不稳定心绞痛患者血浆肌钙蛋白T水平与冠状动脉病变程度及预后的关系

目的:探讨不稳定心绞痛(UA)患者血浆肌钙蛋白T(cTnT)水平与冠状动脉病变程度及预后的关系。方法:400例UA患者根据cTnT是否阳性分为cTnT阳性组(221例),cTnT阴性组(179例),在住院期间行冠脉造影(CAG)并观察其心脏事件的发生情况,对比分析两组UA患者的冠状动脉造影特点及预后。结果:cTnT阳性组冠状动脉造影阳性率为89.1%,3支病变发生率46.2%,冠脉内血栓形成者为21.8%,均明显高于cTnT阴性组;cTnT阳性组cTnT水平与冠状动脉的狭窄程度有相关性,cTnT阳性组近期(30 d)心脏事件发生率37.8%,亦明显高于cTnT阴性组,且两组对比有显著差异。结论:cTnT阳性的UA患者复杂病变多,冠脉内血栓形成率高,预后较差,cTnT水平越高,冠脉狭窄越重。     

Prognostic significance of admission cardiac troponin T in patients treated successfully with direct percutaneous interventions for acute ST-segment elevation myocardial infarction

BACKGROUND: Cardiac troponin T (cTnT) elevations at admission indicate a high-risk subgroup of patients with acute ST-segment elevation myocardial infarction, possibly due to a higher failure rate of reperfusion therapies. OBJECTIVE: We sought to determine the predictive role of admission cTnT in patients with ST-segment elevation myocardial infarction undergoing successful direct percutaneous coronary intervention. METHODS: A total of 218 consecutive patients with ST-segment elevation myocardial infarction were enrolled. Patients were stratified according to admission cTnT and infarct location. They were followed prospectively for short-term and long-term outcomes.RESULTS A positive cTnT (47.7%) was associated with higher mortality rates at 30 days (14.4% vs. 3.5%, p = .003) and 12 months (17.3% vs. 4.4%, p =.007). cTnT allowed discrimination of patients at high and low risk for cardiac death at 30 days and 12 months among anterior (19.2% vs. 7.9%, p = .19, and 25% vs. 13.2%, p = .22, respectively) and, more impressively, among nonanterior acute myocardial infarction (9.6% vs. 1.3%, p = .04, and 11.5% vs. 1.3%, p = .017, respectively). In multivariate analysis, older age, anterior infarct location, and depressed left ventricular function were the most potent independent predictors of future risk. Among clinical variables available at admission, cTnT indicated independently a higher risk of cardiac death (odds ratio, 3.1 [1.07-9.01], p =.038). This increased risk associated with a positive cTnT was almost independent of time delays from onset of symptoms to admission (3.8 vs. 2.3 hrs in cTnT-positive vs. cTnT-negative patients, p <.001). CONCLUSIONS: Admission cTnT is a strong predictor of future cardiac risk in patients with ST-segment elevation myocardial infarction, despite successful restoration of Thrombolysis in Myocardial Infarction grade 3 coronary flow by direct percutaneous coronary intervention.     

Angiographic correlates of a positive troponin T test in patients with unstable angina

OBJECTIVE: To study the angiographic correlates of cardiac troponin T (cTnT)-positive and -negative patients with unstable angina pectoris. BACKGROUND: A positive cTnT test identifies a high-risk subgroup of unstable angina pectoris patients. Only the high-risk cTnT-positive patients seem to benefit from a more aggressive antithrombotic treatment regimen. The underlying coronary pathology in cTnT-positive and -negative patients that explains the predictive power of cTnT on prognosis and response to antithrombotic therapy is largely unknown. METHODS: A total of 197 subsequently admitted patients with unstable angina pectoris underwent cTnT testing by a rapid bedside assay and early qualitative and quantitative angiography. Long-term follow-up was 12 months. RESULTS: Patients with cTnT-positive tests revealed more critical stenoses of culprit lesions (p =.041), more severe reductions of thrombolysis in myocardial infarction flow grades (p <.037), a higher prevalence of intracoronary thrombus (p =.079), and a poorer left ventricular function (p =.047). The odds ratio of cTnT was 5.8 (p <.0001) for presence of thrombus, reduced thrombolysis in myocardial infarction flow, and/or critical stenosis (>90%), and was 3.1 (p =.005) for presence of three-vessel disease, left main disease, and/or reduced left ventricular ejection fraction. Coronary bypass grafting was more frequently performed in the cTnT-positive group. However, event-free survival was not different in our cohort characterized by a high rate of percutaneous coronary interventions. CONCLUSIONS: A positive cTnT test in patients with unstable angina pectoris indicates presence of more severe coronary artery disease and poorer left ventricular function. This finding could explain the differences in short- and long-term outcome and treatment responses to antithrombotic regimens.     

Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.     

cTnT与CK--MB在胸痛危险分层中的作用

目的评价心肌肌钙蛋白T(cTnT)与肌酸激酶同工酶-MB(CK-MB)蛋白量在胸痛危险分层中的作用。方法对所有病例进行12h床边动态监测，包括基线、4、8、12h的连续心律监测和12导联心电图(ECG)测试；与此同时分别于基线、4、8、12h对入选胸痛组的其中383例患者测定cTnT、CK-MB。结果383例CPU患者只有8例(2．1％)CK-MB阳性，39例cTnT阳性。cTnT状态与随访的结果表明，cTnT阳性明显早于CK-MB。89％cTnT阳性患者血管造影术显示发生冠状动脉疾病(CAD)及多支血管病。结论cTnT比CK-MB在评估伴心肌坏死和多支血管病的胸痛危险分层中具有更高的敏感性与特异性；常规测定cTnT更便于胸痛的危险分层与处理。     

Risk stratification of chest pain patients by point-of-care cardiac troponin T and myoglobin measured in the emergency department

A prospective multicenter study including 1410 chest pain patients with suspected acute coronary syndromes was carried out to examine the predictive value of biological cardiac markers for adverse events measured by a point-of-care system. Admission cardiac troponin T (cTnT) and myoglobin were measured in parallel on a point-of-care system in the emergency department and -- together with CK-MB mass -- on lab analyzers. In a one-year follow-up, cardiac and non-cardiac death, acute myocardial infarction, unstable angina pectoris and need for revascularization were registered. Median time between onset of symptoms and admission was 285 min; 172 patients (12.2%) had no event during follow-up. If the cTnT, measured either by the point-of-care system or a conventional lab analyzer, was >0.05 microg/L, then the chance of a cardiac event during the follow-up period was doubled (18% vs. 9%). Serial cTnT measurement did not add any further value to the predictive power of the admission cTnT. Myoglobin and CK-MB mass identified increasing risk with increasing concentration quartiles; cardiac event rates were 2.8- to 4.4-fold higher between the quartiles with the lowest and those with the highest analyte concentration, respectively. There was no difference in non-cardiac death rates between any concentration quartiles. In conclusion, the prediction of clinical events by cardiac troponin T and myoglobin measured with a point-of-care analyzer in the emergency department was as good as that of the same cardiac markers and CK-MB mass measured on lab analyzers.     

Role of "Ischemia modified albumin", a new biochemical marker of myocardial ischaemia, in the early diagnosis of acute coronary syndromes

Background: Diagnosis of cardiac ischaemia in patients attending emergency departments (ED) with symptoms of acute coronary syndromes is often difficult. Cardiac troponin (cTn) is sensitive and specific for the detection of myocardial damage but may not rise during reversible myocardial ischaemia. Ischemia Modified Albumin (IMA) has recently been shown to be a sensitive and early biochemical marker of ischaemia. Methods and Results: This study evaluated IMA in conjunction with ECG and cTn in 208 patients presenting to the ED within three hours of acute chest pain. At presentation, a 12-lead ECG was recorded and blood taken for IMA and cardiac troponin T (cTnT). Patients underwent standardised triage, diagnostic procedures, and treatment. Results of IMA, ECG, and cTnT, alone and in combination, were correlated with final diagnoses of non-ischaemic chest pain, unstable angina, ST segment elevation, and non-ST segment elevation myocardial infarction. In the whole patient group, sensitivity of IMA at presentation for an ischaemic origin of chest pain was 82%, compared with 45% of ECG and 20% of cTnT. IMA used together with cTnT or ECG, had a sensitivity of 90% and 92%, respectively. All three tests combined identified 95% of patients whose chest pain was attributable to ischaemic heart disease. In patients with unstable angina, sensitivity of IMA used alone was equivalent to that of IMA and ECG combined. Conclusions: IMA is highly sensitive for the diagnosis of myocardial ischaemia in patients presenting with symptoms of acute chest pain.     

心肌肌钙蛋白Ⅰ和肌钙蛋白T对急性缺血性心脏病预后相关性分析

目的探讨心肌肌钙蛋白I(cTnI)和肌钙蛋白T(cTnT)对急性缺血性心脏病转归的影响。方法对就诊的急性缺血性心脏病患者定性测定入院时及距胸痛发作间隔10h的cTnI和定量测定相同时点的cTnT。同时随访患者发病后1、3、6、12个月的疾病转归,以心绞痛、心肌梗死、心力衰竭、心源性猝死为终点评价指标。结果cTnI或cTnT异常患者与正常者相比较,不稳定型心绞痛、心肌梗死、心力衰竭、心源性猝死的发生率具有显著性差异(P<0.01)。cTnI或cTnT异常与终点事件(不稳定型心绞痛、心肌梗死、心力衰竭、心源性心源性猝死)发生率呈正相关。结论cTnI或cTnT对急性心肌梗死,尤其是微小心肌坏死诊断具有高度的敏感性和特异性,并与急性缺血性心脏病的预后密切相关。     

The effect of elevated serum soluble CD40 ligand on the prognostic value in patients with acute coronary syndromes

BACKGROUND: Increasing evidence shows that high expression of CD40L plays an important role in the pathogenesis of atherosclerosis and coronary artery disease. We evaluated the clinical predictive value of increased serum soluble CD40 ligand (CD40L) in patients with acute coronary syndromes (ACS) and acute chest pain. METHODS: Serum levels of soluble CD40 ligand were measured by ELISA in 128 patients with ACS and in 68 patients with acute chest pain. Platelet activation was assessed by flow cytometry. RESULTS: The levels of soluble CD40 ligand were increased in 57.8% patients with ACS (>8.0 ng/ml) and in 35 patients with acute chest pain (>8.0 ng/ml), respectively. The level of soluble CD40 ligand was slightly correlated with measured levels of troponin T (r=0.21, p<0.05), and the increased soluble CD40L levels (>8.0 ng/ml) were associated with higher risk for AMI, sudden death and recurrent angina. Patients with elevated serum levels of sCD40L and cTnT showed a significantly increased risk of major adverse cardiovascular events (including AMI, sudden death and recurrent angina) in the two groups during 30 days and 6 months of follow-up. CONCLUSION: In patients with unstable coronary artery disease, elevation of serum soluble CD40L levels indicated an independent increased risk of major adverse cardiovascular events.     

Prognostic value of serum concentration of heart-type fatty acid-binding protein relative to cardiac troponin T on admission in the early hours of acute coronary syndrome

BACKGROUND: Heart-type fatty acid-binding protein (H-FABP) is proposed as an early biomarker for acute myocardial infarction (AMI), but its prognostic value is unclear in acute coronary syndrome (ACS). We evaluated the prognostic value of the H-FABP concentration relative to cardiac troponin T (cTnT) in the early hours of ACS. METHODS: Serum concentrations of H-FABP and cTnT were measured on admission in 328 consecutive patients hospitalized for ACS within 6 h after the onset of chest pain [AMI, 241 (73.5%) patients; ST-segment elevation myocardial infarction, 154 (47.0%) patients; and emergent coronary angiography within 24 h after admission, 287 (87.5%) patients]. Cardiac events, which were defined as cardiac death or subsequent nonfatal AMI, were monitored for 6 months after admission. RESULTS: During the 6-month follow-up period, there were 25 cardiac events, including 15 cardiac deaths and 10 subsequent nonfatal AMIs. Stepwise multivariate analyses including clinical, electrocardiographic, and biochemical variables revealed that increased H-FABP (above the median of 9.8 microg/L), but not increased cTnT (above the median of 0.02 microg/L), was independently associated with cardiac events in all patients [relative risk (RR) = 8.96; P = 0.0004], the subgroup of patients with ST-segment elevation myocardial infarction (RR = 11.3; P = 0.02), and the subgroup of patients with unstable angina and non-ST-segment elevation myocardial infarction (RR = 8.31; P = 0.007). The area under the ROC curve was higher for H-FABP than for cTnT (0.711 vs 0.578; P = 0.08), suggesting that H-FABP concentrations have a greater predictive capacity for cardiac events than cTnT. CONCLUSION: Serum H-FABP is a potential independent predictor of cardiac events within 6 months of patient admission and may provide prognostic information superior to cTnT in the early hours of ACS.     

Laboratory diagnosis of patients with acute chest pain.

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First creatine kinase MB mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins troponin T (cTnT) and troponin I (cTnI) appeared on the scene, displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. On the other hand, the latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For routine clinical laboratory practice we suggest that in diagnosis of patients with chest pain, myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later.     

A rapid troponin-I-based protocol for assessing acute chest pain.

In a prospective randomized open trial with 30-day follow-up, we compared a troponin-I-based protocol to 'standard management' for the diagnosis and risk stratification of patients with acute non-ST-elevation chest pain. Patients with acute chest pain (n=400) were randomized to standard diagnostic tests and management, or a protocol based on the admission ECG and the troponin-I result 6 h after onset of chest pain. Low-risk patients were discharged early from CCU; high-risk patients were treated with medical therapy or referred for in-patient angiography as appropriate. We measured length of CCU stay, and followed all patients for major adverse cardiac events (MACE) of death, non-fatal myocardial infarction (MI), or urgent revascularization during the admission and for 30 days post-discharge. The troponin protocol allowed earlier discharge in the low-risk group (10 vs. 30 h, p<0.001) with no excess of adverse events compared to standard management (3% vs. 5%, p=0.32). It identified a group of patients at moderate risk of cardiac events (15% MACE rate during admission and 30-day follow-up), and a high-risk group (75% MACE rate) more accurately than did standard management. The prognostic power of troponin testing in combination with the admission ECG was higher than with either test used alone. The protocol improved the efficiency of low-risk patient management, and improved patient risk stratification. This study adds to the evidence favouring troponin evaluation as part of the management of acute coronary syndromes.     

Diurnal variation in admission troponin concentrations in patients with chest pain in the emergency department

BackgroundRecent studies have suggested that there may be large diurnal variation in cardiac troponin T (cTnT) concentrations measured with a high sensitive assay.ObjectiveTo investigate if clinically relevant diurnal variation in cTnT concentrations is present in patients with chest pain in the emergency department (ED).MethodsWe included all patients with chest pain, but no myocardial infarction (MI), and no other acute condition that may affect troponin concentrations in the ED at Karolinska University Hospital, Stockholm, Sweden, 2011–2014. Time periods for blood sampling were: 00.00–03.59 am, 04.00–07.59 am, 08.00–11.59 am, 00.00–03.59 pm, 04.00–07.59 pm, and 08.00–11.59 pm. Negative binomial regression models were used to calculate least-square means of admission cTnT concentrations with 95% confidence intervals (CIs).ResultsA total of 19,460 patients were included with a mean age of 54 ± 16 years. Patients who arrived during the night were younger, but other characteristics were similar among the time periods. The greatest mean admission cTnT concentrations for men (9.0 ng/l, 95% CI, 8.7–9.3), and women (8.0 ng/l, 95% CI, 7.8–8.2) were found at 08.00–11.59 am. After adjustment for age and estimated glomerular filtration rate, no significant diurnal variation in admission cTnT concentrations was observed.ConclusionsIn a cohort of unselected patients with chest pain, and no acute condition affecting troponin admission concentrations, we found no evidence of clinically relevant diurnal variation in admission cTnT concentrations. There is no need to take the time point when blood is drawn into account in the assessment of admission cTnT concentrations in the ED.     

Clinical predictors of 30-day cardiac events in patients with acute coronary syndrome at a community hospital

OBJECTIVE: We sought to determine predictors of coronary events (cardiac death, acute myocardial infarction, and urgent revascularization) within 30 days after admission. METHODS: We prospectively collected data on 400 patients admitted through our emergency room for unstable angina and acute coronary syndromes. Patients with ST-segment elevation myocardial infarction and those who required thrombolysis were excluded. RESULTS: Of 383 patients who were eligible, 120 patients had coronary events within 30 days. Statistically significant variables associated with coronary events were advanced age, male sex, family history of premature coronary artery disease (CAD), diabetes mellitus, tobacco abuse, prior congestive heart failure, prior myocardial infarction, and history of CAD. Symptoms at presentation associated with cardiac events were typical angina and shortness of breath. Objective measures of ischemia associated with cardiac events were elevated troponin T, elevated creatine kinase MB, and ischemic electrocardiographic changes. Using forward stepwise regression analysis, we generated a model to predict 30-day major adverse cardiac events. The strongest predicting variable was serum troponin T (accounting for 33% of predicting r2, P < 0.001) followed by typical angina (r2 increasing to 37%), ischemic electrocardiographic changes (40%), prior CAD (42%), family history of premature CAD (44%), shortness of breath (46%), and positive creatine kinase MB (48%). The positive predictive power of the complete model was r2 = 48%, P < 0.001. CONCLUSION: Our model incorporating elements from the patient's demographic, medical history, presentation, and ischemic assessment identified 48% of patients presenting with unstable angina and acute coronary syndromes who will suffer a major adverse cardiac event within 30 days of admission. Although the strongest predictor was identified as serum troponin T, other clinical criteria offered improvement in our predictive abilities. Therefore, good initial clinical evaluation in addition to simple tests such as serum cardiac markers and electrocardiography are valuable in risk stratification of patients presenting with acute coronary syndromes and cardiac chest pain. Additional testing may be necessary to improve the positive predictive value of the model. Cardiac enzymes and electrocardiographic changes have the highest negative predictive value for occurrence of major adverse cardiac events. Identification of high-risk patients is essential to direct resources toward these patients and to avoid unnecessary costs and risk to the low-risk population.     

Time-dependent diagnostic performance of a rapid troponin T version 2 bedside test in patients with acute coronary syndromes

In a prospective trial, the diagnostic performance of the second version of the troponin T rapid assay (Trop T; cutoff 0.2 microg/L) was compared with the quantitative cardiac-specific troponin T assay (cTnT ELISA; cutoff 0.1 microg/L) and other established cardiac markers such as CK, CK-MB activity, CK-MB mass and myoglobin. Additionally, a 30-day follow-up was performed to determine the suitability of the Trop T assay and the reference markers for short-term risk stratification. Two-hundred-and-eighty-six consecutive patients with chest pain and suspected acute myocardial infarction (AMI) were enrolled in two CCU departments. Serial blood specimens were taken at admission and at 3, 6, 12, 24, 48, 72 and 96 h after admission. According to the biochemical criterion CK-MB mass, the patients were classified as having AMI in 154 patients (54%), unstable angina (UAP) in 72 patients (27%) and no evidence for acute cardiac ischemia in 55 patients (19%). Analytical method comparison of Trop T with cTnT ELISA (cutoff 0.1 microg/L) showed a good agreement, Trop T yielded only 4% false-negative and 3% false-positive results. The diagnostic performance of Trop T for the detection of AMI was only slightly inferior compared to cTnT ELISA. Beyond 12 h after admission, Trop T and cTnT ELISA maintained a sensitivity close to 100%, whereas the sensitivity of the other cardiac markers decreased sharply. The diagnostic sensitivity of Trop T for the detection of minor myocardial damage in UAP patients was the same as for cTnT ELISA. Death within 30 days' follow-up occurred only in AMI patients with a positive Trop T test result within the first 6 h after admission. The admission Trop T and cTnT ELISA were the only significant biochemical predictors of major cardiac events. In conclusion, these data show that Trop T has similar diagnostic sensitivity as cTnT ELISA and is a useful tool to confirm acute or subacute myocardial infarction. Trop T is an excellent marker in detecting minor myocardial damage in UAP patients and is suitable for short-term risk stratification.     

Role of coronary angiography before radiofrequency ablation in patients presenting with paroxysmal supraventricular tachycardia

During episodes of paroxysmal supraventricular tachycardia (PSVT), electrocardiograms frequently show ST-segment depressions, and patients may experience typical chest pain prompting invasive coronary angiography. We evaluated 114 patients presenting with PSVT for concomitant coronary artery disease (CAD). Patients were classified as to the type of PSVT, symptoms during PSVT, and cardiovascular risk factors. Maximum heart rate, extent of ST-segment depression, and cardiac troponin levels during PSVT were recorded. Patients were subjected to exercise testing and/or coronary angiography. During PSVT, symptoms suggestive of myocardial ischemia, including chest pain (31%), ST-segment depression (61%), and elevated troponin levels (12%), were common. Sixty-seven patients (59%) underwent coronary angiography. The overall prevalence of significant CAD was found to be low (4%) and did not correlate to symptoms during tachycardia. Routine coronary angiography cannot be recommended in patients with PSVT unless routine evaluation outside episodes of tachycardia suggests the presence of significant CAD.     

Markers of myocardial damage in acute coronary syndromes--therapeutic implications

Patients admitted with suspicion of an acute coronary syndrome (ACS) still constitute a diagnostic, prognostic and therapeutic challenge for the treating physician. The final diagnosis ranges from a noncardiac diagnosis to a full-blown myocardial infarction (MI). Biochemical markers of myocardial damage are essential for diagnosis and, especially troponin T and troponin I, have been shown to be valuable for early risk stratification and for selection of treatment in ACS.Patients identified to be at low risk of future cardiac events might be discharged early, and unnecessary investigations and treatments avoided. On the contrary, a more intense treatment can be started in patients identified to be at high risk. Unstable angina patients with, compared to without, elevation of troponin, have a more activated coagulation system and more frequently complex lesions and visible thrombus in their coronary arteries. Accordingly, antithrombotic and antiplatelet therapies, i.e. l.m.w heparin and GP IIb/IIIa receptor antagonists, have been proved to have beneficial effects in troponin positive patients, but little or no beneficial effects in troponin negative patients. Also, the beneficial effects of an invasive compared to a noninvasive approach seem to be much more pronounced in troponin positive patients.In patients with ST-elevation MI, an elevated troponin T level at admission are associated with an increased mortality. However, the therapeutic implications of this finding remain speculative.Patients admitted with chest pain and left bundle branch block (LBBB) and who develop an MI have a poor prognosis. Current guidelines in acute myocardial infarction state that these patients should receive thrombolysis. Despite that, only a minority of these patients do receive thrombolysis, most probably because of the great diagnostic uncertainty. Rapid testing with a cardiac marker, e.g. myoglobin, would most probably increase the proportion of patients with chest pain and LBBB who receive appropriate reperfusion treatment.     

Troponin T levels in patients with acute heart failure: clinical and prognostic significance of their detection and release during hospitalisation

Aims

Myocardial injury during an episode of acute heart failure (AHF) may be important for patents’ outcome. We hypothesised that an increase of cardiac troponin levels (cTnT) during hospitalisation, in patients with undetectable levels on admission (cTnT release), may be a more specific marker of myocardial damage. With this aim, we assessed the clinical and prognostic significance of high serum cTnT levels at the time of admission and that of cTnT release in 198 consecutive patients admitted for AHF and with no signs of acute coronary syndrome.

Methods and results

cTnT levels were serially measured at the time of admission, and after 6 and 12?h, in 198 consecutive patients admitted for AHF and with no signs of acute coronary syndrome. cTnT was detectable (>0.01?ng/mL) in 102 patients (52?%) and positive for myocardial necrosis (>0.03?ng/mL) in 78 patients (39?%). Negative cTnT at the time of admission became positive at 6 and/or 12?h in 36 (18?%) patients. Patients with increased cTnT levels were more likely to have coronary artery disease, hypertension, diabetes, and renal dysfunction. During a median follow-up duration of 247?days (IQR 96–480?days), the detection of increased cTnT levels was associated with a higher rate of all-cause deaths and, for cTnT release, all-cause death and cardiovascular rehospitalisation rate. CTnT release was an independent predictor of all-cause death and cardiovascular rehospitalisation, along with glomerular filtration rate, and the administration of inotropic agents during the initial hospitalisation.

Conclusions

Increased cTnT levels are a frequent finding in patients with AHF. They are more likely to occur in patients with comorbidities and are associated with poorer outcomes. cTnT release is an independent predictor of poorer outcomes.     

Adverse Cardiac Events in Emergency Department Patients with Chest Pain Six Months after a Negative Inpatient Evaluation for Acute Coronary Syndrome

OBJECTIVE: To evaluate the impact of the diagnostic test setting-inpatient versus outpatient-on adverse cardiac events (ACEs) after six months in emergency department (ED) patients with chest pain who were admitted to the hospital and subsequently had a negative evaluation for acute coronary syndrome (ACS). METHODS: The authors retrospectively studied a consecutive sample of ED patients with chest pain over a nine-month period. All patients were admitted to the hospital and underwent negative evaluations for ACS, defined as the absence of diagnostic changes on serial electrocardiograms or cardiac markers (creatine kinase-MB and troponin T), and a negative diagnostic cardiac study. Subjects were classified according to cardiac diagnostic study setting-either inpatient or outpatient. Diagnostic testing included exercise treadmill, angiography, stress echocardiography, or stress thallium scans. Acute cardiac events at six months were defined as cardiac death, myocardial infarction, unstable angina, cardiac arrest, or emergent revascularization. RESULTS: The six-month rate of ACEs among 157 subjects was 14%, with 2% cardiac mortality. The outpatient group had higher ACE risk when compared with the inpatient group using multivariate logistic regression, both for the entire cohort (OR 3.5, p < 0.03) and for a subgroup excluding patients with prior coronary artery disease (OR 6.7, p < 0.05). The outpatient group included 19 of 52 (37%) noncompliant subjects who did not receive a diagnostic study. CONCLUSIONS: Long-term cardiac morbidity of patients after a negative ACS evaluation may be higher than previously thought. Risk of ACE is significantly higher in subjects scheduled for outpatient diagnostic tests. Inpatient diagnostic testing is justified for subjects at risk for poor compliance.     

A new chest pain strategy in Thunder Bay

Thunder Bay Regional Hospital (TBRH) developed a chest pain strategy (CPS) to support its emergency physicians in making the difficult clinical decisions required to properly evaluate and manage ED "chest pain" patients. This strategy was developed to ensure excellent patient care in a setting of diminished inpatient bed availability and increasing ED congestion. It focuses on rapid risk stratification, using history, electrocardiogram, physical examination and 3 new point-of-care cardiac markers: myoglobin, CK-MB mass, and cardiac troponin I. Following the introduction of the CPS in 1997, TBRH realized significant ($500 000/yr) institutional resource savings through a 60% decrease in the admission rate of non-myocardial infarction, non-unstable angina chest pain patients, a 30% decrease in ED chest pain evaluation time, and improved ED availability of monitored stretchers. The CPS has allowed TBRH to simultaneously decrease costs and improve patient care.