Use Of Cardiac Troponin Research Articles

How to use high-sensitivity cardiac troponins in acute cardiac care

Recommendations for the use of cardiac troponin (cTn) measurement in acute cardiac care have recently been published.1 Subsequently, a high-sensitivity (hs) cTn T assay was introduced into routine clinical practice.2 This assay, as others, called highly sensitive, permits measurement of cTn concentrations in significant numbers of apparently illness-free individuals. These assays can measure cTn in the single digit range of nanograms per litre (=picograms per millilitre) and some research assays even allow detection of concentrations 10% at the 99th percentile URL limiting that ability.5–7 However, the less precise cTn assays do not cause clinically relevant false-positive diagnosis of acute myocardial infarction (AMI) and a CV <20% at the 99th percentile URL is still considered acceptable.8 We believe that hs-cTn assays, if used appropriately, will improve clinical care. We propose criteria for the clinical interpretation of test results based on the limited evidence available at this time. ‘Sensitive’ and ‘high-sensitive’ are terms often used by manufacturers to describe their assays for marketing purposes. In some cases, it reflects higher sensitivity than former assays developed by the same company, and in other situations it reflects a higher sensitivity than most assays on the market. Although there is still no consensus regarding when the terms ‘sensitive’ and ‘high-sensitive’ should be applied, we advocate that cTn assays should be labelled ‘high-sensitive’ only if they fulfil the analytical criteria suggested by …

The significance of second generation cardiac troponin I in early screening of hypoxic-ischemic encephalopathy after perinatal asphyxia

In the last few years the use of cardiac troponin I and T, as diagnostic and prognostic factors of ischemic myocardial injury both in adult and neonatal medicine has been of great interest. The objective of our research was to investigate the significance of cardiac troponin I (cTnl) as an early indicator of the presence and severity of hypoxic-ischemic encephalopathy (HIE) in newborns. We analyzed 55 term newborns with HIE diagnosed based on clinical findings and ultrasonographic examination of the central nervous system. Serum concentration of cTnl-ultra was determined by immunoenzyme method during the first 24-48 hours after birth, and the obtained findings were compared with the values of identical parameter in 36 healthy term newborns. During the first 24-48 hrs after birth, serum concentration of cTnI-ultra was significantly higher (p < 0.0005) in term newborns with HIE (0.135 +/- 0.207 microg/l) and median (0.07, 0.01-006 microg/l) in comparison to control group (0.0183 +/- 0.026 microg/l and median 0.01 (0.01-0.01 microg/l), with the cTnl-ultra level rising proportionally to the clinical HIE stages. The increase of cTnI-ultra of > 0.12 microg/l indicated the development of significant cerebral damage with the sensitivity of 75% and specificity of 72.2%, while the cTnI-ultra level of > 0.13 microg/l was a significant mortality predictor with sensitivity of 76.9% and specificity of 73.8%. The second generation cardiac troponin I assay highly correlates with clinical and ultrasonographic findings in neonates with HIE, so that it can be used as a significant diagnostic and prognostic indicator of this pathological condition.

Trastuzumab-Related Cardiac Dysfunction

The use of trastuzumab in the adjuvant and metastatic treatment of breast cancer is associated with both symptomatic and asymptomatic cardiotoxicity. The long-term significance of these events, isolating known cardiotoxic effects of anthracyclines from those of trastuzumab, and the appropriateness of referring to trastuzumab-related cardiotoxicity as reversible rather than responsive to trastuzumab withdrawal and heart failure medical therapy, are issues that continue to be debated. This article provides an overview of the available cardiac safety data from the major trastuzumab clinical trials in breast cancer, highlighting areas of ongoing controversy. Important recent data documenting the occurrence and prognostic use of cardiac troponin I elevations among patients treated with trastuzumab are placed into context with the mechanistic insight these data provide and the implications for clinical practice today.

High Sensitivity Cardiac Troponins: a Curse or a Blessing?

The use of cardiac troponins (cTn) in lieu of creatine kinase to diagnose myocardial infarction (MI) has allowed us to detect even the smallest myocardial damage. Recently the use of high-sensitivity assays to measure even the tiniest myocardial injuries has led to a substantial increase in the diagnosis of MI. However, the specificity of such tests has been compromised and false positive results are rising. Clinicians should be aware that elevated cTn may be encountered in a variety of conditions of non-thrombotic cardiac damage, but also in a plethora of non-coronary diseases and laboratory interferences. These caveats are herein overviewed and an algorithm is proposed of a step-wise approach to using cTn measurement to triage and manage patients with suspected acute coronary syndromes.

Veterinary and toxicological applications for the detection of cardiac injury using cardiac troponin

The use of cardiac troponin (cTn), the 'gold-standard' biomarker of myocardial injury in humans, is growing in veterinary medicine and in animal safety studies, although there are differences in its application in animals. In this study six new assays for the marker were assessed in 619 animals of six different species (dog, cat, horse, cattle, rat and rabbit), in clinical and drug-safety studies. Healthy animals and clinical cases without cardiac disease served as controls. Several of the tested assays had poor analytic or diagnostic sensitivity and only one test was effective in all species and in all models of cardiac injury. This assay had the highest sensitivity and widest dynamic range, and identified cardiac injury due to anaemia, pancreatitis, uncontrolled Addison's and Cushing's disease, old age, renal disease, severe colic, lymphoma and neoplasia. Detection of the cTnI and cTnT forms correlated with loss of cardiac function in toxicity studies in rodents and rabbit. Increased serum cTnI was not found to correlate with disease aetiology or pathogenesis, but was effective in detecting, monitoring and quantifying ongoing cardiac injury. Cardiac injury, as demonstrated by elevated cTnI in blood, appears to be a common sequel to a wide variety of both primarily cardiac disease and of other diseases that do not primarily involve the cardiovascular system.

Elevated Cardiac Troponin T (cTnT) in the Extreme Elderly Group of Patients: The Short and Long Term Prognostic Implications

Background: There is a wide use of cardiac troponin T (cTnT) for various hospital presentations in the elderly population. The short and long term prognostic implications of an elevated cTnT level, in the extremeelderly, have not been clearly defined. Methods: We analysed 229 consecutive patients ≥80 years of age (mean age 85± 4 years; 62% females) admitted to our hospital, who had cTnT measured, for both non-cardiac and cardiac presentations. The primary study endpoint was all causemortality in hospital and long term follow up. Results: The mean follow up duration was 2 years 11 months. The provisional admission diagnosis (cTnT negative/cTnT positive groups: 61% vs. 46% non-cardiac; 24% vs. 26% acute coronary syndrome; 25% vs. 28% other cardiac diagnosis). Kaplan–Meier curves showed a significantlyhigher all causemortality in the cTnTpositive group dysfunction and heart failure. This study aimed to investigatewhether theendogenousactive levels ofMMP-1, -2, -3 and -9 or tissue inhibitor of metalloproteinases-1 (TIMP1) were altered in the circulation of patients with diastolic dysfunction (DD) in the setting of coronary artery disease (CAD). Methods and results: We studied 153 patients with angiographically proven coronary artery disease and clinically symptom free of angina. Demographic and angiographic characteristics were collected. Plasma samples were analysed for MMPs (active forms of MMP-1, -2, -3, and -9, and the total form of MMP-9) as well as TIMP-1 using ELISA-based isoform sensitive assays. Doppler-echocardiographic assessment of diastolic filling was undertaken with measurements of maximal early (E) and late (A) transmitral velocities in diastole, E/A ratio, E-wave deceleration time and isovolumic relaxation time. Active MMP-9 level was higher in patients with more severe phases of diastolic dysfunction [normal (n= 62): median 1.41 ng/ml; mild (n= 49) 1.52 ng/ml; mildmoderate (n= 23) 2.13 ng/ml; moderate (n= 13) 2.26 ng/ml; severe (n= 6) 2.48 ng/ml; p= 0.007 for trend]. Elevated level of active MMP-9 had an adjusted odds ratios of 6.1 (95% CI: 1.7–21.2, p= 0.005) and 9.1 (95% CI: 2.2-37.2, p= 0.003) for associationwithmild–moderateDDandmoderate and severe DD, respectively. Conclusion: Elevated active MMP-9 level is associated

MicroRNAs as Novel Myocardial Biomarkers

The search for new biomarkers of cardiovascular disease remains a large and growing enterprise. Biomarkers are used to identify the risk, presence, and/or severity of disease; to guide diagnostic and therapeutic interventions; and to provide clues to disease mechanisms and pathophysiological distinctions within clinically similar populations. Among cardiovascular biomarkers, those used for identifying the presence or severity of myocardial injury have the most extensive history. Beginning with the first report 55 years ago that circulating transaminases are increased in acute myocardial infarction (1), the search for new and better biomarkers of myocardial injury has continuously evolved. As recently reviewed (2), cardiac troponin has emerged after decades of clinical and laboratory investigation as a highly diagnostically sensitive and specific biomarker of myocardial injury, with a currently indispensable role in the accurate and timely diagnosis of patients with suspected acute coronary syndromes (ACSs).1 Central to this preeminence is the tissue specificity of cardiac troponin isoforms, increases in assay sensitivity, and an extensive body of evidence validating the diagnostic, prognostic, and therapy-guiding utility of cardiac troponins in diverse clinical settings. Because the benefits of ACS treatments are favorably influenced by the speed with which they are applied, the ideal myocardial injury biomarker must also permit rapid measurement; cardiac troponin assays have also proved satisfactory in this regard. Despite the established strengths of cardiac troponins for prompt and reliable detection of myocardial injury, the ability to reliably detect ischemia in the absence of myocyte necrosis and the ability to distinguish alternative causes and mechanisms of myocyte damage (inflammation, oxidative stress, apoptosis) represent unmet needs and opportunities for new biomarkers, which have been highlighted in recent reviews (2)(3). Resistance to inaccuracy caused by confounding factors such as renal failure is another favorable attribute that is not ideally achieved with cardiac troponin assays. …

Cardiac troponin I as a marker for severity and prognosis of cardiac disease in dogs

The use of cardiac troponin I (cTnI) to assess the severity of disease and prognosis in 120 dogs presented for cardiac evaluation was analysed. cTnI concentrations were measured using a commercially available assay. Dogs were placed into three groups: group 1, cTnI0.15ng/mL; group 2, cTnI 0.151-1.0ng/mL; group 3, cTnI>1.01ng/mL. Dogs in group 1 were significantly younger (P<0.0001) and had no or stable cardiac diseases and longest survival times, whereas those in groups 2 and 3 had severe cardiac diseases and significantly reduced survival times (P<0.0001). Thirty dogs with initially increased cTnI concentrations had a repeat assay less than 2months later with significant reductions in cTnI concentrations (P=0.005). Initial cTnI concentrations could not differentiate dogs that survived in group 3 from those that did not. However, dogs that survived showed significant cTnI reductions (P=0.015) in the repeated assay in contrast to the dogs that died (P=0.22). It was concluded that cTnI is useful in assessing the prognosis and severity of cardiac diseases in dogs, and progression and response to treatment can be assessed by repeat sampling. cTnI concentrations >1.0ng/mL and persistent increases in cTnI concentrations are indicators of a poor prognosis in dogs with cardiac disease.

Prediction of Hemodynamically Significant Coronary Artery Disease Using Troponin I in Hemodialysis Patients Presenting with Chest Pain: A Case-Control Study

Objectives: Controversy exists regarding utility of cardiac troponin I (cTnI) in predicting significant coronary artery disease (CAD) in hemodialysis (HD) patients with chest pain and no acute ischemia on electrocardiogram (non-ST segment elevation myocardial infarction, non-STEMI). We sought to determine if cTnI elevation predicts significant CAD (>70% stenosis) in these patients. Methods: Ninety patients with non-STEMI referred for cardiac catheterization were included, divided equally into HD and non-HD groups. Results: Mean age and baseline characteristics were not significantly different between groups, except for left ventricular hypertrophy which was higher in HD patients (56 vs. 27%, p = 0.012). Initial cTnI correlated with obstructive CAD and was stratified into <0.3 and >0.3 ng/ml. By logistic regression, cTnI >0.3 ng/ml was not predictive of CAD in HD patients [odds ratio = 0.87 (95% CI 0.19–4.0), p = 0.8], while non-HD patients had an increased risk of CAD if first cTnI was >0.3 ng/ml [odds ratio = 1.461 (95% CI 1.01–2.11), p = 0.04] as expected. Sensitivity, specificity, negative and positive predictive values of cTnI in predicting obstructive CAD were better in non-HD patients. Conclusion: cTnI in these patients had no predictive value for obstructive CAD. This contrasts with the general population, suggesting a higher index of suspicion for high-grade CAD irrespective of cTnI levels in HD patients.

Diagnostic utility of cardiac troponin I in neonatal hypoxic myocardial injury

目的 评价心肌肌钙蛋白Ⅰ(cTn Ⅰ)对新生儿窒息心肌损害(MCI)的早期诊断价值.方法 采用双抗夹心免疫测定方法检测51例生后窒息并MCI新生儿(MCI组)血清cTn Ⅰ和CK-MB水平,并以57例窒息无MCI(NMCI组)及45例正常新生儿(NC组)作为对照组.结果 NC组cTn Ⅰ水平在生后7 d内无变化,MCI组生后24 h内和1周时cTn Ⅰ水平均显著高于NMCI组和NC组(P＜0.01).MCI组生后24 h内CK-MB水平显著高于NMCI组和NC组(P＜0.01);生后5～7 d 3组CK-MB水平差异无显著性(P＞0.05),且均明显低于生后24 h内水平.cTn Ⅰ诊断新生儿MCI的敏感度为91%,特异度为88%,准确度89%;CK-MB的敏感度为86.3%,特异度为69%,准确度为74%.结论 血清cTn Ⅰ及CK-MB均可用于新生儿窒息MCI的早期诊断,cTn Ⅰ优于CK-MB。

Cardiac troponins and autoimmunity: Their role in the pathogenesis of myocarditis and of heart failure

Despite the widespread use of cardiac troponins as biomarkers for the diagnosis and quantitation of cardiac injury, the effect of troponin release and a possible autoimmune response to the troponins is unknown. Other investigators reported that programmed cell death-1 (PD-1)-receptor deficient mice developed severe cardiomyopathy with autoantibodies to troponin I. We found that immunization of genetically susceptible mice with troponin I but not troponin T induced a robust autoimmune response leading to marked inflammation and fibrosis in the myocardium. At later times, antibodies to cardiac myosin were detected in troponin-immunized mice. The severity of inflammation correlated with expression of chemokines RANTES, MIP-2, IP-10 and MCP-1 in the myocardium. Prior immunization with troponin I increased the severity of experimental infarctions, indicating that an autoimmune response to troponin I aggravates acute cardiac damage. Cardiac inflammation, fibrosis and functional impairment were transferred from immunized to naive recipients by CD4+ T cells, and the cytokine profile suggested both Th2 and Th17 profiles in A/J mice. Finally we identified an 18-mer of troponin I containing an immuno-dominant epitope.

Novel Biomarkers of Cardiovascular Disease: Myeloperoxidase for Acute and/or Chronic Heart Failure?

Cardiac biomarkers continue to play a prominent role in the diagnosis and management of patients who present to the emergency department with symptoms suggestive of acute cardiovascular disease. The use of cardiac troponin was reaffirmed in 2007 by the European Society of Cardiology, American College of Cardiology, American Heart Association, and World Heart Federation as the single most important biomarker for diagnosis of acute myocardial infarction (1). For acute decompensated heart failure (ADHF),1 the American College of Cardiology and American Heart Association have opined that “measurement of B-type natriuretic peptide (BNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of heart failure is uncertain (level of evidence: A)” (2). Despite these advancements, some clinical needs are not met by measurement of troponin and the natriuretic peptides. For acute coronary syndrome, novel biomarkers are needed for the early diagnosis of acute myocardial infarction, e.g., at the time of emergency department presentation. Biomarkers are also needed for risk stratification for future short-term (30 days) adverse cardiac events (death and acute myocardial infarction). For acute heart failure, new laboratory tests are needed to complement B-type natriuretic peptide and N-terminal pro–B-type natriuretic peptide, because these markers are influenced by obesity, renal failure, and pulmonary disease (3). In general, 2 strategies are employed for the discovery of novel biomarkers. The proteomic/metabolomic approach compares tissue and blood samples from diseased patients with similar samples from healthy or nondiseased individuals (4) …

Identification of Cardiac Troponin I Sequence Motifs Leading to Heart Failure by Induction of Myocardial Inflammation and Fibrosis

Despite the widespread use of cardiac troponins for diagnosis of myocyte injury and risk stratification in acute cardiac disorders, little is known about the long-term effects of the released troponins on cardiac function. Recently, we showed that an autoimmune response to cardiac troponin I (cTnI) induces severe inflammation and subsequent fibrosis in the myocardium. This autoimmune disorder predisposes to heart failure and cardiac death in mice. To investigate the role of cTnI-specific T cells, T cells were isolated from splenocytes of mice immunized with murine cTnI (mcTnI). Wild-type mice that received mcTnI-specific T cells showed high mcTnI-specific antibody titers, increased production of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha, severe inflammation and fibrosis in the myocardium, and reduced fractional shortening. To identify the antigenic determinants of troponin I responsible for the observed inflammation, fibrosis, and heart failure, 16 overlapping 16mer to 18mer peptides covering the entire amino acid sequence of mcTnI (211 residues) were synthesized. Only mice immunized with residues 105 to 122 of mcTnI developed significant inflammation and fibrosis in the myocardium, with increased expression of the inflammatory chemokines RANTES, monocyte chemotactic protein-1, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, macrophage inflammatory protein-2, T-cell activation-3, and eotaxin and the chemokine receptors CCR1, CCR2, and CCR5. Mice immunized with the corresponding human cTnI residues 104 to 121 and the mcTnI residues 131 to 148 developed milder disease. Transfer of troponin I-specific T cells can induce inflammation and fibrosis in wild-type mice, which leads to deterioration of contractile function. Furthermore, 2 sequence motifs of cTnI that induce inflammation and fibrosis in the myocardium are characterized.

2008 Usefulness of cardiac troponin T for prediction of microvascular obstruction as determined by contrast-enhanced cardiac magnetic resonance imaging

Methods Eighty-nine consecutive patients with reperfused AMI after PCI were enrolled in the study. cTnT was measured serially at admission and after 24, 48, 72 and 96 hours. Contrast-enhanced cardiac magnetic resonance imaging (CE-MRI) was performed on a 1.5 T scanner 4 ± 1 days after AMI. To evaluate myocardial distribution of hyperenhancement, data were aquired 15 min after bolus injection of 0.2 mmol Gd-DTPA (Magnevist®) using an inversion-recovery three-dimentional turbo-gradient echo technique. Data were evaluated on a regular workstation (Philips Viewforum). MVO was visually defined as hypoenhanced area within hyperenhancement and was manually contoured. All single measurements, peak cTnT and concentration-time integral of cTnT over 96 hours were related to size of myocardial infarction and MVO as determined by CE-MRI. Results CE-MRI was feasible in all patients with excellent image quality. 39% of the patients presented with MVO. cTnTtime concentration kinetics in the presence of MVO differs from cTnT release in the absence of MVO showing a higher peak and a slower release. At single point measurement 24 h-cTnT correlates at least as well with the presence of MVO (p = 0.0015) as peak cTnT (p = 0.0204) and sampling over 96 h (p = 0.0106). Using ROC analysis, at single measurement a cTnT concentration > 2.52 μg/L at 24 hours was the best predictor of MVO (AUC 0.7) with a sensitivity of 67% and a specificity of 85%. Multivariate regression analysis demonstrated that infarct size and cTnT at 24 hours after admission remained independent predictors of MVO after adjustment for duration of ischemia, and spontaneous preinterventional TIMI grade 3 flow. Figures 1 and 2.

Troponins and natriuretic peptides in the monitoring of anthracycline cardiotoxicity

Anthracycline-related cardiotoxicity has a substantial negative impact on long-term survivors of childhood cancer. The detection of cardiotoxicity is currently based on echocardiography or radionuclide angiography. However, as they depict only the final outcome of myocardial injury in terms of reduced heart contractility, heart specific biomarkers of myocardial destruction or dysfunction could be advantageous by allowing for an earlier detection of cardiotoxicity. In the present study, the usefulness of cardiac troponins and natriuretic peptides, the most commonly used biomarkers of myocardial destruction and ventricular dysfunction respectively, to detect and to predict the development of anthracycline cardiotoxicity has been reviewed.

Cardiac troponins

AbstractObjective: To review the use of cardiac troponins as biomarkers for myocardial injury in human and veterinary medicine.Data sources: Data sources included scientific reviews and original research publications.Human data synthesis: Cardiac troponins have been extensively studied in human medicine. Finding an elevated cardiac troponin level carries important diagnostic and prognostic information for humans with cardiovascular disease. Troponin assays are used primarily to diagnose acute myocardial infarction in patients with ischemic symptoms such as chest pain. However, elevated blood levels may be found with any cause of myocardial injury.Veterinary data synthesis: Several studies have shown that cardiac troponins are sensitive and specific for myocardial damage in veterinary patients and may have utility in diagnosis and prognosis for certain disease states. Human assays may be used in most animals due to significant homology in the troponin proteins between species.Conclusions: Cardiac troponins are sensitive and specific markers of myocardial injury although they do not give any information regarding the mechanism of injury. They have redefined how acute myocardial infarction is diagnosed in humans. Their use in the clinical management of veterinary patients is limited at this time. Further prospective studies are warranted.

New Definition of Myocardial Infarction: Impact on Long-term Mortality

Background The use of cardiac troponin allows the identification of additional patients developing myocardial necrosis during an acute coronary syndrome. Novel guidelines of European and American cardiac societies recommend labeling these events as myocardial infarction. Our study evaluated the long-term mortality in the group of patients with non-ST segment elevation myocardial infarction not meeting the older World Health Organization (WHO) criteria (creatine phosphokinase) but additionally identified by the novel definition of myocardial infarction. Methods This cohort study included 1024 consecutive patients with non-ST segment elevation acute coronary syndrome classified into “unstable angina,” myocardial infarction according to the WHO definition (“WHO criteria”), and myocardial infarction additionally identified by the novel definition (“additional criteria”). All patients were treated with an early invasive strategy. The primary end point was all-cause mortality during follow-up of up to 36 months. Results During long-term follow-up (median 16 months, interquartile range 6-29 months), 67 deaths occurred. Kaplan-Meier analysis showed cumulative 3-year mortality rates of 5.6% in patients with “unstable angina,” 9.1% in patients identified by “WHO criteria,” and 17.5% in patients identified by “additional criteria” ( P <.001). Cox regression analysis confirmed the “additional criteria” as a significant predictor of mortality (hazard ratio 3.1; 95% confidence interval, 1.9-5.0; P <.001). Conclusions The new definition of myocardial infarction based on cardiac troponin testing identifies a high-risk group of additional patients with acute coronary syndrome that is, therefore, appropriately classified as myocardial infarction. In fact, long-term mortality in “additional criteria” patients is higher than in “WHO criteria” patients.

The role of cardiac troponin measurements

The use of cardiac troponin as the definitive test for MI has enabled an improved standard of care.

Postmortem cardiac troponin-I levels predict intramyocardial damage at autopsy

Serum cardiac troponin levels are now widely used in the diagnosis of myocardial infarct (MI) and injury in living patients, but their utility in postmortem diagnosis has not been established. We evaluated postmortem cardiac troponin-I (cTnI) levels in serum from 53 hospital patients undergoing autopsy and correlated the levels with anatomic findings at postmortem examination. Among patients with nonischemic cardiac disease, those with intramyocardial disease (e.g., cardiac transplant rejection, intramyocardial tumor) had significantly higher cTnI levels than those with disease confined to the pericardium (e.g., epicardial tumor implants, pericarditis) (p = 0.004). No correlation was found between recent MI and cTnI level. There was also no correlation between cTnI level and the presence of chronic ischemic features, a history of cardiopulmonary resuscitation, or postmortem interval. We conclude that cTnI is detectable in postmortem serum samples and, although its levels did not correlate specifically with ischemia or infarction in our series, its levels appear to correlate significantly with intramyocardial injury. Use of cardiac troponin in the postmortem diagnosis of cardiac disease may be warranted.

Clinical Utility of Cardiac Troponin I in the Diagnosis of Acute Coronary Syndrome in Patients With Renal Failure

To analyze sensitivity and specificity of cardiac troponin I (cTnI) in detecting obstructive coronary artery disease in African American population with renal insufficiency presenting with acute coronary syndrome. Retrospective analysis of 108 patients who underwent coronary angiography over a 3-year period in a single institution. A troponin I level of 0.1 ng/mL or higher was considered abnormal troponin I. Renal insufficiency was defined as creatinine of 1.2 mg/dL or higher. Obstructive coronary artery disease (CAD) was defined as luminal diameter reduction of 70% or more (or total occlusion) in at least 1 coronary artery. Patients were divided into group 1 (renal insufficiency without need for hemodialysis, n = 76, mean age = 65) and group 2 (patients requiring hemodialysis, n = 32, mean age = 60). Access Accu TnI method was used to quantitate cTnI where murine monoclonal antibodies specifically bind to the C-terminal end of cTnI. In group 1, 41 (54%) patients had abnormal troponin of whom 37 (90%) had CAD and 4 (10%) had normal angiogram; 35 (46%) patients had normal troponin, of whom 25 (71%) had CAD and 10 (29%) had normal angiogram yielding a sensitivity of 60% and specificity of 71% (P = 0.003; 95% confidence interval). In group 2, 20 (63%) had abnormal troponin of whom 19 (95%) had CAD and 1(5%) had normal angiogram; 12 (38%) had normal troponin of whom 7 (59%) had CAD and 5 (41%) had normal angiogram yielding a sensitivity of 73% and specificity of 83% (P = 0.06; 95% confidence interval). cTnI has a sensitivity of 60% and specificity of 71% in acute coronary syndrome patients with renal insufficiency. In patients on hemodialysis, troponin I has a sensitivity of 73% and specificity of 83% for detection of obstructive CAD.