Prognostic significance of troponin T elevation in patients without chest pain

Increased cardiac troponin with chest pain is important for the diagnosis, triage, and treatment of patients in the emergency department. However, the use of troponin for the diagnosis and triage of patients without chest pain is poorly established. The aim of this study was to determine 30-day and 1-year mortality and morbidity of troponin T increases in patients without chest pain. This retrospective study compared 92 hospitalized patients without (study group) and 91 patients with chest pain (control group), followed up for 1 year. Study group patients had troponin T >0.04 mug/L, normal creatine kinase or creatine kinase-MB fraction <5%, and no electrocardiographic ischemia. Excluded were high-risk patients with end-stage kidney disease, those with left ventricular ejection fraction <40%, and the critically ill. Outcome variables included 30-day and 1-year death, myocardial infarction, unstable angina, and coronary revascularization rates. Thirty-day (13.0% vs 4.4%; p = 0.032) and 1-year (33% vs 4.6%; p <0.001) mortality rates were significantly higher in the study group, whereas myocardial infarction, unstable angina, and revascularization were infrequent. In conclusion, patients with increased troponin T and no chest pain had a high mortality rate and required careful follow-up.     

Implication of different cardiac troponin I levels for clinical outcomes and prognosis of acute chest pain patients

OBJECTIVES: We compared outcomes in patients with non-ST-segment elevation acute coronary syndromes (ACS) according to the degree of cardiac troponin I (cTnI) elevation. BACKGROUND: Controlled trials of high-risk patients have found that troponin elevations identify an even higher risk subset. It is unclear whether outcomes are similar among a lower risk, heterogeneous patient group. Also, few studies have reported outcomes other than myocardial infarction (MI) or death, based on the peak troponin value. METHODS: Consecutively, admitted patients without ST-segment elevation on the initial electrocardiogram underwent serial marker sampling using creatine kinase (CK), CK-MB fraction, and cTnI. Patients were grouped according to peak cTnI: negative = no detectable cTnI; low = peak greater than the lower limit of detectability but less than the optimal diagnostic value; intermediate = peak greater than or equal to the optimal diagnostic value but less than the manufacturer's suggested upper reference limit (URL); and high = peak greater than or equal to the URL. Thirty-day outcomes included cardiac death, MI based on CK-MB, revascularization, significant disease, and a reversible defect on stress testing. Six-month mortality was also determined. Negative evaluations for ischemia included nonsignificant disease, no reversible stress defect, and negative rest perfusion imaging. RESULTS: Of the 4,123 patients admitted, 893 (22%) had detectable cTnI values. Cardiac events and positive test results at 30 days and 6-month mortality increased significantly with increasing cTnI values. Negative evaluations for ischemia were significantly and inversely related to peak cTnI values. Although adverse events were significantly more common in patients with a low cTnI value than in those with negative cTnI, negative evaluations for ischemia were frequent. CONCLUSIONS: Increased cTnI values are associated with worse outcomes. Although low cTnI values are associated with adverse events, they do not have the same implication as higher cTnI values, and nonischemic evaluations are frequent.     

非特异性胸痛患者运动试验前后血清心肌肌钙蛋白I水平的变化

目的探讨以非特异性胸痛(ACP)患者运动负荷前、后血清心肌肌钙蛋白I(cTnI)值的变化,间接推断其是否存在心脏微血管病变的可能性.方法冠状动脉造影结果正常的ACP患者33例,健康正常人17例和冠心病心绞痛患者16例,均进行运动平板试验,并分别于运动前,运动后1小时、24小时进行血清cTnI浓度、CK值和LDH值的测定.结果ACP组中运动试验阳性者及冠心病心绞痛组患者运动后1小时及24小时血清cTnI浓度明显升高(P<0.01及 P<0.05),提示ACP组运动试验阳性者可能存在心脏微血管病变;ACP组中运动试验阴性者运动前、后血清cTnI浓度的变化无显著性差异.在冠心病心绞痛组患者中,运动试验后1小时血清cTnI浓度随患者病变程度的加重而逐渐增加,且变化有显著性差异(P<0.05).结论ACP患者运动负荷前后血清cTnI值的检测有助于间接推断患者是否存在心脏微血管病变,且其升高程度可以间接反映冠状动脉的病变程度.     

Evaluation of the Emergency Department chest pain patient

Patients presenting to the Emergency Department with chest pain are common and often present diagnostic difficulties. Because of the limitations of the initial evaluation, the majority of patients are admitted, although many are later found to have noncardiac causes for their symptoms. Recognition of these limitations has driven the investigation of newer evaluation techniques and protocols in an attempt to improve diagnostic sensitivity without increasing overall costs. These have included modifications of the standard ECG, and use of newer myocardial markers such as mass assays for CK-MB and troponin T and I. Use of acute rest myocardial perfusion imaging has also been shown to be a highly valuable technique for risk stratification of the intermediate- to low-risk chest pain patient.     

Clinical impact of the troponin 99th percentile cut-off and clinical utility of myoglobin measurement in the early management of chest pain patients admitted to the Emergency Cardiology Department

OBJECTIVE: To verify the clinical impact of different low cut-offs for troponin I/cardiac troponin I (99th percentile to 10% CV) and for myoglobin, in early risk stratification of patients with suspected acute coronary syndrome. METHODS: A total of 516 consecutive non-ST-elevation patients admitted to hospital were followed. The first measurement of cardiac markers was performed at the point-of-care in the Emergency Cardiology Department, using Stratus CS. The lowest cardiac troponin I concentration with a CV0.07 microg/l in the Emergency Cardiology Department (P>0.05). Using lowering cut-off values, the difference between the fraction of patients that was positive compared with the diagnosis according to European Society of Cardiology and American College of Cardiology criteria and had remained statistically significant (P<0.05) up to 0.03 microg/l (99th percentile upper reference limit) was considered (85 patients, 16.5%, n.s.). Relative operating characteristic analysis confirmed that the best clinical cut-off was related to the cardiac troponin I concentration that meets the 99th percentile upper reference limit. The diagnostic accuracy of myoglobin in detecting the minimum cardiac damage was significantly lower, independently from the cut-offs considered. CONCLUSION: The diagnostic accuracy in detecting myocardial damage early in the Emergency Cardiology Department improves when the 99th percentile is used as a decisional value of cardiac troponin I; the use of this cut-off makes the measurement of myoglobin unnecessary.     

Symptomatic myocardial infarction without chest pain: Prevalence and clinical course

Symptomatic myocardial infarction without chest pain was identified in 26 of 102 patients (25.5 percent) admitted to the hospital with acute myocardial infarction. As a group, these patients had a significantly lesser prevalence of a history of angina (P < 0.05) and cigarette smoking (P < 0.01). Their mean age was 69.1 years compared with 58.7 years for patients with chest pain (P < 0.001). The group had a significantly greater median delay between the onset of symptoms and (1) arrival at the hospital (P < 0.05), (2) examination by a physician in the emergency room (P < 0.05), (3) diagnosis of possible myocardial infarction (P < 0.001), and (4) transfer from the emergency room to the intensive care unit (P < 0.001). They had significantly higher admission values for mean heart rate, respiratory rate, temperature and white blood cell count and more frequent in-hospital complications of pneumonia (P < 0.001) and cardiogenic shock (P < 0.05). Mortality in the group was 50 percent compared with 18 percent in the group with chest pain (P < 0.05). Discriminant function analysis identified an at-risk population with 80 percent reliability.     

Characteristics of elevated cardiac troponin I in patients with acute ischemic stroke

Objective To study prognostic characteristics of cardiac troponin I (cTnI) elevation in acute ischemic stroke. Methods We retrospectively studied patients (n = 248) with acute ischemic stroke, acute ST-segment elevation myocardial infarction, and acute non-ST-elevation myocardial infarction who were treated between January 2013 and October 2015. Baseline demographic data and changes in cTnI levels among these three groups were compared. Patients with acute ischemic stroke were assigned to either the cTnI elevation group (cTnI > 0.034 ng/mL) or the no cTnI elevation group (cTnI ≤ 0.034 ng/mL). Logistic regression analysis was used to identify risk factors associated with elevated serum cTnI in patients with acute ischemic stroke. Moreover, the duration of hospital stay and incidence of major cardiovascular outcomes were compared in patients with acute ischemic stroke, with or without elevated cTnI. Results In this study population of patients with acute ischemic stroke (n = 178), acute ST-segment elevation myocardial infarction (n = 35), and acute non-ST-elevation myocardial infarction (n = 35), patients with acute ischemic stroke with elevated cTnI comprised 18.54% of subjects. Patients with elevated cTnI were older and more likely to have a history of hypertension. In addition, these patients had higher levels of inflammatory markers, reduced renal functions, increased D-dimer levels, higher NIH stroke scores, and lower left ventricular ejection fractions. Logistic regression analysis showed that both percentage of neutrophil and NIH stroke scores were elevated; estimated glomerular filtration rate and left ventricular ejection fraction were decreased in patients with acute ischemic stroke who had elevated cTnI, and they had more frequent major cardiovascular events during hospital stay. Conclusion Elevated cTnI detected in patients with acute ischemic stroke, indicated a greater likelihood of poor short-term prognosis during hospital stay.     

Prognostic value of myocardial contrast echocardiography in patients presenting to hospital with acute chest pain and negative troponin

We hypothesized that myocardial contrast echocardiography (MCE) could be used to stratify risk in patients with suspected acute coronary syndrome but a nondiagnostic electrocardiogram and negative troponin. Pretest Thrombolysis In Myocardial Infarction (TIMI) scores were determined. Exercise electrocardiographic data in those patients undergoing treadmill stress echocardiography as part of risk evaluation were analyzed independently of echocardiographic data. On a separate day, low-power MCE at rest and during vasodilator stress was performed. All patients were followed for cardiac events (cardiac death, myocardial infarction, and revascularization). Of 148 patients, 27 demonstrated abnormal myocardial contrast echocardiographic results and had higher cardiac event rates compared with those with normal myocardial contrast echocardiographic findings (59% vs 7%, p <0.0001) at follow-up (8 +/- 5 months). Hard cardiac event rates (death and nonfatal myocardial infarction) were low (3%) in patients with normal myocardial contrast echocardiographic findings. Cardiac events in patients with abnormal myocardial contrast echocardiographic findings (59%) were significantly higher than those predicted by a high-risk TIMI score (33%, p = 0.0023) and compared with those predicted by high-risk exercise electrocardiography (80% vs 57%, p = 0.0003). In conclusion, stress MCE was superior to TIMI risk score and exercise electrocardiography in the assessment of risk in patients with suspected acute coronary syndrome, nondiagnostic electrocardiogram, and negative troponin.     

Superiority of combined CK-MB and troponin I measurements for the early risk stratification of unselected patients presenting with acute chest pain

BACKGROUND: Recent studies have suggested that positive troponin I tests are associated with an increased risk of cardiac death during short-term follow-up. However, it is unknown if troponin I tests alone or in addition to CK-MB measurements are superior to predict unfavorable outcome during long-term follow-up. PATIENTS AND METHODS: In a prospective, double-blind study we assessed the prevalence and prognostic value of combined troponin I and CK-MB tests in an unselected cohort of patients (n = 292) admitted to the emergency department for acute chest discomfort. Patients were grouped according to the diagnosis on discharge in those with acute myocardial infarction (1), unstable angina (2), and noncardiac chest pain (3). Six months after enrollment, death rates were obtained and follow-up interviews were performed with respect to survival, recurrence of chest pain, and myocardial infarction. RESULTS: In patients with evidence of coronary heart disease, the mortality rate for abnormal troponin I and normal CK-MB levels was 5.0%. Baseline troponin I and elevated CK-MB levels were associated with a mortality rate of 4.0%. However, the mortality rate was significantly higher (11.1%) in patients presenting with elevated troponin I and CK-MB values. In patients without myocardial infarction on admission, 10.5% with positive troponin I tests died compared to 1.6% with negative tests. The mortality rate in patients without myocardial infarction was 2.7% for patients with elevated CK-MB but normal troponin I values. In patients with both markers elevated a significantly higher mortality rate (16.7%) was found, representing a 6-fold increase in the death event rate. With the additional knowledge of troponin I values, it could be demonstrated that certain cases were misclassified as having noncardiac chest pain. At least some of the latter patients with above-normal values of troponin I were retrospectively to be reclassified as unstable angina. Acute non-Q-wave myocardial infarctions were occasionally misdiagnosed as either angina pectoris or nonischemic chest pain. CONCLUSIONS: Our data suggest the superiority of combined CK-MB and troponin I measurements in clinical practice for the early risk stratification of patients presenting with acute chest pain. In nonmyocardial infarctions, both CK-MB and troponin I convey independent prognostic information with regard to fatal outcome. Troponin I tests in addition to CK-MB measurements contribute to a lower rate of misdiagnoses.     

Prognostic significance of an elevated creatine kinase in the absence of an elevated troponin I during an acute coronary syndrome

In patients with troponin-negative acute coronary syndromes, creatine kinase (CK)-MB elevation predicts a significantly higher risk of death and major acute cardiac events compared with CK-MB negative patients. This risk is accentuated in troponin-negative, CK-MB positive patients who do not demonstrate ST elevation by electrocardiogram.     

Prevalence of increased cardiac troponin I levels in patients with and without acute pulmonary embolism and relation of increased cardiac troponin I levels with in-hospital mortality in patients with acute pulmonary embolism

Cardiac troponin I levels were increased in 24 of 147 patients (16%) with documented acute pulmonary embolism and in 20 of 594 patients (3%) without pulmonary embolism (p <0.001). In patients with acute pulmonary embolisms, 8 of 24 (33%) with increased cardiac troponin I levels and 9 of 123 (7%) with normal cardiac troponin I levels died during hospitalization (p <0.001).     

Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes

OBJECTIVES

We prospectively evaluated the relation between cardiac troponin T (cTnT) level, the presence and severity of coronary artery disease (CAD) and long-term prognosis in patients with chest pain but no ischemic electrocardiographic (ECG) changes who had short-term observation.

BACKGROUND

Cardiac TnT is a powerful predictor of future myocardial infarction (MI) and death in patients with ECG evidence of an acute coronary syndrome. However, for patients with chest pain with normal ECGs, it has not been determined whether cTnT elevation is predictive of CAD and a poor long-term prognosis.

METHODS

In 414 consecutive patients with no ischemic ECG changes who were triaged to a chest pain unit, cTnT and creatine kinase, MB fraction (CK-MB) were evaluated ≥10 h after symptom onset. Patients with adverse cardiac events, including death, MI, unstable angina and heart failure were followed for as long as one year.

RESULTS

A positive (>0.1 ng/ml) cTnT test was detected in 37 patients (8.9%). Coronary artery disease was found in 90% of 30 cTnT-positive patients versus 23% of 144 cTnT-negative patients who underwent angiography (p < 0.001), with multivessel disease in 63% versus 13% (p < 0.001). The cTnT-positive patients had a significantly (p < 0.05) higher percent diameter stenosis and a greater frequency of calcified, complex and occlusive lesions. Follow-up was available in 405 patients (98%). By one year, 59 patients (14.6%) had adverse cardiac events. The cumulative adverse event rate was 32.4% in cTnT-positive patients versus 12.8% in cTnT-negative patients (p = 0.001). After adjustment for baseline clinical characteristics, positive cTnT was a stronger predictor of events (chi-square = 23.56, p = 0.0003) than positive CK-MB (>5 ng/ml) (chi-square = 21.08, p = 0.0008). In a model including both biochemical markers, CK-MB added no predictive information as compared with cTnT alone (chi-square = 23.57, p = 0.0006).

CONCLUSIONS

In a group of patients with chest pain anticipated to have a low prevalence of CAD and a good prognosis, cTnT identifies a subgroup with a high prevalence of extensive and complex CAD and increased risk for long-term adverse outcomes.     

Prognostic value of troponin T, myoglobin, and CK-MB mass in patients presenting with chest pain without acute myocardial infarction.

OBJECTIVE: To assess the prognostic value of minor myocardial damage in patients presenting with chest pain without myocardial infarction. DESIGN: The relative risk of suffering a cardiac event in the next six months was assessed in patients with minor myocardial damage assessed by the cardiac markers CK-MB, myoglobin, and troponin T. SETTING: Emergency department of a large university hospital. PATIENTS: In 128 consecutive patients with chest pain, acute myocardial infarction (by WHO criteria) was ruled out; of these, 39 had a rise and fall of one or more markers, indicating minor myocardial damage. The presence of a documented history of coronary artery disease was assessed on admission. RESULTS: 24 patients had a subsequent event (cardiac death, acute myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting) in the next six months. An abnormal troponin T predicted a subsequent event while abnormal CK-MB or myoglobin did not. The relative risk for troponin T was 2.8 (95% confidence interval: 1.0 to 7.9), for myoglobin 1.0 (0.3 to 3.2), and for CK-MB 0.9 (0.2 to 3.4). A documented history of coronary artery disease predicted subsequent events with a relative risk of 3.9 (1.3 to 11.3). CONCLUSIONS: Troponin T was the only marker that predicted future events, but a documented history of coronary artery disease was the best predictor in patients in whom an acute myocardial infarction had been ruled out.