Cardiac troponin T in acute coronary syndrome with renal insufficiency

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

Impact of troponin T determinations on hospital resource utilization and costs in the evaluation of patients with suspected myocardial ischemia

The evaluation and triage of patients with suspected myocardial ischemia in the emergency department remains challenging and costly. Previous studies of cardiac troponins have focused predominantly on patients with chest pain and have not randomized patients to different diagnostic strategies. Eight hundred fifty-six patients with suspected myocardial ischemia were prospectively randomized to receive a standard evaluation, including serial electrocardiographic and creatine phosphokinase-MB determinations (controls) or a standard evaluation with the addition of serial troponin T determinations (troponin group). The primary end points were length of stay and hospital charges. Significant reductions in length of hospital stay were seen in troponin T patients both with (3.6 vs 4.7 days; p = 0.01) and without (1.2 vs 1.6 days; p = 0.03) acute coronary syndromes compared with controls. Total hospital charges were reduced in a similar fashion in troponin patients with and without acute coronary syndromes ($15,004 vs $19,202; p = 0.01, and $4,487 vs $6,187; p = 0.17, respectively) compared with controls. Troponin patients without acute coronary syndromes had fewer hospital admissions (25% vs 31%; p = 0.04), whereas troponin patients with acute coronary syndromes had shorter telemetry and coronary care unit lengths of stay (3.5 vs 4.5 days; p = 0.03) compared with controls. Thus, utilization of troponin T in a broad spectrum of emergency department patients with suspected myocardial ischemia improves hospital resource utilization and reduces costs.     

Chest pain in clinical practice: impact of routine troponin determination on clinical manifestations and care

INTRODUCTION AND OBJECTIVES. To study the significance of chest pain in the clinical practice of a Spanish hospital and to evaluate the impact of routine troponin determination. METHODS: In our institution, routine serial measurements of troponins I and T were made in the evaluation of chest pain in 2000. We compared the results obtained in 1999 for all patients who visited the emergency room for chest pain and the patients who were hospitalized. We recorded the diagnosis at discharge, duration of the hospital stay, and associated costs. RESULTS: In 2000, 1,820 patients with chest pain visited the emergency department, which was equivalent to 1.9% of visits and 7.5 cases per 1,000 people and year: 43% of these patients were hospitalized for suspected acute coronary syndrome as compared to 49% in 1999 (-12%; p > 0.001). Among the patients admitted, 28% were discharged with a diagnosis of non-ischemic chest pain. Troponin determinations were associated with a lower probability of admission due to unstable angina (11.5 vs 16.0%; -28%; p < 0.001) and non-ischemic chest pain (12.1 vs 14.5%; -16%; p < 0.05), and an increase in diagnoses of non-Q wave acute myocardial infarction (3.4% vs 1.8%; +89%; p < 0.01). Non-ST elevation acute coronary syndrome ACS required 3,751 days of hospitalization and 1,003,420 euros of cost, and troponin determinations were associated with a reduction in hospital stays of 832 days (-18.2%) and 185,100 euros (-15.6%). CONCLUSION: Chest pain had a high incidence, 7.5, and generates high costs in hospital admissions. The routine use of serial troponin determinations was associated with a reduction in hospital admissions due to unstable angina and non-ischemic chest pain, and costs.     

Ability of troponins to predict adverse outcomes in patients with renal insufficiency and suspected acute coronary syndromes: a case-matched study

ObjectivesThe purpose of this study was to investigate the utility of cardiac troponin T and troponin I for predicting outcomes in patients presenting with suspected acute coronary syndromes and renal insufficiency relative to that observed in similar patients without renal disease.BackgroundCardiac troponin T and troponin I have shown promise as tools for risk stratification of patients with acute coronary syndromes. However, there is uncertainty regarding their cardiac specificity and utility in patients with renal disease.MethodsWe measured troponin T, troponin I and creatine kinase MB in 51 patients presenting with suspected acute coronary syndromes and renal insufficiency and in 102 patients without evidence of renal disease matched for the same peak troponin T or I value, selected from a larger patient cohort. Blood samples were obtained at presentation to an emergency room 4 hours, 8 hours and 16 hours later. The ability of biochemical markers to predict adverse outcomes in both groups including infarction, recurrent ischemia, bypass surgery, heart failure, stroke, death or positive angiography/angioplasty during hospitalization and at six months was assessed by receiver-operator curve analysis. The performance of both troponins was compared between groups.ResultsThirty-five percent of patients in the renal group and 45% of patients in the nonrenal group experienced an adverse initial outcome; over 50% of patients in all groups had experienced an adverse outcome by 6 months, but these differences were not significant. The area under the curve (AUC) for the ROC curve for troponin T as predictor of initial outcomes was significantly lower in the renal group than in the nonrenal group: 0.56 ± 0.07 and 0.75 ± 0.07, respectively. The area under the curve was also significantly lower in the renal group compared with the nonrenal group for troponin T as predictor of six month outcomes: 0.59 ± 0.07 and 0.74 ± 0.07, respectively. The area under the curve was also significantly lower in the renal group compared to the nonrenal group for troponin I as predictor of both initial and six month outcomes: 0.54 ± 0.06 vs. 0.71 ± 0.07 and 0.53 ± 0.06 vs. 0.65 ± 0.07, respectively. The sensitivity of troponin T for both initial and six month adverse outcomes was significantly lower in the renal group than in the nonrenal group at a similar level of specificity (0.87): 0.29 vs. 0.60 and 0.45 vs. 0.56, respectively. Troponin I also exhibited similar differences in sensitivity in the renal group (0.29 vs. 0.50 and 0.33 vs. 0.40, respectively).ConclusionsThe ability of cardiac troponin T and troponin I to predict risk for subsequent adverse outcomes in patients presenting with suspected acute coronary syndromes is reduced in the presence of renal insufficiency.     

Effect of Intracoronary and Intravenous Melatonin on Myocardial Salvage Index in Patients with ST-Elevation Myocardial Infarction: a Randomized Placebo Controlled Trial

Melatonin has attenuated myocardial ischemia reperfusion injury in experimental studies. We hypothesized that the administration of melatonin during acute myocardial reperfusion improves myocardial salvage index in patients with ST-elevation myocardial infarction. Patients (n = 48) were randomized in a 1:1 ratio to intracoronary and intravenous melatonin (total 50 mg) or placebo. The myocardial salvage index assessed by cardiac magnetic resonance imaging at day 4 (± 1 day) after primary percutaneous coronary intervention was similar in the melatonin group (n = 22) at 55.3% (95% CI 47.0–63.6) and the placebo group (n = 19) at 61.5% (95% CI 57.5–65.5), p = 0.21. The levels of high-sensitive troponin T, creatinine kinase myocardial band, and oxidative biomarkers (advanced oxidation protein products, malondialdehyde, myeloperoxidase) were similar in the groups. The frequency of clinical events at 90 days did not differ between the groups. In conclusion, melatonin did not improve the myocardial salvage index after primary percutaneous coronary intervention in patients with ST elevation myocardial infarction compared with placebo.     

Different characteristics of cardiac biomarkers to decide and predict the culprit lesions in patients with suspicious acute coronary syndrome

This multicenter prospective study was conducted to assess high-sensitivity troponin T (hs-TnT) and other biomarkers to decide and predict culprit lesions indicated for emergency percutaneous coronary intervention (PCI) in patients with suspicious acute coronary syndrome (ACS). We have reported Hs-TnT is the most sensitive biomarker for earlier diagnosis and decision making in patients with suspected ACS. In this study, we had conducted subanalysis investigating the usefulness for prediction of ACS culprit lesion. The patients with suspicious ACS and initially negative whole-blood rapid troponin T test, who underwent coronary angiogram (CAG), were enrolled (n = 74). Hs-TnT, quantitative assay for conventional troponin T (c-TnT), creatine kinase MB isozyme (CK-MB), and heart-type fatty acid-binding protein (H-FABP) were simultaneously measured. ACS culprit lesion was described as total occlusion, subtotal occlusion, and/or angiographical unstable lesion such as thrombosis, ulceration or irregularity. The CAG revealed that 49 cases had ACS lesions to be indicated for emergency PCI. The areas under the ROC curves and ROC-optimized cut-off of hs-TnT, c-TnT, CK-MB, and H-FABP were 0.75, 0.67, 0.68, and 0.75, respectively, and 18, 11, 2.0, and 4.6 ng/ml, respectively. In patients with total occlusion and 90–99 % of diameter stenosis (TIMI 2 or 3), hs-TnT could predict emergency PCI with significantly higher sensitivity compared with H-FABP (hs-TnT >14 ng/ml; 71 %, and H-FABP >6.2 ng/dl; 51 %, p = 0.021) and other biomarkers. Meanwhile, H-FABP displayed significant correlations with number of diseased vessels and presence of thrombotic lesion. The present study first revealed different characteristics of correlation between the angiographic culprit lesions and each cardiac biomarker. For prediction of ACS lesions requiring emergency PCI, hs-TnT had the highest sensitivity with satisfied analytical precision.     

Fracción aminoterminal del propéptido natriurético cerebral y troponina ultrasensible en el dolor torácico agudo de origen incierto. Un subestudio del estudio PITAGORAS

Introduction and objectives

High-sensitivity troponin assays have improved the diagnosis of acute coronary syndrome in patients presenting with chest pain and normal troponin levels as measured by conventional assays. Our aim was to investigate whether N-terminal pro-brain natriuretic peptide provides additional information to troponin determination in these patients.

Methods

A total of 398 patients, included in the PITAGORAS study, presenting to the emergency department with chest pain and normal troponin levels as measured by conventional assay in 2 serial samples (on arrival and 6 h to 8 h later) were studied. The samples were also analyzed in a central laboratory for high-sensitivity troponin T (both samples) and for N-terminal pro-brain natriuretic peptide (second sample). The endpoints were diagnosis of acute coronary syndrome and the composite endpoint of in-hospital revascularization or a 30-day cardiac event.

Results

Acute coronary syndrome was adjudicated to 79 patients (20%) and the composite endpoint to 59 (15%). When the N-terminal pro-brain natriuretic peptide quartile increased, the diagnosis of acute coronary syndrome also increased (12%, 16%, 23% and 29%; P=.01), as did the risk of the composite endpoint (6%, 13%, 16% and 24%; P=.004). N-terminal pro-brain natriuretic peptide elevation (>125 ng/L) was associated with both endpoints (relative risk= 2.0; 95% confidence interval, 1.2-3.3; P=.02; relative risk=2.4; 95% confidence interval, 1.4-4.2; P=.004). However, in the multivariable models adjusted by clinical and electrocardiographic data, a predictive value was found for high-sensitivity T troponin but not for N-terminal pro-brain natriuretic peptide.

Conclusions

In low-risk patients with chest pain of uncertain etiology evaluated using high-sensitivity T troponin, N-terminal pro-brain natriuretic peptide does not contribute additional predictive value to diagnosis or the prediction of short-term outcomes.Full English text available from:www.revespcardiol.org/en.     

Cardiac emergency triage and therapeutic decisions using whole blood rapid troponin T test for patients with suspicious acute coronary syndrome

Emergency triage and therapeutic decisions using the recently developed whole blood rapid troponin T test were evaluated and compared with conventional electrocardiographic (ECG) diagnosis in a total of 155 patients with chest pain who visited 16 emergency outpatient clinics in the Tokyo metropolitan area. Thirty-seven patients (23.9%) had a final diagnosis of acute myocardial infarction or high-risk unstable angina requiring emergency coronary intervention and these events were defined as acute coronary syndrome. Diagnostic values using the second-generation rapid troponin T test were evaluated according to 3 time-windows in 85 patients. The sensitivity of the test was 10% for patients assessed within 3 h after the onset, 62.5% for 3-6 h after, and 75% for more than 6h, whereas conventional ECG diagnosis had 100% sensitivity at any time-window. In contrast, the specificity of the rapid troponin T test was 100%, 100%, and 97.4%, whereas that of conventional ECG diagnosis was 25%, 57.1%, and 42.2%, respectively for the 3 time-windows. The positive predictive value of ECG diagnosis was inferior to the rapid troponin T test, which reflected the prudent attitude of physicians taking ECG decisions as positive when myocardial ischemia was suspected. The diagnostic efficacy of the rapid troponin T test was remarkable in patients with the non-ST elevation type of acute coronary syndrome. A questionnaire survey on therapeutic decisions revealed that only 10% of Tokyo outpatient institutes performed prehospital thrombolytic therapy, 30-33% administered aspirin or nitrate, and 16.7% gave heparin. The rapid troponin T test is extremely useful for cardiac emergency triage and therapeutic decision making. There is a requirement for practical guidelines for the primary therapeutic decisions for patients with suspicious acute coronary syndrome.     

A rapid troponin I assay is not optimal for determination of troponin status and prediction of subsequent cardiac events at suspicion of unstable coronary syndromes

BACKGROUND: Troponin is a specific marker of myocardial damage. For early prediction of coronary events in patients with suspicion of acute coronary syndromes the assay also needs to be highly sensitive. METHODS AND RESULTS: A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial. A quantitative troponin T analysis was later performed on blood samples obtained at randomization by a central laboratory. There was an agreement between the rapid troponin I assay and troponin T (< or =/>0.1 microg/l) in 3596 (80.9%) patients. A positive rapid troponin I was identifying any elevation of troponin T (>0.01 microg/l) in 1990 patients (90.4%) whereas a negative rapid troponin I was corresponding to negative troponin T (< or =0.01 microg/l) in only 1217 patients (54.2%). Patients with a positive versus negative rapid troponin I had an increased risk of death or myocardial infarction at 30 days (9.3 vs. 5.9%; odds ratio, O.R. 1.64; 95% confidence interval, 1.31-2.06). Troponin T elevation (>0.1 microg/l) provided a better (10.5 v. 4.9%, O.R. 2.26; C.I. 1.79-2.85) risk stratification. Regardless of a positive or a negative rapid troponin I, the troponin T result (>0.1 vs. < or =0.1 microg/l) stratified the patients into high and low risk of events at 30 days, (10.3 vs. 5.7%, P=0.002) and (11.5 vs. 4.8%, P<0.001), respectively. CONCLUSION: In a population with non-ST elevation acute coronary syndrome a positive rapid troponin I assay is a specific indicator of troponin elevation and a predictor of early outcome. However, a negative rapid troponin I is not a reliable indicator of the absence of myocardial damage and does not indicate a low risk of subsequent cardiac events. A rapid troponin I assay was performed prior to inclusion in 4447 acute coronary syndrome patients in the GUSTO-IV trial and related to a centrally analyzed quantitative troponin T test. A positive rapid troponin I was well corresponding to any elevation of troponin T (>0.01 microg/l) and predicted an unfavorable outcome at 30 days. However, a negative rapid troponin I was corresponding to troponin T < or =0.01 microg/l in only half of the patients. Troponin T >0.1 microg/l vs. < or =0.1 microg/l provided a better risk stratification than the rapid troponin I result. For patients with troponin T elevation (>0.1 microg/l) the 30 day event rate was high regardless of the rapid troponin I result.     

Acute heart failure in the emergency department: a follow-up study

Acute heart failure (AHF) is a major public health issue due to high incidence and poor prognosis. Only a few studies are available on the long-term prognosis and on outcome predictors in the unselected population attending the emergency department (ED) for AHF. We carried out a 1-year follow-up analysis of 1234 consecutive patients from selected Italian EDs from January 2011 to June 2012 for an episode of AHF. Their prognosis and outcome-associated factors were tested by Cox proportional hazard model. Patients’ mean age was 84, with 66.0 % over 80 years and 56.2 % females. Comorbidities were present in over 50 % of cases, principally a history of acute coronary syndrome, chronic obstructive pulmonary disease, diabetes, chronic kidney disease, valvular heart disease. Death occurred within 6 h in 24 cases (1.9 %). At 30-day follow-up, death was registered in 123 cases (10.0 %): 110 cases (89.4 %) died of cardiovascular events and 13 (10.6 %) of non-cardiovascular causes (cancer, gastrointestinal hemorrhages, sepsis, trauma). At 1-year follow-up, all-cause death was recorded in 50.1 % (over 3 out of 4 cases for cardiovascular origin). Six variables (older age, diabetes, systolic arterial pressure <110 mm/Hg, high NT pro-BNP, high troponin levels and impaired cognitive status) were selected as outcome predictors, but with limited discriminant capacity (AUC = 0.649; SE 0.015). Recurrence of AHF was registered in 31.0 %. The study identifies a cluster of variables associated with 1-year mortality in AHF, but their predictive capacity is low. Old age and the presence of comorbidities, in particular diabetes are likely to play a major role in dictating the prognosis.     

急性冠状动脉综合征患者C-反应蛋白升高与远期死亡率和心力衰竭的相关性分析

目的评估C-反应蛋白(CRP)与急性冠状动脉综合征(ACS)患者远期预后的相关性。方法收集我院急诊ACS患者的资料并检测其CRP水平。入选患者随访3年,内容包括死亡,因急性心肌梗死(AMI)和充血性心力衰竭(CHF)而再次住院情况。结果共有446名患者入选,CRP升高的患者的死亡率和因CHF的再次住院率均高于CRP正常的患者(P<0.05)。校正心肌肌钙蛋白T(cTnT)水平后,急性期CRP>7.44 mg/L与发病后3年内的死亡率和因CHF再住院的风险增加仍显著相关。结论在胸痛早期就出现CRP升高的ACS患者的晚期死亡率和CHF风险增加。     

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.

Prognostic usefulness of marginal troponin T elevation

Marginal elevations of troponin T among patients with chest pain are often considered to be insignificant. We sought to define the prognostic value of marginal troponin T elevations in patients presenting to the emergency department with suspected myocardial ischemia. Four hundred twenty-eight consecutive patients presenting to the emergency department with ongoing chest pain were evaluated, followed through their hospital course, and contacted for follow-up 4 months after discharge. Two hundred ninety-nine patients had undetectable troponin T levels (<0.01 microg/L), 76 had marginal troponin T elevations (0.01 to 0.09 microg/L), and 53 had frank troponin T elevations (> or =0.1 microg/L). Patients with either marginally or frank elevated troponin levels were older and more likely to be men, but did not differ from patients with undetectable troponin levels with regard to the prevalence of coronary artery disease risk factors, history of coronary disease, or race. While in the hospital, the undetectable and marginal troponin groups were referred for cardiac testing in equal proportions (58% and 59%, respectively), whereas 87% of the elevated group underwent further testing. After adjustment for possible confounders, a significantly increased rate of death/myocardial infarction/revascularization was observed in the marginal troponin group compared with the undetectable troponin group (p = 0.004). Marginal elevations of troponin T identified a currently underevaluated high-risk subgroup of patients with suspected myocardial ischemia who are more likely to have adverse clinical outcomes than those with undetectable troponin levels.     

Mild troponin elevation in patients admitted to the emergency department with atrial fibrillation: 30-day post-discharge prognostic significance

Patients with atrial fibrillation (AF) often undergo troponin (Tn) testing in the emergency department (ED), but the clinical significance of mildly elevated values remains unclear. We evaluated short-term 30-day post-discharge outcomes in AF patients according to troponin levels. Out of 2181 AF patients evaluated in the ED (June 2014 to June 2015), we included consecutive admitted patients. Patients were grouped into those with normal Tn values (≤ 0.05 ng/mL), mild elevations (> 0.05–0.5 ng/mL, 10× URL) and marked elevations (> 0.5 ng/mL). Outcomes included acute coronary syndrome (ACS), revascularization, all-cause mortality and combined end point; the secondary outcome was ischemic stroke. A total of 348 patients (90.9%) had Tn testing, which was associated with longer in-hospital stay (median 2.04 vs. 0.74 days in unmeasured Tn, p = 0.014); 37.1% did not have clinical suspicion of ACS. Mild Tn elevation occurred in 19.0% and 6.3% had markedly elevated values. Compared to normal values, mild elevations had higher absolute incidence, without statistical significance, of ACS (1.5 vs. 0.0%, p = 0.202), revascularization (1.5 vs. 0.0%, p = 0.202), all-cause mortality (12.1 vs. 6.9%, p = 0.200), combined end point (13.3 vs. 6.9%, p = 0.084) or ischemic stroke (4.5 vs. 2.3%, p = 0.394). Tn testing is routine in admitted AF patients, even without suspicion of ACS, and is associated with prolonged stay. Mild Tn elevation is associated with a nonsignificant trend toward higher adverse events. Larger-scale studies are needed to evaluate the cost-effectiveness of Tn testing for prognosis in admitted AF patients, as this prolongs stay and has unclear impact on patient management.     

The HEART score with high-sensitive troponin T at presentation: ruling out patients with chest pain in the emergency room

The HEART score is a simple scoring system, ranging from 0 to 10, specifically developed for risk stratification of patients with undifferentiated chest pain. It has been validated for the conventional troponin, but not for high-sensitive troponin. We assess a modified version of the HEART score using a single high-sensitivity troponin T dosage at presentation, regardless of symptom duration, and with different ECG criteria to evaluate if the patients with a low HEART score could be safely discharged early. The secondary aim was to confirm a statistically significant difference in each HEART score group (low 0–3, intermediate 4–6, high 7–10) in the occurrence of major adverse cardiac events at 30 and 180 days. We retrospectively analyzed the HEART score of 1597 consecutive patients admitted to the Emergency Department of our Hospital for chest pain between January 1 and June 30, 2014. Of these, 190 did not meet the inclusion criteria and 29 were lost to follow-up. None of the 512 (37.2 %) patients with a low HEART score had an event within 180 days. The difference between the cumulative incidences of events in the three HEART score groups was statistically significant (P < 0.0001). We demonstrate that it might be possible to safely discharge Emergency Department chest pain patients with a low modified HEART score after an initial determination of high-sensitive troponin T, without a prolonged observation period or an additional cardiac testing.     

Causes of Troponin Elevation and Associated Mortality in Young Patients

Background

While increased serum troponin levels are often due to myocardial infarction, increased levels may also be found in a variety of other clinical scenarios. Although these causes of troponin elevation have been characterized in several studies in older adults, they have not been well characterized in younger individuals.

Predictors of left main or three-vessel disease in patients who have acute coronary syndromes with non-ST-segment elevation

To identify an early, simple, noninvasive predictor of left main (LM) or 3-vessel disease (3-VD), we retrospectively studied clinical variables on admission in 310 patients with acute coronary syndromes with non-ST-segment elevation. Univariate analysis indicated that many factors were related to LM/3-VD. Multivariate analysis showed that ST-segment elevation in lead aVR of >/=0.5 mm was the strongest predictor of LM/3-VD, followed by positive troponin T (odds ratio 19.7, p <0.001, and odds ratio 3.08, p = 0.048, respectively). ST-segment elevation in lead aVR of >/=0.5 mm and positive troponin T identified LM/3-VD with sensitivities of 78% and 62%, specificities of 86% and 59%, positive predictive values of 57% and 26%, and negative predictive values of 95% and 87%, respectively (p <0.05). Our findings suggest that in patients with non-ST-segment elevation acute coronary syndromes, ST-segment elevation in lead aVR of >/=0.5 mm and positive troponin T on admission (especially the former) are useful predictors of LM/3-VD.     

The prognostic value of markers of inflammation in patients with troponin T-negative chest pain before discharge from the emergency department

PURPOSE: To assess the prognostic value of markers of inflammation for rule-out purposes in patients admitted to the emergency department with troponin T-negative chest pain. METHODS: Patients presenting to the emergency department within 6 hours of symptom onset and who had a normal or nondiagnostic electrocardiogram were eligible. The standard rule-out protocol, which included serial creatine kinase and creatine kinase-MB measurements, was applied, and markers of inflammation (C-reactive protein, erythrocyte sedimentation rate, and total white blood cell count and differential count) were measured. The study group comprised patients with negative serial troponin T results (<0.06 microg/L) who were discharged home after unstable coronary artery disease was ruled out. Endpoints during the 6-month follow-up were cardiac death, myocardial infarction, or rehospitalization for unstable angina. RESULTS: A total of 382 troponin T-negative patients were discharged, of whom 2 died, 2 had a myocardial infarction, and 7 were rehospitalized for unstable angina. A positive C-reactive protein test result (>0.3 mg/dL) was associated with future clinical events (hazard risk [HR] = 4.5; 95% confidence interval [CI]: 1.2 to 17.0; P = 0.03), as was a positive test (>13 mm/h) for erythrocyte sedimentation rate (HR = 5.6; 95% CI: 1.5 to 22.2; P = 0.01). Patients with positive results for both tests were at highest risk of clinical events (9.3%) compared with patients with other combinations of test results (1.1% to 2.1%; HR = 7.5; 95% CI: 2.2 to 25.5; P = 0.001). CONCLUSION: The combination of C-reactive protein and erythrocyte sedimentation rate had prognostic value in patients with troponin T-negative chest pain and a normal or nondiagnostic electrocardiogram in whom unstable coronary artery disease was ruled out.     

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.