Normal Troponin I Research Articles

Troponin I Levels and Postoperative Myocardial Infarction following Renal Transplantation

Background: The relationship of routine postoperative troponin I (TnI) monitoring in kidney transplant recipients and in-hospital myocardial infarction (MI) is not known. Methods: This observational study evaluated the prevalence of abnormal postoperative TnI (Ortho Clinical Diagnostics assay) in 376 consecutive kidney or kidney/pancreas transplant recipients. In-hospital MI was adjudicated using the universal definition. Rates of death and coronary revascularizations at 1 year were studied. Logistic regression analysis was performed to identify independent predictors of abnormal TnI. Results: Ninety-five (25%) recipients had abnormal TnI (>0.04 ng/ml) following transplantation. Abnormal TnI levels were more common in older (mean age: 52.2 ± 13.4 vs. 48.3 ± 13.2 years, p = 0.01), diabetic (57.9 vs. 45.6%, p = 0.04), and prior coronary artery disease (31.6 vs. 20.3%, p = 0.02) patients. In-hospital MI occurred in 6 patients (1.6%). All subsequent in-hospital cardiovascular events occurred in the abnormal postoperative TnI group; most in those with TnI levels >1 ng/ml. Previous coronary artery disease was the only independent predictor of a postoperative TnI level >1 ng/ml in multivariate analysis (odds ratio 4.61, 95% confidence interval 1.49–14.32). At 1 year there was no significant difference in death (3.2 vs. 1.8%, p = 0.42) and borderline significant difference in coronary revascularization (5.3 vs. 1.4%, p = 0.049) in abnormal versus normal TnI groups. Conclusions: In-hospital MI was infrequent, but abnormal TnI highly prevalent following renal transplantation. Normal TnI levels following renal transplantation had a high negative predictive value in excluding patients likely to develop subsequent postoperative MI. The role of a higher TnI cut-off for screening for postoperative MI in high-risk subgroups deserves future prospective evaluation.

Predictors of cardiac events in high‐risk patients undergoing emergency surgery

The aim of this study was to determine the incidence of myocardial damage and left ventricular myocardial dysfunction and their influence on outcome in high-risk patients undergoing non-elective surgery. In this prospective observational study, 211 patients with American Society of Anesthesiologists classification III or IV undergoing emergent or urgent surgery were included. Troponin I (TnI) was measured pre-operatively, 12 and 48 h post-operatively. Pre-operative N-terminal fragment of B-type natriuretic peptide (NT-proBNP), as a marker for left ventricular systolic dysfunction, was analyzed. The diagnostic thresholds were set to TnI >0.06 microg/l and NT-proBNP >1800 pg/ml, respectively. Post-operative major adverse cardiac events (MACE), 30-day and 3-months mortality were recorded. Elevated TnI levels were detected in 33% of the patients post-operatively. A TnI elevation increased the risk of MACE (35% vs. 3% in patients with normal TnI levels, P<0.001) and 30-day mortality (23% vs. 7%, P=0.003). Increased concentrations of NT-proBNP were seen in 59% of the patients. Elevated NT-proBNP was an independent predictor of myocardial damage post-operatively, odds ratio, 6.2 [95% confidence interval (CI) 2.1-18.0] and resulted in an increased risk of MACE (21% vs. 2.5% in patients with NT-proBNP < or = 1800 pg/ml, P<0.001). Myocardial damage is common in a high-risk population undergoing unscheduled surgery. These results suggest a close correlation between myocardial damage in the post-operative period and increased concentration of NT-proBNP before surgery. The combinations of TnI and NT-proBNP are reliable markers for monitoring patients at risk in the peri-operative period as well as useful tools in our risk assessment pre-operatively in emergency surgery.

Diagnostic Uncertainty and Costs Associated With Current Emergency Department Evaluation of Low Risk Chest Pain

Of all stress tests done in low risk Emergency Department observation units (OU), a small, but significant number may be reported as positive or indeterminate. The objective of this study is to quantify the prevalence and costs associated with positive and indeterminate stress tests that result in negative cardiac catheterization. Retrospective observational cohort study over 9 months. All patients undergoing the chest pain protocol who got cardiac stress testing in the OU were eligible for inclusion. Cost data were derived from an institutional activity-based cost system utilizing actual costs. Chart review was completed on all patients with positive and indeterminate stress tests and a randomly chosen sample of those with negative stress tests. Of the 1194 patients who met the inclusion criteria, 1084 (90.8%) had a negative stress test. Sixty-two (5.2%) had a positive stress test, and 48 (4.0%) had an indeterminate stress test. Of all 59 patients who underwent catheterization, 41 (69.5%) were negative cardiac catheterizations. The prevalence among all OU stress test patients of positive or indeterminate stress tests with subsequent negative cardiac catheterization was 41/1194 (3.4%; 95% CI 2.5%-4.6%). The prevalence of significant coronary artery disease at cardiac catheterization was 18/1194 (1.5%; 95% CI 1.0%-2.4%). Patients with a positive or indeterminate stress test who had a negative catheterization incurred increased OU costs ($1385 vs. $1,039, P = 0.012), total costs ($7298 vs. $1562, P < 0.001) and length of inpatient stay (1.83 days vs. 0.00 days) when compared with those who had a negative stress test. The probability of going to the OU and having a positive or indeterminate stress test resulting in a subsequent negative catheterization was double the probability of having a stress test result in catheterization that detected significant coronary artery disease. These patients incurred 5 times the total cost when compared with those patients with negative stress testing. Further investigation is warranted to determine alternative risk stratification methods for these low risk chest pain patients with positive stress tests.

Elevated Troponin I after Implantation of Drug-Eluting Stents: Incidence, Predictors, and Prognostic Value

Background and Objectives: The presence of elevated troponin after percutaneous coronary intervention (PCI) is considered to reflect irreversible myocardial injury. However, its prognostic value remains unclear. The purpose of this study was to investigate the incidence, risk factors, and clinical outcomes of troponin I (TnI) elevation after the implantation of drug-eluting stent (DES). Subjects and Methods: We performed a retrospective analysis of 335 patients who had undergone PCI with DES. Patients who had acute coronary syndrome with elevated TnI levels before PCI were excluded. TnI levels were measured 6 and 24 hours after PCI. Results: Baseline clinical characteristics were similar in the elevated TnI and normal TnI groups. Elevated postprocedural TnI (>1.5 ng/mL) occurred in 52 patients (15.5%). Univariate analysis revealed that the clinically significant variables were multi-vessel disease (p<0.001), multiple stent implantation (p=0.003), total stent length (p=0.001), side-branch occlusion (p<0.001), and bifurcation lesion (p=0.003). Multivariate analysis indicated that the independent predictors of elevated TnI after DES implantation were multi-vessel disease (p=0.019), side-branch occlusion (p=0.001), and bifurcation (p= 0.011). There were no significant differences in major adverse cardiovascular events between the elevated TnI and normal TnI groups (p=0.461). Conclusion: Multi-vessel disease, side-branch occlusion, and bifurcation were independent predictors of elevated TnI following DES implantation. The elevation of TnI after successful PCI with DES was not associated with worse 400-day clinical outcomes. (Korean Circ J 2008;38:12-16)

Cardiotoxicity in Patients with Multiple Myeloma Treated with Tandem Autologous Hematopoetic Stem Cell Transplantation.

BACKGROUND. Tandem autologous hemopoetic stem cell transplantation (HSCT) was recognised as effective treatment modality in patients with multiple myeloma (MM). During the treatment period patients are treated with high doses of cyclophosphamide followed twice with high doses of melphalan. There are scant data, if any, regarding potential cardiotoxic side effects of this treatment modality. METHODS. We included 30 patients with newly diagnosed multiple myeloma. After they were treated with three cycles of chemotherapy, they received high doses of cyclophosphamide 4 mg/m2 (cycle CY), followed by two autologous tandem HSCT, where patients received melphalan 200 mg/m2 (cycle MEL I and cycle MEL II). During each fifteen-day treatment period blood was routinely controlled for biochemical parameters troponin I (TnI), brain natriiuretic peptide (BNP) and endothelin-1 (ET-1) at six time points. All patients underwent conventional and tissue Doppler echocardiographic examination before treatment with cyclophosphamide (Eho 0), before cycle MEL I (Eho 1), before cycle MEL II (Eho 2) and three months after completion of the therapy (Eho 3). RESULTS. None of the patients developed clinical signs of heart insufficiency. Highest TnI values in all three cycles of chemotherapy were observed on the eighth, eleventh and fifteenth day of treatment. But all TnI values in patients were lower than 0.04 μg/L. During all three cycles we noticed a significant increase in BNP values compared with the basal values and values on day one after treatment with cyclophosphamide and melphalan (CY: P = 0.0001, MEL I: P = 0.001, MEL II: P= 0.001). In cycle CY this was also the highest BNP value (0.517 ± 0.391 μg/L). The maximum BNP values in cycles MEL I and MEL II were noticed on day four after chemotherapy (MEL I 0.376 ± 0.418 μg/L; MEL II 0.363 ± 0.379 μg/L). The highest ET-1 values in all three cycles were noticed on day one after chemotherapy (CY 1.146 ± 1.313 ng/L; MEL I 1.054 ± 2.242 ng/L; MEL II 0.618 ± 0.539 ng/L). We observed a significant increase in ET-1 values compared with the basal values only in cycle MEL II (P = 0.003). Concerning the parameters of diastolic left ventricular function, the duration of wave a in Doppler pulmonary vein flow signal significantly increased compared with it's basal value (Eho 0/Eho 1: P = 0.008, Eho 0/Eho 3; P = 0.026). The ratio A/a in flow velocities significantly decreased with cycles of chemotherapy (Eho 0/Eho 1: P = 0.002, Eho 0/Eho 3: P < 0.0001). Early diastolic tissue Doppler velocities (Em) decreased significantly within individual cycles of chemotherapy (P = 0.006). After the treatment a significant increase in mitral regurgitation was observed (Eho 0/Eho 3; P = 0.003). Pericardial effusion was observed in six patients (20.6%). CONCLUSIONS. Treatment of MM patients with autologous tandem HSCT is cardiotoxic. Patients did not develop clinical signs of overt heart failure and normal TnI values excluded myocardial necrosis. On the other hand, increased plasma BNP and ET-1 levels confirm transient neurohormonal activation of heart failure, likely in combination with toxic endothelial damage. Doppler echocardiography studies prove worsening of the left ventricular diastolic function and appearance of functional mitral regurgitation. The age of the patients has no influence on the clinical, laboratory and echocardiography parameters of cardiotoxicity.

Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release

Background Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. Methods The study included 50 ICU patients with SS ( n = 25) and NSS ( n = 25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop−). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. Results ACStrop+ (1525 [25th–75th percentile: 790–3820] pg/L) and NSS (687 [254–1552]) patients showed increased NT-proBNP levels above those of UAtrop− patients (107 [43–450], p < 0.001) and controls (52 [42–99], p < 0.001), but SS patients exhibited still higher levels (11,335 [4716–25,769], p < 0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specifity (area under ROC curve: 0.946 [95% confidence interval, 0.872–1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ ( p < 0.001) and SS patients ( p = 0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels ( p < 0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. Conclusions SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.

Suspected Acute Coronary Syndrome Patients With Diabetes and Normal Troponin-I Levels Are at Risk for Early and Late Death

Clinicians use a variety of methods (1,2) to risk stratify patients with acute coronary syndromes (ACSs). Based on elevated risk, patients are often triaged to an aggressive strategy, including early angiography (3,4) and upstream use of intravenous glycoprotein IIb/IIIa inhibitors (5–7). The current American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines for the Management of Patients with Unstable Angina and Non-ST-segment Elevation Myocardial Infarction do not recognize diabetes as a high-risk ACS indicator. Therefore, we sought to clarify the relative risk of diabetes in early and late death in suspected ACS patients. In this study, a prospective registry of consecutive ACS patients with and without diabetes ( n = 864) was used. ACS was diagnosed as either myocardial infarction (8) or unstable angina (9) using standard definitions. Patients with ST-segment elevation myocardial infarction were excluded. All potential unstable angina patients who had a diagnostic angiographic, nuclear, or echocardiographic stress test that excluded obstructive coronary disease or who had an additional diagnostic study confirming an alternative explanation for presentation were excluded. Diabetes was defined by reported history or new antidiabetic therapy initiated during …

B-type Natriuretic Peptide as a Diagnostic Tool for Acute Myocardial Infarction in Patients With Chest Pain in the Emergency Department

Background: B-type natriuretic peptide (BNP) is a protein produced by the heart and found to be elevated in cardiac failure and acute myocardial infarction (AMI), having important prognostic role. However, its value for the diagnosis of AMI is unknown. This study was undertaken to determine if BNP measured in patients with suspicious chest pain on admission to the emergency department can identify those with AMI. Methods: From January 1, 2002, to September 30, 2003, 631 consecutive patients with chest pain suspicious of cardiac ischemia and no ST-segment elevation seen in a chest pain unit (age = 67.3 ± 13.6, males = 54%, patients with diabetes = 20%, normal/nonspecific admission electrocardiogram [ECG] = 81%) were prospectively evaluated with admission BNP (immunofluorescence, BIOSITE), serial myocardial necrosis markers and ECG, and stress test (when applicable). Results: Non-ST segment elevation AMI and unstable angina (UA) were diagnosed in 72 and 183 patients, respectively, and their median (first through third quartile) admission BNP values were 203.5 (52.1–494.5) and 77.9 (25.8–240.0) pg/mL, respectively, versus 27.7 (9.1–76.8) in 174 non-AMI/UA patients (P = 0.0000, Kruskal-Wallis). The remaining 202 patients could only be ruled out for AMI, with BNP of 45.7 (17.3–127.0). Sensitivity, specificity, and positive and negative predictive values of admission BNP >100 pg/mL (vs admission CK MB mass >5.0 ng/mL) for AMI were 71% (vs 46%, P = 0.0000), 69% (vs 98%, P = 0.0000), 23% (vs 79%, P = 0.0000), and 95% (versus 93%, P = NS), respectively. Admission troponin-I did not perform significantly better than CK MB. The combined used of BNP, troponin-I, and CK MB on admission was significantly better for sensitivity (87%, P = 0.0000) and negative predictive value (97%, P <0.002), but worse for specificity (66%, P = 0.0000) than CK MB and troponin alone. In patients with normal troponin-I on admission, a BNP >100 pg/mL implied a 4-fold greater risk of AMI than a normal BNP. By multivariate logistic regression analysis, admission troponin (odds ratio [OR] = 36.7, P = 0.0000), admission CK MB (OR = 11.9, P = 0.0000), admission ST-segment depression (OR = 6.0, P = 0.0002), BNP (OR = 3.2, P = 0.0026), and diabetes (OR = 2.5, P = 0.0238) were independent predictors of AMI. Diagnostic performance of BNP was independent of interaction with previous or admission evidence of heart failure or serum creatinine levels. Conclusions: In patients with chest pain and no ST-segment elevation, admission BNP seems to have an adjunctive role for the immediate identification of those with and without AMI.

3355 Troponin i determination to detect subclinical cardiac ischemia during ercp.

Introduction: Methodological/procedural risks of ERCP are well known, but cardiac risks have not been studied, specifically. Troponin I (TnI) is a cardio-selective enzyme that can aid in detection of even small amounts of myocardial damage. This prospective study examined the TnI levels of patients before and after ERCP to assess for cardiac injury, e.g. caused by administration of antimotility agents that can produce tachycardias (Scopolamine, Glucagon). Methods: 100 patients (57 f, 43 m, age 20-93, mean 62 y) were randomized prospectively to administration of Scopolamine or Glucagon as the antimotility agent during ERCP (30% diagnostic, 70% therapeutic). 65% of patients had one or more cardiovascular risk factors. TnI [normal value 0-0.4 ng/ml] was measured at baseline, at 8 h, and, if elevated, at 20 h post ERCP. Patients were sedated with Midazolam, Midazolam/Pentazocin or Propofol, given nasal O₂(2 l/min), and were monitored during ERCP for heart rate, blood pressure, pulse oximetry. Results: Mean duration of ERCP was 28 min. 8 patients (5 with Scopolamine, 3 with Glucagon) had elevated TnI levels: 6 already had elevated levels at baseline (0.5-2.5ng/ml; mean 1.13), with subsequent decrease to normal in 4 patients over the 8/20 h after ERCP. The remaining 4 (2 with TnI elevations at baseline, 2 with normal TnI at baseline) had a rise in TnI levels from 0-1.3 (mean 0.47) ng/ml at baseline to 0.9-18.4 (mean 5.48) ng/ml at 8 h, to 0.6-7.8 (mean 2.75) ng/ml at 20 h after ERCP. 3 of these 4 patients had ERCP's of more than 30 min in duration (range 32-115 min). In the patients with a rise in TnI no cardiac symptoms or complication occurred during or after the ERCP. There was no correlation of an increase in TnI with tachycardias (pulse >120), hypoxic episodes (O₂- Sat < 95%), or systolic BP elevations (>160 mm Hg). No difference was found between administration of Scopolamin versus Glucagon: Heartrates of >100/min and/or systolic BP >160 mm Hg occurred in 33 patients after Scopolamin and 34 patients after Glucagon without change in TnI. 22 patients had stable vital signs. Conclusions: In this study an increasing TnI level was observed in 4% of patients undergoing ERCP. This correlated only with duration of the procedure (>30 min). No difference was found with regard to choice of antimotility agent (Scopolamine versus Glucagon). No clinically relevant cardiac symptoms or cardiovascular problems resulted in any patient with TnI elevation. In this study ERCP appeared to be safe from a cardiovascular standpoint, even for multimorbid patients.