Elevated cTnI Levels Research Articles

Cardiac Findings in Asymptomatic Chronic Hemodialysis Patients with Persistently Elevated Cardiac Troponin I Levels

Background. The prevalence and significance of higher than normal cardiac troponin I (cTnI) levels in asymptomatic chronic hemodialysis (HD) patients remains a source of discussion. The aim of the present study was to evaluate the prevalence of higher than normal cTnI levels in asymptomatic HD patients, as determined by the last generation of immunoassay, and to perform further cardiological investigations in those patients with persistently elevated cTnI levels. Methods. All chronic HD patients in our center who had exhibited no symptoms of coronary artery disease (CAD) during the previous four weeks were screened. cTnI levels were determined before dialysis in all patients using the last generation AccuTnI™ assay (UniCel DxI 800, Beckman Coulter). The cTnI levels of those patients with elevated cTnI at the screening evaluation were then measured monthly for six months. We were thus able to identify a group of patients with persistently elevated cTnI levels (> 3 consecutive months) who subsequently underwent cardiac echography and dipyridamole-exercise (D-E) thallium testing. If stress myocardial ischemia was detected, a coronary angiography was then performed. Results. Fifty patients (32 males) were included: mean age 62.8 ± 13.6 years, 20 (40%) with a history of CAD, and 21 (42%) diabetic. At the initial screening, the mean cTnI concentration was 0.05 ± 0.06 μg/L and the cTnI levels were higher than normal (> 0.09 μg/L) in six patients (12%). In the follow-up, the cTnI normalized immediately in two patients but remained persistently elevated (range, 0.10–0.48 μg/L) in four (8%). These four patients (all males, one diabetic) had a mean age of 70.2 ± 6.6 years, and all had heart failure with a history of severe CAD with previous myocardial infarction (n = 4), coronary stenting (n = 3), and/or bypass (n = 2). D-E thallium imaging showed reversible myocardial ischemia in all. The stress ischemia involved one to four cardiac segments and was slight to moderate in three patients and severe in the diabetic patient. A coronary angiogram was performed in all patients, and showed lesions of variable severity: severe three-vessel CAD with severe systolic dysfunction in two patients (including the diabetic), and non-critical/peripheral coronary stenosis in the other two. Conclusions. Among the asymptomatic HD patients in our center, we identified four (8%) with persistently elevated cTnI levels, as determined using the last generation AccuTnI™ assay. All of them had a history of severe CAD with heart failure and exhibited reversible myocardial ischemia upon D-E thallium imaging; coronary angiography revealed coronary lesions of variable severity. Overall, our data indicate that persistent low-grade cTnI elevation occurs in HD patients having longstanding severe cardiac disease, but, from our data, it is difficult to reach a conclusion as to the best clinical approach for this group of patients.

Donor Cardiac Troponin I Levels Do Not Predict Recipient Survival After Cardiac Transplantation

Serum levels of cardiac troponin I (cTnI) are frequently measured in the evaluation of potential heart donors. However, the utility of cTnI levels for predicting recipient outcomes remains controversial. This study was performed to determine whether donor cardiac cTnI levels exceeding 1.0 microg/liter are associated with adverse recipient outcomes. All donors managed by the California Transplant Donor Network between January 2001 and July 2002 with consent for donor evaluation and at least 1 measured cTnI level were included in the study if 1-year recipient mortality data were available. Each study subject was classified as having elevated cTnI if any level exceeded 1.0 microg/liter. Donor variables, recipient risk of 30-day and 1-year mortality, and recipient need for mechanical circulatory support were compared between the 2 groups. A total of 263 potential donors were evaluated, and 98 had elevated cTnI levels. Of these potential donors, 139 were accepted for transplantation. The cTnI levels were normal in 96 and elevated in 43. Most donors (77%) with elevated cTnI levels had levels of less than 10 microg/liter. Donor cardiopulmonary resuscitation was associated with cTnI elevations. Donors with elevated cTnI levels did not require higher doses of inotropic drugs before transplantation and had similar hemodynamic profiles compared with donors with normal cTnI levels. Although there was a trend towards longer post-transplant hospitalization in recipients of grafts from donors with elevated cTnI levels (17 days vs 15 days, p = 0.044), there was no significant difference in the recipient need for mechanical circulatory support or 30-day and 1-year mortality between the 2 groups. In this study, a modestly elevated donor cTnI was not associated with a higher risk of recipient mortality or need for post-transplant mechanical circulatory support. A potential donor heart should not be discarded solely because the troponin level is elevated.

Persistent Cardiac Troponin I Elevation in Stabilized Patients After an Episode of Acute Coronary Syndrome Predicts Long-Term Mortality

In patients with non-ST-elevation acute coronary syndrome, any troponin elevation is associated with an increased risk for cardiovascular events. However, the prevalence and prognostic importance of persistent troponin elevation in stabilized patients after an episode of non-ST-elevation acute coronary syndrome are unknown and were therefore assessed in this study. Cardiac troponin I (cTnI) was measured in 1092 stabilized patients at 6 weeks and 3 and 6 months after enrollment in the FRagmin and Fast Revascularization during InStability in Coronary artery disease (FRISC-II) trial. cTnI was analyzed with the Access AccuTnI assay with the application of different prognostic cutoffs. Outcomes were assessed through 5 years. Elevated cTnI levels >0.01 microg/L were found in 48% of the study patients at 6 weeks, in 36% at 6 months, and in 26% at all 3 measurements. cTnI elevation was associated with increased age and other cardiovascular high-risk features. The lowest tested cTnI cutoff (0.01 microg/L) was prognostically most useful and was independently predictive of mortality (hazard ratio, 2.1 [95% confidence interval, 1.3 to 3.3]; P=0.001) on multivariable analysis adjusted for cardiovascular risk factors and randomization to an invasive versus noninvasive treatment strategy, whereas it was related to myocardial infarction only on univariate analysis. Persistent minor cTnI elevation can be detected frequently in patients stabilized after an episode of non-ST-elevation acute coronary syndrome with the use of a sensitive assay. Elevated cTnI levels >0.01 microg/L predict mortality during long-term follow-up. Our results emphasize the importance of further troponin testing in non-ST-elevation acute coronary syndrome patients after hospital discharge.

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Recently, a high prevalence of small persistent cardiac troponin I (cTnI) elevations has been reported in patients who had been stabilized after a recent episode of acute coronary syndrome (ACS). We now have studied the associations of persistently elevated cTnI levels to cardiac performance, inflammation, coagulation, coronary status, and treatment strategy in these patients.Cardiac troponin I was determined at 6 weeks, 3 months, and 6 months after randomization in 898 stabilized ACS patients from the FRagmin and Fast Revascularization during InStability in Coronary artery disease (FRISC) II trial and using the high-sensitive Access AccuTnI assay (Beckman Coulter, Fullerton, CA). All patients were followed up for at least 5 years. Persistent cTnI elevation >0.01 μg/L at the 3 measurement instances was detected in 233 patients (26%). N-terminal pro-brain natriuretic peptide (NT-proBNP) at 6 months (OR 2.5, 95% CI 2.0-3.1), male sex (OR 2.2, 95% CI 1.4-3.7), and randomization to an early invasive strategy (OR 1.8, 95% CI 1.2-2.7) independently predicted persistently elevated cTnI levels. Persistently cTnI-positive patients in the invasive cohort had significantly lower NT-proBNP levels compared to noninvasively treated patients, indicating that the mechanisms causing cTnI elevation in this group may be prognostically less harmful. No independent associations were found for markers of inflammation or coagulation.Persistent cTnI elevation occurs frequently late after an ACS. The NT-proBNP level at 6 months was the strongest predictor for elevated cTnI levels that thus appear to be predominantly related to impaired left ventricular function.

Postmortem cardiac troponin I and creatine kinase MB levels in the blood and pericardial fluid as markers of myocardial damage in medicolegal autopsy

The present study investigated cardiac troponin I (cTnI) and creatine kinase MB (CK-MB) in the blood and pericardial fluid from medicolegal autopsy cases ( n = 234, within 48 h postmortem) with regard to the cause of death. The cTnI and CK-MB levels in cardiac, peripheral blood and pericardial fluid generally showed a mild and gradual postmortem time-dependent elevation ( r = 0.231–0.449, P < 0.05–0.001). However, postmortem elevation of cTnI was larger for specific causes of death including acute myocardial infarction (AMI), cerebrovascular diseases (CVD), hyperthermia, fatal methamphetamine (MA) abuse and carbon monoxide (CO) intoxication and insignificant for recurrent myocardial infarction (RMI), chronic congestive heart diseases (CHD) and drowning, while that of CK-MB was greater for CO intoxication and insignificant for drowning. Cardiac blood and pericardial cTnI levels were relatively high for AMI, RMI, hyperthermia, MA abuse and CO intoxication, and was low for drowning. Elevated CK-MB level was observed for cardiac blood in asphyxiation and MA abuse cases and for peripheral blood in hyperthermia and MA abuse cases. When the cTnI/CK-MB ratio was estimated, it was independent of postmortem time, and the ratios for cardiac blood and pericardial fluid were significantly higher in cases of AMI, RMI, hyperthermia and CO intoxication but lower in cases of drowning. Elevations of cTnI levels in cardiac blood and pericardial fluid were related to the morphological severity of myocardial damage. These findings suggest that elevated cTnI and CK-MB levels in blood and pericardial fluid are related to ischemic, hypoxic and/or cytotoxic myocardial damage, which are characteristic of the cause of death, although the levels increase after death depending on myocardial damage at the time of death.

Atrial Fibrillation and Plasma Troponin I Elevation After Cardiac Surgery: Relation to Inflammation-Associated Parameters

Recent studies have demonstrated correlation between inflammation to plasma troponin (cTnI) levels elevation and atrial fibrillation (AF) in noncardiac surgery settings. The goal of this prospective study was to examine the relation between inflammation associated parameters (IAPs) to post cardiac surgery cTnI elevation and AF. A single post CABG cTnI measurement was assessed in 156 consecutive patients. Clinical, operative and postoperative data, IAPs (hypophosphatemia, preoperative statin treatment, immediate postoperative fever, and prolonged mechanical ventilation) and in-hospital AF episodes were prospectively recorded. Mean cTnI level was 14.4 +/- 12.4 ng/mL. In the two in-hospital deaths (1.2%) cTnI concentration was less than 12 ng/mL. Cardiac troponin-I levels were significantly higher in patients not preoperatively treated with statins (21.6 +/- 4.1 vs. 13.3 +/- 0.9, p = 0.05), in patients who needed intraoperative cardioversion (16.7 +/- 2.2 vs. 12.2 +/- 0.9, p = 0.07), in patients with postoperative hypophosphatemia (16.9 +/- 10.0 vs. 11.1 +/- 13.7, p = 0.04), postoperative fever (18.6 +/- 3.0 vs. 13.7 +/- 1.0, p = 0.07) and postoperative respiratory complications (23.9 +/- 4.3 vs. 13.5 +/- 1.0, p = 0.04). Step-wise logistic regression analysis revealed the following parameters as independently associated with elevated cTnI levels: preoperative statin treatment (CI 95%-15.9; -1.7, p = 0.02), intraoperative ventricular arrhythmia (CI 95%-0.7; 13.8, p = 0.08), hypophosphatemia (CI 95% 0.9; 8.6, p = 0.02), postoperative fever (CI 95% 0.9; 11.0, p = 0.02), and postoperative respiratory complications (CI 95% 0.1; 0.5, p = 0.01). Of the 156 patients, 50 (32.1%) had postoperative AF. The first episode of AF occurred between postoperative day 1 and 6 (mean-day 2). Mean duration of AF was 21.8 +/- 8.1 hours. Postoperative AF was significantly associated with age above 75 (50% vs. 29.4%, p = 0.01), hypertension (37% vs. 18%, p = 0.02), preoperative calcium channel blockers treatment (44% vs. 26%, p = 0.02), furosemide treatment (58% vs. 30%, p = 0.05), and preoperative left atrial diameter above 40 mm (56% vs. 29%, p = 0.01). Postoperatively, AF was significantly associated with postoperative renal failure (70% vs. 29%, p = 0.01), respiratory complications (61% vs. 29%, p = 0.02), and prolonged hospital stay (OR 1.1; CI 1.0-1.3; p < 0.05). No association was found between troponin levels and postoperative AF. Multivariable analysis found only left atrial enlargement and prolonged hospital stay independently associated with AF. A significant correlation between clinical IAPs and cTnI plasma level elevation was found after cardiac surgery. There was no correlation between these parameters and postoperative AF, and there was no correlation between postoperative plasma cTnI levels and the occurrence of AF. Preoperative treatment with statins may be beneficial in reducing postoperative inflammatory response but further study has to be carried out.

Can elevated troponin I levels predict complicated clinical course and inhospital mortality in patients with acute pulmonary embolism?

Objective The purpose of this study was to evaluate the value of elevated cardiac troponin I (cTnI) for prediction of complicated clinical course and in-hospital mortality in patients with confirmed acute pulmonary embolism (PE). Methods and Results This study was a retrospective chart review of patients diagnosed as having PE, in whom cTnI testing was obtained at emergency department (ED) presentation between January 2002 and April 2006. Clinical characteristics; echocardiographic right ventricular dysfunction; inhospital mortality; and adverse clinical events including need for inotropic support, mechanical ventilation, and thrombolysis were compared in patients with elevated cTnI levels vs patients with normal cTnI levels. One hundred sixteen patients with PE were identified, and 77 of them (66%) were included in the study. Thirty-three patients (42%) had elevated cTnI levels. Elevated cTnI levels were associated with inhospital mortality ( P = .02), complicated clinical course ( P < .001), and right ventricular dysfunction ( P < .001). In patients with elevated cTnI levels, inhospital mortality (odds ratio [OR], 3.31; 95% confidence interval [CI], 1.82-9.29), hypotension (OR, 7.37; 95% CI, 2.31-23.28), thrombolysis (OR, 5.71; 95% CI, 1.63-19.92), need for mechanical ventilation (OR, 5.00; 95% CI, 1.42-17.57), and need for inotropic support (OR, 3.02; 95% CI, 1.03-8.85) were more prevalent. The patients with elevated cTnI levels had more serious vital parameters (systolic blood pressure, pulse, and oxygen saturation) at ED presentation. Conclusion Our results indicate that elevated cTnI levels are associated with higher risk for inhospital mortality and complicated clinical course. Troponin I may play an important role for the risk assessment of patients with PE. The idea that an elevation in cTnI levels is a valuable parameter for the risk stratification of patients with PE needs to be examined in larger prospective studies.

Association of platelet‐monocyte aggregates with platelet activation, systemic inflammation, and myocardial injury in patients with non‐st elevation acute coronary syndromes

Platelet-monocyte aggregates (PMA) and C-reactive protein (CRP) are increased in unstable coronary disease. The interrelation of PMA with platelet activation, systemic inflammation, and their association with markers of myocardial injury has not been studied extensively. The study was undertaken to evaluate the association of CRP, PMA, and cardiac troponin I (cTnI) in patients admitted with non-ST elevation acute coronary syndromes (NSTE-ACS). In all, 69 consecutive patients with NSTE-ACS, 58 patients with stable angina pectoris (SAP), and 46 control patients without coronary artery disease were selected; PMA, sP-selectin, sCD40L inter leukin, (IL)-6, CRP, and cTnI concentrations were measured in these patients at the time of admission. Patients with NSTE-ACS were classified into two groups: those with troponin normal (cTnI < 0.06 ng/ml) and those with troponin elevation (cTnI > or = 0.06 ng/ml). Their risk for clinical in-hospital cardiac events (death and nonfatal myocardial infarction) was analyzed. Compared with SAP and control, patients with NSTE-ACS exhibited higher levels of PMA, sP-selectin, sCD40L, IL-6, and CRP. All these parameters were found to be higher (p < 0.001 ) in patients with troponin elevation than in those with normal troponin. There was a significant relationship between PMA and CRP (r =0.628, p < 0.001) and cTnI (r = 0.557, p < 0.001) in patients with NSTE-ACS. Logistic analysis further demonstrated that the presence of elevated PMA, CRP, and cTnI levels each confers and increases risk of future cardiac events. Levels of PMA and CRP were significantly increased in patients with NSTE-ACS, especially in those with troponin elevation. This increase is strongly related to the risk of in-hospital cardiac events. A panel of PMA, CRP, and cTnI may provide important information additional to current laboratory data for the treatment of NSTE-ACS.

Prognostic value of SPECT myocardial perfusion imaging in patients with elevated cardiac troponin I levels and atypical clinical presentation

We determined the prognostic value of myocardial perfusion imaging (MPI) in patients with atypical clinical presentations and unexpected elevation of cardiac troponin I (cTnI) levels. In 156 consecutive patients with atypical presentations for acute coronary syndromes (ACS) and elevated cTnI levels undergoing MPI within 30 days, rates of all-cause mortality (100% follow-up; median follow-up, 611 days) and 6-month cardiac death and nonfatal myocardial infarction (96% follow-up; median follow-up, 167 days) were determined. The mean age of the patients was 68 +/- 14 years. The majority of the study cohort (96%) was at low to intermediate clinical risk for ACS (Thrombolysis in Myocardial Infarction score for unstable angina/non-ST-segment elevation myocardial infarction <5). The overall event rate was high, with 45 deaths (28.8%). There were 13 cardiac deaths/nonfatal myocardial infarctions in 6 months (8.3%). A normal MPI result was associated with a high event-free survival rate, whereas an abnormal MPI result was associated with a 3-fold and 7-fold higher risk of all-cause mortality and 6-month cardiac events, respectively. An abnormal MPI result was an independent predictor of all-cause death. In patients with cTnI elevation and a low to intermediate risk for ACS, a normal MPI result portends a good prognosis. Patients with abnormal MPI results have a higher 6-month cardiac event rate and a worse survival rate.

Prognostic Value of Preoperative Cardiac Troponin I in Patients Undergoing Emergency Coronary Artery Bypass Surgery With Non–ST-Elevation or ST-Elevation Acute Coronary Syndromes

Cardiac troponin I (cTnI) is a highly sensitive and specific biomarker which has been shown to predict patient outcome pre- and postoperatively following elective coronary artery bypass surgery (CABG). Whether preoperatively elevated cTnI levels similarly predict the outcome in patients undergoing emergency CABG with acute myocardial infarction (AMI) is currently unknown. A possible correlation between preoperative cTnI and in-hospital mortality and major adverse cardiac events (MACE) was investigated in 57 patients with ST-elevation AMI (STEMI) in group 1 and 197 with Non-ST-elevation AMI (NSTEMI) in group 2, who were operated within 24 hours after onset of symptoms. Primary study end point was all-cause in-hospital mortality. Secondary end points were low cardiac output syndrome (LCOS) and hospital course. CTnI levels on admission were higher in group 1 compared with group 2 (7.1+/-1.8 versus 1.4+/-1.8 ng/mL; P<0.001). Overall in-hospital mortality was higher in group 1 compared with group 2 (14.3 versus 4.1%; odds ratio [OR], 3.9, 95% confidence interval [CI], 1.3 to 12.3; P<0.01). LCOS occurred in 16/57 (28.1%), and 18/197 (9.1%) patients, respectively (OR, 3.9, 95% CI, 1.7 to 8.8; P<0.001). Postoperative ventilation time, intensive care, and hospital stay were significantly longer in group 1 versus group 2. Multivariate logistic regression analyses revealed preoperative cTnI as the strongest independent predictor for in-hospital mortality (P<0.001) and MACE (P<0.001) in all AMI patients, regardless whether ST-elevation was included as an additional risk factor or not. Preoperative cTnI measurement before emergency CABG appears as a powerful and independent determinant of in-hospital mortality and MACE in acute STEMI and NSTEMI.

Elevated troponin levels are associated with higher mortality following intracerebral hemorrhage

Elevated troponin levels are an independent indicator of poor outcome in ischemic stroke. The authors performed a retrospective study to ascertain whether elevated cardiac troponin I (cTnI) influences outcome from intracerebral hemorrhage (ICH). Patients were included if they had a cTnI level measured and a head CT performed within 24 hours of presentation with a spontaneous ICH. Those with recent stroke, angina, or myocardial ischemia were excluded. CT scans were reviewed to determine the hematoma size, location, presence of intraventricular or subarachnoid hemorrhage, hydrocephalus, and midline shift. Of the 729 ICH patients admitted over 4 years, 235 were included in the analysis. Most exclusions were for medical reasons or because of lack of a CT. Mortality was higher in the 18% with a peak cTnI level > 0.4 ng/mL (58 vs 34%, p = 0.009) and having elevated cTnI was an independent predictor of in-hospital mortality (Exp [beta] 3.68, 95% CI 1.2 to 11.2, p = 0.023). Three patients (1.2%) died due to cardiac events, all of whom had an elevated cTnI level on admission. Elevated cardiac troponin I (cTnI) values occur frequently in ICH and are independently associated with higher in-hospital mortality. Although cardiac causes of death were higher in those with elevated cTnI levels, due to its very low frequency (1.2%) this finding remains preliminary.

Troponin I Testing in Dialysis Patients Presenting to the Emergency Room: Does Troponin I Predict the 30-Day Outcome?

Background: Troponins are often measured in acutely ill chronic dialysis patients admitted to the emergency room, irrespective of their clinical presentation. The significance of an elevated troponin level in this setting is unclear. Methods: We identified all chronic dialysis patients presenting over 1 year to a tertiary care hospital emergency room who also had at least one cardiac troponin I (cTnI) level determination. We evaluated presenting complaints, risk factors for cardiac disease, cTnI levels, and major cardiac events (MCE; occurrence of cardiovascular death, myocardial infarction, de novo heart failure, or coronary revascularization) within 30 days by chart review in 149 patients (79 on hemodialysis, 70 on peritoneal dialysis). Results: Chest pain was documented in only 29% of the patients. Twenty-two patients (15%) experienced an MCE. The incidence of an MCE was the same in patients with and without chest pain. A cTnI level >0.1 ng/l was a significant predictor of an MCE (odds ratio 15.2, 95% confidence interval CI 5.26, 43.6). The likelihood ratios for MCEs were 0.32 (CI 0.16, 0.63) for a cTnI level <0.1 ng/l, 0.72 (CI 0.09, 5.5) for cTnI concentrations 0.1–0.3 ng/l, 7.8 (CI 4.2, 15) for a cTnI level >0.3, and 11.7 (CI 4.4, 31) for a cTnI concentration >2.0 ng/l. Conclusion: In acutely ill chronic dialysis patients presenting to a hospital emergency room, an elevated cTnI level indicates an increased 30-day cardiac risk, regardless of their clinical presentation.

Long-term Outcome of Patients With Perioperative Myocardial Infarction as Diagnosed by Troponin I After Routine Surgical Coronary Artery Revascularization

Diagnosis of perioperative myocardial infarction (P-MI) after coronary artery bypass graft (CABG) surgery traditionally relied on a combination of electrocardiographic and enzyme assay changes. Patients with Q-wave P-MIs who survive to hospital discharge have a poorer long-term prognosis. Troponin assays are more sensitive and specific for detecting minor P-MI, with an increased incidence of P-MI being reported. This study investigated if P-MI after CABG surgery, as defined by troponin-I isozyme (cTn-I), correlated with long-term outcome. A prospective, observational study. A single-institution, cardiothoracic specialty hospital. Seventy patients undergoing elective CABG surgery. Patients (n = 70) were stratified into low-risk and high-risk groups according to the absence (cTn-I <15 microg/L) or presence (cTn-I >or=15 microg/L) of P-MI after CABG surgery. Patients with (n = 24) and without (n = 46) P-MI were then followed for 3 years after CABG surgery to determine the impact of cTn-I-defined P-MI on long-term outcome. Most patients felt that their quality of life and activity index had improved and that their symptoms of angina had lessened at 12-month follow-up. However, cardiovascular event-free survival was significantly less in patients with P-MI (p = 0.01) 3 years postoperatively. The incidence for cardiovascular events was 0.24 versus 0.65 (p = 0.049) in those patients without and with P-MI, respectively. The hazard ratio (2.9; 95% confidence interval, 1.3-9.4) for cardiovascular incidents was also significantly greater in patients with P-MI. More specifically, the incidence of arrhythmia was 2.4% versus 26.1% (p < 0.01), and the incidence of vascular events was 4.9% versus 26.1% (p = 0.02) in patients without and with P-MI, respectively. It was shown that P-MI as defined by cTn-I is associated with an increased long-term incidence of adverse cardiovascular events. An elevated peak cTn-I level (>or=15 microg/L) identified patients at increased risk but did not have a powerful positive predictive value for either cardiovascular (48%) or vascular (26%) complications. However, a peak cTn-I <15 microg/L was a negative predictor of adverse vascular outcome (95%). This may have implications for postoperative patient follow-up.

Frequency of clinically unsuspected myocardial injury at a children's hospital

Ill children are at risk but rarely screened for myocardial injury. The frequency of such injury in ill children is unknown. Elevated levels of plasma cardiac troponin I (cTnI) can detect subclinical myocardial injury. We measured cTnI levels from 283 Children's Hospital, Boston patients (median age 2.10 years, range 0.13-22.4 years) seen in an outpatient or emergency clinic without clinically apparent cardiac disease. We took > or = 0.5 ng/mL as an indication of myocardial injury. We also measured plasma creatine kinase-MB, total creatine kinase, and myoglobin, and performed a chart review. Fifteen (7.8%) of the 193 acutely ill children and 4 (4.4%) of the 90 well children had an elevated cTnI level (P = .44). Within the acutely ill group, the children with elevated cTnI were younger and had lower mean hemoglobin and hematocrit levels. Cardiac troponin I levels correlated with creatine kinase-MB (r = 0.22; P < .001) but not with creatine kinase or myoglobin. The 4 children with cTnI > 0.89 ng/mL, who also had plasma cardiac troponin T measured, showed cardiac troponin T elevations that were consistent with unstable angina levels in adults. Four children had high-level cTnI elevations (> 2 ng/mL) consistent with acute myocardial infarction levels in adults. Elevated cTnI levels occur in children without clinically apparent cardiac disease and can be at adult unstable angina or acute myocardial infarction levels. Prospective studies to determine the clinical significance of these findings and their relationship to the development of cardiomyopathy are warranted.

Positive Interference from Contrast Media in Cardiac Troponin I Immunoassays

Cardiac troponin I (cTnI) has been found to be a sensitive and reliable marker of myocardial damage, and elevated levels of cTnI can indicate high risk for acute coronary syndrome. To determine how to intervene in possible cases of acute coronary syndrome, cTnI levels must be measured by immunoassay. However, cTnI immunoassay results are prone to interference from many substances such as heparin and common drugs. The contrast media used in the coronary angiography might also interfere with results. To explore this possibility, we performed two in vivo and two in vitro studies. In the first in vivo study, we evaluated the effects of contrast media on cTnI immunoassays by collecting blood samples from 45 patients undergoing coronary angiography before and after the procedure. We used the Opus Magnum immunoassay system to measure cTnI levels. In the second in vivo study, we collected 25 blood samples from another group of patients also undergoing angiography at various times before and after the procedure to determine cTnI values by both the Opus Magnum and ACCESS systems. In the first in vitro study, 12 different contrast media were treated as samples to disclose the potential interference of measurement in the two assay systems. In the second in vitro study, we made sequential dilutions of iopromide (Ultravist; Schering) with serum to explore their potential for interfering with the detection of cTnI by the Opus Magnum and ACCESS assays. In the first in vivo study using the Opus Magnum assay, cTnI concentrations in samples taken after angiography were significantly higher at 5 minutes than at 30 minutes, and, at 60 minutes, all cTnI concentrations had dropped below the cutoff point. In the second in vivo study, we found a substantial difference in detection of cTnI by the Opus Magnum and ACCESS assays. All cTnI concentrations checked by ACCESS assay were below the cutoff value. In our first in vitro study, the Opus Magnum assay gave false positive results for all 12 contrast media; the ACCESS assay gave a positive result for only one contrast medium, poppy-seed oil (Lipiodol; Guebert). In our second in vitro study, we found that, in the Opus Magnum assay, the more concentrated the contrast medium, the higher the cTnI value, but not in the ACCESS assay. We conclude that contrast media may cause false-positive results in cTnI assays and that, when contrast media are being used for angiography, cTnI results, especially those based on samples taken within the first hour of the procedure, should be interpreted carefully.

Cardiac troponin in the general adult critical care unit: solution or problem

Cardiac troponin T (cTnT) and troponin I (cTnI) are the most sensitive and specific biochemical markers of myocardial injury available, but do not indicate the mechanism of such injury [1]. There are many problems with their interpretation in the critical care setting. A recent editorial has highlighted that frequent determination of troponin in the ICU patient can lead to 'troponinitis'! [2]. The editorial quotes various studies, including those showing association between elevated cTnI levels and mortality. After analysis of 346 samples measured over 22 months from our general adult ICU (annual admissions 850), we also found a statistical relationship between levels of elevated cTnI and both ICU and hospital mortality (Table ​(Table1)1) using chi-square testing. However, we have not found this to be clinically significant. A hospital mortality of 51.2% may be high, but not so high as to precipitate the withdrawal of intensive care treatment. Table 1 Due to the low specificity and positive predictive value of cTnI in mixed adult general critical care patients, it is difficult for us as intensivists to place elevated troponin levels in their clinical context. We also have difficulty in using elevated troponin levels to influence patient management in the absence of a classical history and ECG changes. Thrombolysis, ACE-inhibitors and β-blockers can be doubled-edged swords in the critically ill; echocardiography in the resting patient provides scant meaningful information; a pulmonary artery catheter is invasive – and all this before we consider the risks associated with coronary angiography. We therefore believe that cardiac troponins in a mixed adult ICU should only be requested when it could confirm an acute coronary syndrome. In the ICU setting, this would almost always entail obtaining new ECG changes before requesting a cTnI level.

We-W30:1 Genetic determinants of plasma lipoproteins

The independent predictive value of d-dimer and inflammatory markers for the risk of recurrent adverse events in patients with acute chest pain but normal levels of cardiac troponin I (cTnI) remains unclear.We studied 391 patients admitted to the hospital in 1 year with acute ischemic-type chest pain. Creatine kinase-myocardial band isoenzyme (CK-MB) mass and cTnI levels were measured in initial and 12-hour samples. Soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, sP-selectin, sE-selectin, high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), fibrinogen, and d-dimer levels were measured in initial samples. A 1-year incidence of death, myocardial infarction (MI), revascularization, or readmission with chest pain was determined (with death/MI as the primary end point).Patients with normal levels of CK-MBmass and cTnI (195/391[50%]) were at a lower risk than patients with elevated levels of CK-MBmass or cTnI, but still had an important incidence of events (77/195[39%]). Marker elevation was defined as >75th percentile (upper quartile). Elevated d-dimer levels (>580 ng/mL) was predictive of death/MI (odds ratio, 5.4; 95% CI, 1.5-20.2; P = .005). Elevated sP-selectin levels (>152 ng/mL; odds ratio, 3.2; 95% CI, 0.9-11.6; P = .06) trended to increased death/MI rates, with weaker trends for elevated levels of hsCRP (>7.1 mg/L), IL6 (>10.7 pg/mL), and ST depression. Other markers, other electrocardiogram changes, or classic risk factors were not predictive of death/MI. With a multivariate analysis, d-dimer and sP-selectin were found to be of independent significance for death/MI after adjustment for inflammatory, hemostatic, and electrocardiogram markers and d-dimer after adjustment for classic risk factors.Normal cTnI levels after acute chest pain does not confer absence of future risk. Concurrent assessment of d-dimer and inflammatory markers may improve risk stratification.

Myocardial Injury in Critically Ill Patients: Relation to Increased Cardiac Troponin I and Hospital Mortality

<h3>Objective</h3> To examine the relationship between myocardial injury, assessed by cardiac troponin I (cTnI) levels, and outcome in selected critically ill patients without acute coronary syndromes or cardiac dysfunction. <h3>Design and setting</h3> Prospective, observational study in the emergency ICU of a university teaching hospital. <h3>Population</h3> Over a 6-month period, 217 consecutive patients admitted to the ICU were studied. <h3>Methods and results</h3> cTnI assays were performed in all patients on admission to the ICU. The incidence of myocardial injury, defined by cTnI level > 0.1 ng/mL, was 32% (69 of 217 patients). Overall mortality was 27% (58 of 217 patients). Patients with myocardial injury had a mortality rate of 51%, compared with only 16% mortality for those without myocardial injury (p < 0.001). The hospital mortality rate was highest among older patients (71 ± 14% vs 58.5 ± 20%, p < 0.0001) and patients with higher simplified acute physiology scale (SAPS) II score (62 ± 25% vs 37 ± 17%, p < 0.0001). Mechanical ventilation was associated with higher in-hospital death (50% vs 31%, for patients who died in the hospital vs those who were discharged alive; p=0.03). Elevated blood levels of cTnI were found to be independently associated with hospital mortality, regardless of the presence of SAPS II score and mechanical ventilation, in the logistic regression analysis (odds ratio, 2.09; 95% confidence interval, 1.06 to 4.11; p=0.01). <h3>Conclusions</h3> This study demonstrates the high frequency of myocardial injury (32%) in critically ill patients without acute coronary syndromes or cardiac dysfunction on admission to ICU. Myocardial injury is an independent determinant of hospital mortality. Assessment of myocardial injury on admission to ICU would make it possible to identify patients at increased risk of death.

PROGNOSTIC VALUE OF PREOPERATIVE CARDIAC TROPONIN I IN PATIENTS UNDERGOING EMERGENCY CORONARY ARTERY BYPASS RAFTING DUE TO NON-ST VERSUS ST-ELEVATION ACUTE CORONARY SYNDROMES

PURPOSE: Cardiac troponin I (cTnI) is a highly sensitive and specific marker for myocardial damage, which has been shown to predict patients outcome pre- and postoperatively following elective coronary artery bypass surgery (CABG). Wether preoperatively elevated cTnI levels similarily predict the outcome in patients undergoing emergency CABG due to acute coronary syndromes (ACS) is currently unknown.

Risk stratification with cardiac troponin I in patients undergoing elective coronary artery bypass surgery☆

Cardiac troponin I (cTnI) is a highly sensitive and specific marker for postoperative prediction of patients outcome after coronary artery bypass surgery (CABG). Whether preoperatively elevated cTnI levels similarly predict the outcome in patients scheduled for elective CABG is currently unknown. Therefore, a possible correlation between preoperative cTnI levels and perioperative major adverse events and in-hospital mortality after CABG was investigated. CTnI was measured within 24h before surgery in 1405 out of 3124 consecutive elective CABG patients. Out of these patients, 1178 had a preoperative cTnI level below 0.1ng/ml (group 1), 163 patients had a cTnI level between 0.11 and 1.5ng/ml (group 2), and 64 patients had a cTnI level above 1.5ng/ml (group 3). CTnI levels, electrocardiograms, clinical data, adverse events and in-hospital mortality were recorded prospectively. Patients with ST-elevation myocardial infarction less than 7 days before surgery were excluded from the study. Perioperative myocardial infarction (PMI) occurred in 69/1178 patients (5.9%) in group 1, 14/163 patients (8.6%; odds ratio (OR) 1.5, 95% confidence interval (CI): 0.8-2.8) in group 2, and 11/64 patients (17.2%; OR 3.3, CI: 1.6-7.0) in group 3 (overall: P<0.001, Cochran-Armitage trend test). Low cardiac output syndrome (LCOS) occurred in 19/1178 patients (1.6%), 9/163 (5.5%; OR 3.6, CI: 1.5-8.5), and 7/64 patients (10.9%; OR 7.5, CI: 2.7-19.8) (overall: P<0.001, group 1 vs. group 2: P<0.002), respectively. In-hospital mortality was 1.7% in group 1 and 3.1% in group 2, but 6.3% (OR 3.9, CI: 1.1-12.5) in group 3 (overall: P<0.01, group 1 vs. group 2: P=NS). Intensive care and hospital stay were significantly longer in group 3 compared to groups 1 and 2. Univariate and multivariate logistic regression analysis confirmed the statistically significant relationship between cTnI and PMI, LCOS and in-hospital mortality, respectively (P<0.001). Risk stratification by measurement of cTnI levels within 24h before elective CABG clearly identifies a subgroup of patients with increased risk for postoperative adverse outcome and in-hospital mortality.