meier analysis demonstrated that significantly fewer (P < 0.000001) patients with, than without elevated cTnT remained free of events (hospitalization due to cardiovascular or cerebrovascular disease, n = 34). Stepwise Cox multivariate analysis revealed that elevated cTnT (hazard ratio, 6.58; P = 0.000001) and smoking (hazard ratio, 2.24; P = 0.04) were independent predictors of events.The present findings indicate that cTnT is a novel and useful predictor of future cardiovascular or cerebrovascular events in hypertensive patients.     

Risk stratification using a combination of cardiac troponin T and brain natriuretic peptide in patients hospitalized for worsening chronic heart failure

We prospectively evaluated whether the combination of admission measurements of a marker for myocardial cell injury and a marker for left ventricular overload would effectively risk stratify patients with acutely decompensated heart failure. We measured serum concentrations of cardiac troponin T (cTnT) using a second-generation assay, as well as serum cardiac troponin I (cTnI) and plasma atrial and brain natriuretic peptide (BNP) concentrations on admission in 98 consecutive patients hospitalized for worsening chronic heart failure (mean age 69 years; 5 patients were in New York Heart Association functional class II, 35 were in class III, and 58 patients were in class IV). During a mean follow-up period of 451 days, there were 37 cardiac events, including 21 cardiac deaths (14 in-hospital deaths) and 16 readmissions for worsening heart failure. In a stepwise Cox regression analysis, including these biochemical markers, age, sex, functional class, and left ventricular ejection fraction, cTnT, and BNP were found to be significantly independent predictors of both cardiac death (p <0.05) and cardiac events (p <0.01). A cTnT >0.033 microg/L and/or a BNP >440 pg/ml on admission was correlated with an incremental increase in in-hospital cardiac mortality, overall cardiac mortality, and cardiac event rate. Kaplan-Meier analysis revealed that this combination could reliably stratify the patients into low-, intermediate-, and high-risk groups for cardiac events. Measuring the combination of admission concentrations of cTnT and BNP may be a highly effective means of risk stratification of patients hospitalized for worsening chronic heart failure.     

The significance of elevated troponin T in patients with nondialysis-dependent renal insufficiency: a validation with coronary angiography

BACKGROUND: Patients with elevated troponin are at high risk of adverse outcomes, future cardiac events, and are more likely to have hemodynamically significant coronary artery stenoses. Elevated troponin T (cTnT) in patients with poor renal function portends a poor prognosis; however, findings of significant coronary artery disease (CAD) by coronary angiography have not been demonstrated in patients with poor renal function and elevated cTnT. HYPOTHESIS: The purpose of this study was to correlate the angiographic findings of patients with elevated cTnT with respect to renal function in patients with nondialysis-dependent renal insufficiency. METHODS: We retrospectively identified 342 patients with elevated cTnT who underwent coronary angiography in the setting of acute coronary syndrome. Patients were divided into poor (< 40 ml/min) and normal (> 40 ml/min) renal function by measuring their glomerular filtration rate. Our primary outcome was CAD stenosis, defined as epicardial stenosis > or = 70%. Secondary outcomes were rates of contrast nephropathy, initiation of hemodialysis, revascularization, length of stay (LOS), and in-hospital mortality. RESULTS: There was no significant difference in the prevalence of CAD between patients who had positive cTnT with poor renal function versus patients with positive cTnT and normal renal function (87.1 vs. 89.7%, p = 0.54). This finding persisted after stratifying by age. Patients with impaired renal function had a higher mortality, longer LOS, and a higher rate contrast nephropathy requiring hemodialysis. CONCLUSION: The association between elevated cTnT and significant CAD stenosis does not vary with renal function.     

Persistently increased serum concentrations of cardiac troponin in patients with acutely decompensated heart failure are predictive of adverse outcomes.

BACKGROUND: Persistently increased serum concentrations of cardiac troponin (cTn) are a prognostic marker in patients suffering from chronic congestive heart failure (CHF), but the significance in acute cardiac decompensation is unclear. METHODS AND RESULTS: Serial blood samples were collected from 52 patients presenting with acute cardiac decompensation in the absence of an acute coronary event. Serial serum concentrations of cTnI, creatine kinase (CK)-MB, and brain natriuretic peptide (BNP) were measured by rapid assay. BNP and CK-MB steadily decreased from 902+/-529 pg/ml and 2.3+/-1.6 ng/ml at baseline to 453+/-427 pg/ml and 1.2+/-1.6 ng/ml on day 7, respectively, (p<0.0001 for both comparisons). In contrast, cTnI did not decrease significantly and, in 17 patients (35%), increased from 0.063+/-0.047 ng/ml at baseline to 0.167+/-0.181 ng/ml on day 1 (p<0.05). By single variable regression analysis, systolic blood pressure (SBP), use of inotropes or inodilators, vasodilators, and an initially elevated cTnI were predictors of elevated cTnI on day 1. By multiple variable analysis, an elevated SBP (as a mitigating factor) (odds ratios (OR) 0.12; 95% confidence intervals (CI): 0.02-0.76; p=0.0248), and high baseline cTnI (OR 13.85; 95%CI: 1.97-97.54; p=0.0083) were significant predictors of an elevated cTnI on day 1. Patients with elevated cTnI on day 1 had higher rates of worsening CHF and death from CHF than patients without such an increase (p<0.05). CONCLUSIONS: Persistently increased serum concentrations of cTn in patients with acutely decompensated heart failure are predictive of adverse outcomes.     

Elevated Cardiac Troponin T in Patients With Skeletal Myopathies

Background

Cardiac troponins are often elevated in patients with skeletal muscle disease who have no evidence of cardiac disease.

Clinical performance of three cardiac troponin assays in patients with unstable coronary artery disease (a FRISC II substudy)

The assay of cardiac-specific troponins (cTroponins) is a sensitive and specific means to diagnose myocardial injury. Several assays for the measurement of cardiac-specific troponin I (cTnI), but only 1 for the assay of cardiac specific troponin T (cTnT), are commercially available. The aim of this study was to compare 3 of these assays (i.e., Access AccuTnI [cTnI], AxSym [cTnI], and Elecsys 3(rd) generation [cTnI]) and their clinical performances in a group of patients (n = 1,763) with unstable coronary artery disease (Fragmin and fast Revascularisation during InStability in Coronary artery disease [FRISC II] trial). Clinical events after 1-year follow-up, such as death and death and/or acute myocardial infarction, were recorded and the effects of invasive or noninvasive treatment evaluated in relation to cTroponin levels. Overall the 2 cTnI methods showed good correlation (r(s) = 0.96), whereas correlations to the cTnT assay were somewhat lower (r(s) = 0.93). Patients with nonelevated levels, as measured with any of the 3 biomarkers, had a significantly better prognosis than patients with elevated levels (p <0.001). A cohort of 10% to 12.4% of patients with a poor prognosis was identified only by the Access AccuTnI assay. Invasive treatment reduced clinical events only in the group of patients with elevated cTroponin levels. We conclude that stratification of patients with unstable coronary artery disease by means of cTroponin measurements is important in clinical management. It is also apparent that assays with superior sensitivity, such as the Access AccuTnI, identify more patients with poor prognosis who are candidates for early invasive procedures.     

Cardiac troponin T in acute coronary syndrome with renal insufficiency

Cardiac troponin levels are frequently elevated in patients with chronic renal failure, hence diagnosis of myocardial necrosis is difficult. The prevalence of elevated serum troponin T was determined and its diagnostic value in acute coronary syndrome was assessed in patients with chronic renal insufficiency. A retrospective cross-sectional analysis was performed in 227 patients with chronic renal insufficiency and a diagnosis of unstable angina, non-ST or ST-segment elevation myocardial infarction. All patients had baseline serum troponin T levels measured at previous visits; the baseline troponin T level was raised in 53.3%. Cardiac troponin T levels did not correlate with creatinine levels, and were not affected by dialysis. Mortality after an acute coronary event was high (46.3%). Because of the elevated baseline cardiac troponin T levels, detection of acute coronary syndrome in patients with chronic renal failure requires evaluation of serial cardiac enzyme measurements and serial 12-lead electrocardiograms. Early and definitive cardiac interventions may contribute towards decreasing the mortality rate in this group of patients.     

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.     

Temporal pattern of cardiac troponin I after thoracotomy and lung surgery

BACKGROUND: Several studies have shown that patients with perioperative myocardial infarction (MI) are at higher risk for subsequent cardiac events and the identification of these patients is important. However, the diagnosis of perioperative MI can be difficult in many cases. The cardiac troponins are biomarkers with high cardiospecificity, and the aim of this study was to assess cTnI and cTnT among other cardiac biomarkers after thoracotomy and lung surgery. METHODS: 24 consecutive patients were included in the final analysis. Venous blood samples were drawn prior to the procedure, 1-3, 4-6, 16-18 and 30-32 h after surgery. Thoracotomy was performed as a standard posterolateral incision on the left or right side under general anesthesia. RESULTS: Both cTnI and cTnT were completely unaffected by the thoracotomy and the lung surgery. Furthermore, no single value of the troponins was above the 99th percentile at any time. In contrast, CK-MB was elevated in nearly half the patients, although the mean values complied well with the reference limit. CK and myoglobin were both considerably elevated and did not discriminate between acute myocardial infarction and release of the markers due to extracardiac injury. CONCLUSIONS: Only the troponins were unaffected by extracardiac surgery and were, thus, reliable markers of myocardial injury in patients who underwent thoracotomy and lung surgery. If the troponins are unavailable, CK-MB mass combined with the CK-MB/CK percentage should be preferred.