Cardiac troponins in renal insufficiency: review and clinical implications

Patients with renal insufficiency may have increased serum troponins even in the absence of clinically suspected acute myocardial ischemia. While cardiovascular disease is the most common cause of death in patients with renal failure, we are just beginning to understand the clinical meaning of serum troponin elevations. Serum troponin T is increased more frequently than troponin I in patients with renal failure, leading clinicians to question its specificity for the diagnosis of myocardial infarction. Many large-scale trials demonstrating the utility of serum troponins in predicting adverse events and in guiding therapy and intervention in acute coronary syndromes have excluded patients with renal failure. Despite persistent uncertainty about the mechanism of elevated serum troponins in patients with reduced renal function, data from smaller groups of renal failure patients have suggested that troponin elevations are associated with added risk, including an increase in mortality. It is possible that increases in serum troponin from baseline in patients with renal insufficiency admitted to hospital with acute coronary syndrome may signify myocardial necrosis. Further studies are needed to clarify this hypothesis.     

Non-acute myocardial infarction-related causes of elevated high-sensitive troponin T in the emergency room: a cross-sectional analysis

To systematically investigate putative causes of non-coronary high-sensitive troponin elevations in patients presenting to a tertiary care emergency department. In this cross-sectional analysis, patients who received serial measurements of high-sensitive troponin T between 1 August 2010 and 31 October 2012 at the Department of Emergency Medicine were included. The following putative causes were considered to be associated with non-acute coronary syndrome-related increases in high-sensitive troponin T: acute pulmonary embolism, renal insufficiency, aortic dissection, heart failure, peri-/myocarditis, strenuous exercise, rhabdomyolysis, cardiotoxic chemotherapy, high-frequency ablation therapy, defibrillator shocks, cardiac infiltrative disorders (e.g., amyloidosis), chest trauma, sepsis, shock, exacerbation of chronic obstructive pulmonary disease, and diabetic ketoacidosis. During the study period a total of 1,573 patients received serial measurements of high-sensitive troponin T. Of these, 175 patients were found to have acute coronary syndrome leaving 1,398 patients for inclusion in the study. In 222 (30 %) of patients, no putative cause described in the literature could be attributed to the elevation in high-sensitive troponin T observed. The most commonly encountered mechanism underlying the troponin T elevation was renal insufficiency that was present in 286 patients (57 %), followed by cerebral ischemia in 95 patients (19 %), trauma in 75 patients (15 %) and heart failure in 41 patients (8 %). Non-acute coronary syndrome-associated elevation of high-sensitive troponin T levels is commonly observed in the emergency department. Renal insufficiency and acute cerebral events are the most common conditions associated with high-sensitive troponin T elevation.     

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.     

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.     

New features of troponin testing in different clinical settings

Abstract. Omland T. (Institute of Clinical Medicine, University of Oslo, Oslo and Division of Medicine, Akershus University Hospital, Lørenskog, Norway) New features of troponin testing in different clinical settings (Review). J Intern Med 2010; 268 : 207–217. Cardiac troponin levels are routinely measured for diagnosing acute myocardial infarction. Cardiac troponin measurements also provide information concerning prognosis and the effect of early intervention in patients with acute coronary syndromes. The recent development of highly sensitive cardiac troponin assays permits detection of very low circulating levels. Use of sensitive troponin assays improves overall diagnostic accuracy in patients with suspected acute coronary syndromes, and these assays provide strong prognostic information in stable coronary artery disease and chronic heart failure. However, increased sensitivity comes with a cost of decreased specificity, and serial testing, as well as clinical context and judgment, is likely to become increasingly important in the interpretation of troponin assay results.     

Outcomes of hospitalized patients with non-acute coronary syndrome and elevated cardiac troponin level

Objective

Cardiac troponin levels help risk-stratify patients presenting with an acute coronary syndrome. Although cardiac troponin levels may be elevated in patients presenting with non-acute coronary syndrome conditions, specific diagnoses and long-term outcomes within that cohort are unclear.

Methods

By using the Veterans Affairs centralized databases, we identified all hospitalized patients in 2006 who had a troponin assay obtained during their initial reference hospitalization. On the basis of the diagnostic codes of the International Classification of Diseases, 9th Revision, primary diagnoses were categorized as acute coronary syndrome or non-acute coronary syndrome conditions.

Results

Of a total of 21,668 patients with an elevated troponin level who were discharged from the hospital, 12,400 (57.2%) had a non-acute coronary syndrome condition. Among that cohort, the most common diagnostic category involved the cardiovascular system, and congestive heart failure (N = 1661) and chronic coronary artery disease (N = 1648) accounted for the major classifications. At 1 year after hospital discharge, mortality in patients with a non-acute coronary syndrome condition was 22.8% and was higher than in the acute coronary syndrome cohort (odds ratio 1.39; 95% confidence interval, 1.30-1.49). Despite the high prevalence of cardiovascular diseases in patients with a non-acute coronary syndrome diagnosis, use of cardiac imaging within 90 days of hospitalization was low compared with that in patients with acute coronary syndrome (odds ratio 0.25; 95% confidence interval, 0.23-0.27).

Conclusions

Hospitalized patients with an elevated troponin level more often have a primary diagnosis that is not an acute coronary syndrome. Their long-term survival is poor and justifies novel diagnostic or therapeutic strategy-based studies to target the highest risk subsets before hospital discharge.     

The role of cardiac troponin t and other new biochemical markers in evaluation and risk stratification of patients with acute chest pain syndromes

Background and hypothesis: Increased serum creatinine kinase (CK) and CK-MB enzyme levels have been used for years to detect myocardial infarction (MI). However, serum myoglobin and CK-MB mass or protein levels may indicate MI earlier; cardiac troponin T is the most specific marker of myocardial injury and it can detect even minor myocardial necrosis. The diagnostic and prognostic utility of the traditional and new markers of cardiac injury in the emergency evaluation of patients with acute chest pain syndromes were therefore compared. Methods: One hundred and fifteen consecutive patients with an acute coronary syndrome, and 64 controls recruited during the same period, were examined. The time elapsed from onset of symptoms to blood collection was recorded. Cardiac markers were measured in specimens collected upon arrival (0 h), and 2 and 5–9 h, and later in cases of longer observation. The major cardiac events occurring up to 40 months after the index examination were recorded. Results: cTnT levels provided unique information: they were the most specific indicators of myocardial damage and identified unstable angina patients at high risk of future major events. Up to 6 h after the onset of chest pain, the new markers were elevated more frequently than the traditional ones and permitted earlier MI recognition. The worst prognosis (nonfatal myocardial infarction or death) was noted in subjects with chest pain at rest within 48 h before the index examination and elevated cTnT levels. Conclusions: The new markers, particularly cardiac troponin T, offer considerable advantages and they should be more widely used in the diagnosis and risk stratification of acute coronary syndromes.     

Elevated troponin level is not synonymous with myocardial infarction

BACKGROUND: Elevated troponin I in the absence of angiographically visible coronary lesions is seen in up to 10-15% of those undergoing angiography for suspected coronary artery disease. This study aims to elucidate the etiology of elevated cardiac troponin I in patients with normal coronary arteries on angiography. METHODS: We identified 1551 (8.6%) patients with normal coronary arteries from our catheterization database of 17,950 patients from Jan 2000 to Jun 2004. Elevated troponin I levels were found in 217 (14%) of 1551 patients with normal coronary arteries. Of these 217 patients, 73 surgical patients were excluded, and the remaining 144 patients formed the study population. The study population was compared with age and gender matched patients with myocardial infarction and coronary artery disease (Group II). RESULTS: The patients with elevated cardiac troponin I (cTnI) with normal coronary arteries had significantly lower prevalence of atherosclerotic risk factors and significantly higher left ventricular ejection fractions. The cTnI in patients with normal coronary arteries was elevated due to a number of causes including tachycardia, myocarditis, pericarditis, severe aortic stenosis, gastrointestinal bleeding, sepsis, left ventricular hypertrophy, severe congestive heart failure, cerebrovascular accident, electrical trauma, myocardial contusion, hypertensive emergency, myocardial bridging, pulmonary embolism, diabetic ketoacidosis, chronic obstructive pulmonary disease exacerbation and coronary spasm. CONCLUSIONS: Cardiac troponin I could be elevated in a number of conditions, apart from acute myocardial infarction, and could reflect myonecrosis. Acute myocardial infarction is a clinical diagnosis as the laboratory is an aide to, not a replacement for, informed decision making.     

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.     

Troponins in acute coronary syndromes

Cardiac troponins have replaced creatine kinase-MB as the preferred biomarker for establishing the diagnosis of myocardial infarction (MI). Expert recommendations set the diagnostic decision-limit for each assay at the 99th percentile of troponin levels in an apparently healthy reference population, which due to a lack of standardization, will vary depending upon the manufacturer. Among patients presenting with an acute coronary syndrome (ACS), even low-level elevations of cardiac troponin T or I correlate with higher risk of death and recurrent ischemic events compared to patients with levels of troponin below the decision limit. Renal failure does not appear to diminish the prognostic value of troponins among patients with a high clinical probability of ACS. Moreover, patients with elevated levels of troponin derive the most benefit from more intense medical therapy with antithrombin and antiplatelet medications, as well as an early invasive management strategy. Whereas cardiac troponins are extremely specific for myocardial necrosis, they do not discriminate between ischemic and non-ischemic etiologies of myocardial injury. Clinicians must, therefore, determine whether a patient's presenting symptoms are consistent with ACS. Combining troponin with other cardiac biomarkers may offer complimentary information on the underlying pathobiology and prognosis in an individual patient. Future generations of troponin assays may detect specific posttranslational modifications of troponins that may increase the analytic sensitivity for myocardial damage and offer insight into the timing and mechanism of myocardial injury.     

Cardiac troponin I in systemic diseases. A possible role for myocardial strain.

Cardiac troponin I levels are frequently above normal values in several disease states in which myocardial necrosis is not a prominent aspect, particularly in pulmonary embolism, heart failure, liver cirrhosis, septic shock, renal failure and arterial hypertension. Sub-clinical myocardial necrosis has been postulated to be the cause of the phenomenon. Studies performed so far have not included pathological data to confirm this hypothesis. Increased troponin I plasma levels may be the result of myocardial strain, especially the type of strain that accompanies some forms of cardiac dilatation or hypertrophy. Troponin I may act as a marker of myocardial strain, either acute (in pulmonary embolism, septic shock and acute heart failure) or chronic (in chronic cardiac, renal and hepatic failure, as well as in arterial hypertension). The apparent paradox of elevated levels of troponin I without elevated levels of creatine kinase in several disease states might be solved if troponin I could be released from myocardial cells without the disruption of myocardial cell plasma membranes. Precise pathological studies are needed to elucidate whether increased troponin I with normal CK is associated with myocyte death, and, if so, with necrosis or with apoptosis.     

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.     

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.     

A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction

A 71-year-old man presented with left upper quadrant abdominal pain. Serial electrocardiograms (ECGs) demonstrated an evolving left bundle branch block, a sign of acute myocardial infarction (AMI). However, a coronary angiogram demonstrated minimal coronary artery disease, and serum troponin T was undetectable in serial serum measurements. Later, serum pancreatic enzyme levels were elevated and a computed tomography scan of the abdomen was consistent with pancreatitis. In patients presenting with acute pancreatitis and ECG changes suggesting AMI, measurement of serum troponin T concentrations can aid in differentiating ECG changes driven by acute pancreatitis from those of true myocardial ischemia or infarction.     

Troponins in acute coronary syndromes

Delivering superior clinical specificity and sensitivity for myocardial necrosis, cardiac troponin has replaced creatine kinase-MB as the preferred biomarker for establishing the diagnosis of myocardial infarction. On the basis of expert recommendations, present convention sets the diagnostic decision-limit for each assay at the 99th percentile of troponin levels in an apparently healthy reference population. Owing to a lack of standardization between different assays, this level, corresponding to the 99th percentile, will vary depending upon the manufacturer. Among patients presenting with an acute coronary syndrome (ACS), even low-level elevations of cardiac troponin T or I are associated with higher risk of death and recurrent ischemic events compared with patients with a troponin level below the appropriate decision limit. Renal failure does not appear to diminish the prognostic value of troponins among patients with a high clinical probability of ACS. In addition, patients with elevated levels of troponin appear to gain the most benefit from more aggressive medical therapy with antithrombin and antiplatelet medications as well as an early invasive management strategy. Cardiac troponins offer extremely high tissue specificity but do not discriminate between ischemic and nonischemic mechanisms of myocardial injury; thus, presently the clinician must assess whether a patient's presenting symptoms are consistent with ACS. It is possible that future generations of troponin assays will detect specific post-translational modifications of troponins that may increase the analytic sensitivity for myocardial damage and offer insight into the timing and mechanism of myocardial injury.     

Cardiovascular outcome in hospitalized patients with minimal troponin I elevation and normal creatine phosphokinase

BACKGROUND: Among patients with acute coronary syndrome, elevated cardiac troponin and creatine phosphokinase MB fraction levels have both prognostic and diagnostic values. However, in hospitalized patients, cardiac biomarkers are measured in a variety of clinical situations including but not limited to acute coronary syndrome. Moreover, these patients may have elevated troponin levels with no increase in creatine phosphokinase MB fraction levels. OBJECTIVE: To evaluate the cardiovascular outcome of acutely ill, hospitalized patients with minimal troponin I increase with normal creatine phosphokinase MB fraction. METHODS: We identified 64 patients retrospectively from our database with minimal troponin I increase and normal creatine phosphokinase MB fraction hospitalized between November 1998 and April 2000. Discharged patients were questioned about re-hospitalization for myocardial infarction, unstable coronary syndrome, congestive heart failure and percutaneous coronary intervention by means of a structured questionnaire. For those patients who died during hospitalization, data were collected from hospital records. For patients who died at home or at a different institution, a surviving relative completed the questionnaire. Primary outcomes were death, myocardial infarction and the need for revascularization or re-hospitalization. RESULTS: Composite endpoint of death, myocardial infarction, percutaneous coronary intervention or coronary artery bypass grafting and re-hospitalization for cardiac cause occurred in 35.95% of patients within 1 year. CONCLUSIONS: There is a significant composite event rate of death, myocardial infarction or re-hospitalization for cardiac causes in acutely ill, hospitalized patients with normal creatine phosphokinase MB fraction and minimally elevated troponin I, regardless of the cause for hospitalization.     

High-sensitive cardiac troponin T

Cardiac troponin is the preferred biomarker for the diagnosis of acute myocardial infarction (AMI). The recent development of a high-sensitive cardiac troponin T (hs-cTnT) assay permits detection of very low levels of cTnT. Using the hs-cTnT assay improves the overall diagnostic accuracy in patients with suspected AMI, while a negative result also has a high negative predictive value. The gain in sensitivity may be particularly important in patients with a short duration from symptom onset to admission. Measurement of cardiac troponin T with the hs-cTnT assay may provide strong prognostic information in patients with acute coronary syndromes, stable coronary artery disease, heart failure and even in the general population; however, increased sensitivity comes at a cost of decreased specificity. Serial testing, as well as clinical context and co-existing diseases, are likely to become increasingly important for the interpretation of hs-cTnT assay results.     

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.     

Prevalence,Determinants, and Clinical Associations of High-Sensitivity Cardiac Troponin in Patients Attending Emergency Departments

Background

High-sensitivity cardiac troponin assays may improve the diagnosis of myocardial infarction but increase the detection of elevated cardiac troponin in patients without acute coronary syndrome.