Validation of a tool to safely triage selected patients with chest pain to unmonitored beds

Objective: To externally validate a chest pain protocol that triages low risk patients with chest pain to an unmonitored bed. Methods: Retrospective study of all patients admitted from the emergency department of a tertiary referral public teaching hospital with an admission diagnosis of ‘unstable angina’ or suspected ischemic chest pain. Data was collected on adverse outcomes and analysed on the basis of intention‐to‐treat according to the chest pain protocol. Results: There were no life‐threatening arrhythmias, cardiac arrests or deaths within the first 72 h of admission in the group assigned to an unmonitored bed by the chest pain protocol ([0/244]; 0.0%: 95% confidence interval 0.0–1.5%). Four patients had an uncomplicated myocardial infarction, two patients had recurrent ischemic chest pain and one patient developed acute pulmonary oedema ([7/244]; 2.9%: 95% confidence interval 1.2–5.8%). Conclusion: This retrospective study externally validated the chest pain protocol. Care in a monitored bed would not have altered outcomes for patients triaged to an unmonitored bed by the chest pain protocol. Compared to current guidelines, application of the chest pain protocol could increase the availability of monitored beds.     

Multicenter Study of Creatine Kinase-MB Use: Effect on Chest Pain Clinical Decision Making

Objective: To determine whether creatine kinase-MB isomer (CK-MB) levels affect initial physician decisions regarding patients with potential cardiac chest pain.
Methods: A prospective, multicenter, observational cohort study was performed at seven university teaching hospital EDs. Hemodynamically stable chest pain patients >25 years old and without ST-segment elevation on their ECGs were observed with one to two sets of CK-MB level determinations obtained three hours apart prior to disposition. The physicians committed to a dichotomous (yes/no) absolute decision regarding the diagnosis of myocardial infarction (MI), need for hospital admission, and need for coronary care unit (CCU) admission both before and after enzyme results were obtained. The physicians ranked the perceived importance of initial history and physical, serial clinical observation, initial ECG, and CK-MB level to their decision making (rank score: 1 = most important, 4 = least important).
Results: Of the 1,042 patients enrolled, 777 (74.6%) were admitted to the hospital. For the 67 MI patients (8.6% of the admissions), changes in absolute decisions about the diagnosis of MI and planned CCU admission were associated with increased CK-MB importance (p = 0.04 and p = 0.02, respectively). Of the 146 patients who had new-onset angina or unstable angina, changes in absolute decisions were not associated with CK-MB importance. No patient who had MI or unstable angina was released from the ED. There were three of 67 (4%) MI patients and one of 146 (1%) unstable/new-onset angina patients initially slated for release home who were admitted to the hospital.
Conclusions: For a minority of the patients who had subsequently proven MI, the CK-MB result helped guide disposition decisions. The CK-MB availability did not adversely impact the disposition of the patients who had unstable or new-onset angina.     

Chest pain evaluation unit: a cost-effective approach for ruling out acute myocardial infarction

We compared a "cardiac profile" test with standard creatine kinase (CK) and lactic dehydrogenase (LD) electrophoresis in 798 cases of possible acute myocardial infarction (MI). The cardiac profile enzyme screen (CK-B, CK, LD) used on 495 patients who came to the emergency department with chest pain suggestive of acute MI but without diagnostic ECG changes. Instead of admission to the coronary care unit, they were placed on observation status (Chest Pain Evaluation Unit) for a period up to 20 hours (average 11.1 hours). Using the results of the cardiac profile, 327 were able to be sent home. Of the 168 patients admitted, only 30 (18%) had subsequent enzyme evidence of myocardial necrosis. Use of the chest pain evaluation unit resulted in an 80% reduction in cost of ruling out acute MI for the 327 patients not admitted.     

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.     

Contemporary diagnosis and management of unstable angina

Unstable angina (UA) is one of the acute coronary syndromes, a group of conditions that also includes non-ST elevation myocardial infarction (MI) and ST elevation MI. The underlying pathogenic substrate of all these entities is the unstable coronary plaque with an overlying intracoronary thrombus. Initial management for the patient with suspected UA includes a resting electrocardiogram and oral administration of aspirin. ST-segment elevation indicates acute MI with the need for urgent reperfusion therapy. Patients without ST-segment elevation commonly have a mixture of UA and non-ST elevation MI; initial management is similar with assessment of near-term risk of MI or death as the next step. Features of UA indicating high risk include persistent ST-segment depression, persistent ischemic pain, elevated troponin level, or features of heart failure. Such patients undergo intensive medical therapy with heparin (unfractionated or low-molecular-weight), beta-blockade, and IIb/IIa antiplatelet agents, usually followed by coronary angiography and percutaneous intervention. The timing of intervention depends on the patient's response to therapy. Intermediate- or low-risk patients (including those presenting to the emergency department) can be managed with a chest pain unit strategy, and those with normal results on serial electrocardiograms, cardiac marker studies, and functional testing can be safely discharged home. Others are admitted for elective angiography, intensive medical therapy, or both. Assessment of coronary risk factors and their modification is an important component of long-term therapy for both high-risk and low-risk patients with UA, as well as those determined to have had non-ST elevation MI.     

The role of cardiac markers in the emergency department.

The emergency department (ED) evaluation of patients with potential acute coronary syndromes (ACS) has traditionally included initial cardiac marker testing for suspected acute myocardial infarction (AMI). While ED management decisions for patients with ACS have largely been based on history, physical examination, and a presenting 12-lead electrocardiogram (ECG), there is ample evidence that markers impact treatment decisions and provide risk stratification. Newer, more sensitive markers of myocardial necrosis have blurred the distinction between patients with and without classically defined AMI, and have focused attention on the continuum of ACS from angina to transmural Q-wave MI. Newer antiplatelet agents, the glycoprotein IIb/IIIa receptor blockers, are likely to receive increased ED utilization. This use will be partially driven by ED cardiac marker determination. Bedside, point-of-care testing is reliable technology that may shorten time to diagnosis and treatment of ACS in the emergency setting. The ED-based chest pain center (CPC) has become a popular tool to evaluate patients at low- to moderate-risk for ACS and a non-diagnostic ECG. Such centers use serial cardiac marker testing as a mainstay for evaluation and risk stratification. Cost issues have driven many diagnostic patient evaluations from the inpatient setting to such ED observation units. As this becomes more common for low- to moderate-risk patients with chest pain, serial assessment of cardiac markers, and their interpretation by emergency physicians, will become essential.     

Differences between Chest Pain Observation Service Patients and Admitted "Rule-out Myocardial Infarction" Patients

Objective: To compare and contrast the patient characteristics of ED patients at low risk for acute cardiac ischemia who were assigned to a chest pain observation service vs those admitted to a monitored inpatient bed for "rule-out acute myocardial infarction" (R/O MI).
Methods: This was a retrospective, cross-sectional comparison of adult patients considered at relatively low risk for cardiac ischemia and who were evaluated in 1 of 2 settings: a short-term observation service and an inpatient monitored bed. All patients had an ED final diagnosis of "chest pain," "R/O MI," or "unstable angina" during the 7-month study period. Demographic features and presenting clinical features were examined as a function of site of patient evaluation.
Results: Of 531 study patients, 265 (50%) were assigned to the observation service. Younger age (OR = 1.75, 95% CI 1.26, 2.44, for each decrement of 20 years), the complaint of "chest pain" (OR = 2.35, 95% CI 1.34, 4.12), and the absence of prior known coronary artery disease (OR = 1.64, 95% CI 1.13, 2.38) were the principal independent factors associated with assignment to a chest pain observation service bed. Conclusions: Patients evaluated in a chest pain observation service appear to have different clinical characteristics than other individuals admitted to a monitored inpatient bed for "R/O MI." Investigators should address differences in clinical characteristics when making outcome comparisons between these 2 patient groups.     

Detection of chest pain of non-cardiac origin at the emergency room by a new non-invasive device avoiding unnecessary admission to hospital

Recent advances in the treatment of acute coronary syndromes has raised awareness that prompt presentation for chest pain may be life saving. Most patients presenting with chest discomfort have a non-ischaemic ECG on presentation, but are routinely admitted to hospital because of diagnostic uncertainty for occult MI or ischaemia.

We tested a new non-invasive device that measures central aortic pressure changes (dP/dt_ejc): an accepted index of myocardial performance that could be added to the diagnostic triage of ischaemia in the ER avoiding unnecessary admissions.

We followed 85 patients presenting at the ER with acute chest pain. In 72 patients, negative ECG and myocardial enzyme dynamics ruled out coronary origin during the first 24 h after admission. In 8 of the 72 patients, coronary catheterisation found normal coronary arteries. In this group, average dP/dt_ejc was 163 (range 92–232). In 35 patients in whom the new non-invasive cardiac performance index dP/dt_ejc was above a threshold of >150, acute MI was ruled out. In 13 patients, acute chest pain had coronary origin confirmed by ECG and/or positive enzymes. The average dP/dt_ejc in this group was 117 (range 61–149). The dP/dt_ejc values were found to be significantly higher in patients without acute MI (p<0.001).

Preliminary findings suggest that nearly 40% of patients presenting with acute chest pain could be spared the risks and costs of unnecessary hospital admission and more invasive cardiac testing by simply adding a easy to use, immediately obtained, test to the diagnostic protocol, and using a threshold of dP/dt_ejc >150 to rule out heart attack.

     

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.     

Circulating stress hormone and insulin concentrations in acute coronary syndromes: identification of insulin resistance on admission.

We re-examined, in the context of modern practice, plasma insulin and stress hormone concentrations in patients admitted to hospital with acute coronary syndromes. Venous blood sampling was carried out prior to anti-thrombotic therapy in 148 patients with myocardial infarction (MI); 76 patients with unstable angina (UA) pectoris were also studied, together with 27 patients with non-cardiac chest pain (NCP). There were significant progressive increases in the concentrations of catecholamines, cortisol, glucose and insulin from NCP to UA to MI patients. Hyperglycaemia (glucose >8 mmol/l) was present in over 50% of MI patients. The plasma cortisol and insulin levels were both significantly positively correlated with the glucose concentration on admission. Only the cortisol concentration was correlated with peak cardiac enzyme levels. The glucose and insulin concentrations on admission in 141 MI and UA patients were related to insulin resistance, as judged from subsequent insulin and glucose concentrations measured while fasting and during a glucose tolerance test. The product of admission insulinxglucose (divided by 25; the admission insulin-resistance index, or AIRI) was significantly correlated with indices of insulin resistance, and was significantly higher (approximately double) in the MI group (7. 81+/-0.76) and the UA group (6.88+/-1.19) than in the control NCP group (3.59+/-0.06; Kuskul-Wallis: P=0.0001), implying that the insulin levels in the first two groups were approximately twice as high as is appropriate for the glucose levels. The ethnic origin of 20% of the patients was the Indian subcontinent; admission insulin and glucose levels in this subgroup were higher than in the non-Asians across all the groups with chest pain. Cortisol was the only stress hormone that was raised in proportion to the size of the infarct, and is a likely partial cause of the elevation in blood glucose. The high insulin levels were related to the prevalence of insulin resistance, and this was particularly important in the Asian subgroup presenting with MI and UA. Thus it appears feasible to identify acute coronary syndrome patients who are insulin-resistant at a time (on admission) when alternative early therapeutic strategies can be instituted.     

Utility of Troponin I in Patients with Cocaine-associated Chest Pain

Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. OBJECTIVE: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. METHODS: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). RESULTS: Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. CONCLUSIONS: Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.     

Evaluation of acute coronary syndromes by cardiac magnetic resonance imaging

The use of cardiovascular magnetic resonance (CMR) imaging for the evaluation of patients with acute chest pain and acute coronary syndromes has great potential. The strength of CMR relies on its ability to provide information on anatomy, physiology, and function in a single scanning session in a noninvasive manner without the need for iodinated contrast, radiation, or the need to undergo invasive procedures. Specifically, with regard to imaging patients with acute chest pain and/or myocardial infarction (MI), CMR has the ability to qualitatively and quantitatively evaluate global and regional right and left ventricular systolic functions, myocardial edema, myocardial perfusion, and myocardial infarct size and transmurality/viability. This review will focus on CMR imaging for the following applications: (1) imaging for the evaluation of ventricular function and infarct size in patients with acute chest pain and/or acute MI, (2) for triage and prognosis of patients presenting to the emergency department with acute chest pain, (3) for evaluating patients after sustaining an acute MI, and (4) for stem cell research.     

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.     

B型尿钠肽对无ST段抬高急性心肌梗死患者的诊断价值

目的:评价B型尿钠肽(BNP)对伴急性胸痛但心电图无ST段抬高的急性心肌梗死(AMI)患者的诊断价值。方法:对156例门诊及急诊急性胸痛或胸部不适患者进行前瞻性研究,测定BNP和肌钙蛋白I(cTnI),评价BNP对无ST段抬高的AMI患者的早期诊断价值。结果:156例患者中,不伴有心电图ST段抬高AMI患者,其入院时BNP水平显著高于不稳定型心绞痛和非急性冠状动脉综合征患者。BNP诊断无ST段抬高的AMI的敏感度为0.63,特异度为0.42。联合应用BNP及cTnI可显著提高对无ST段抬高AMI的诊断敏感度(0.99),阴性预测值可提高至0.98。经多元回归分析发现,对于诊断无ST段抬高AMI,BNP是一个显著的独立指标。结论:对于伴有急性胸痛但无ST段抬高的AMI患者,尤其是cTnI还未达到AMI诊断阈值时,BNP联合cTnI可能成为其有效的早期诊断指标之一。     

急性胸痛患者血清缺血修饰白蛋白检测及其意义研究

【目的】探讨缺血修饰白蛋白(IMA)在急性胸痛患者检测的应用价值。【方法】选取2014年2月至2015年7月本院收治的100例急性胸痛发作3 h 内胸痛患者,将其分为缺血性胸痛组(59例)和非缺血性胸痛组(41例),缺血性胸痛组进一步分为不稳定型心绞痛组(39例)和急性心肌梗死组(20例)。于入院后即刻、3 h、24 h 分别采集静脉血分离血清,检测肌酸激酶同工酶(CK-MB)、肌钙蛋白 I(cTnI)、IMA。【结果】入院后即刻和入院后3 h,缺血性胸痛组 IMA 高于非缺血性胸痛组,差异有统计学意义(P <0.05);cTnI 、CK-MB 水平比较差异无统计学意义(P >0.05)。入院后24 h,缺血性胸痛组 IMA 与非缺血性胸痛组比较无统计学意义(P >0.05);而 cTnI 和 CK-MB 均高于非缺血性胸痛组,差异有统计学意义(P <0.05)。入院后即刻、3 h、24 h 不稳定型心绞痛组和急性心肌梗死组IMA 水平比较差异均无统计学意义(P >0.05)。【结论】IMA 是早期诊断非缺血性胸痛和缺血性胸痛的敏感指标,但其并不能诊断区别不稳定型心绞痛和急性心肌梗死。     

Outcome from a rapid-assessment chest pain clinic

Chest pain accounts for much of the rising numbers of emergency admissions, but in-patient assessment is not necessarily the best way of dealing with these patients. We ran a 'rapid-assessment chest pain clinic' to provide an alternative route of assessment, and audited its outcome. General practitioners referred patients with recent-onset chest pain, increasing chest pain, chest pain at rest, or other chest pain of concern, on the understanding that they would be seen within 24 h. During 8 1/2 months, 334 patients were referred and 317 patients were seen, most of whom had exercise electrocardiography. A median of 6 months later, 278 patients were personally contacted to determine outcome. Of these, 18% had been admitted immediately with acute coronary syndromes, and 49% had been diagnosed as non-coronary chest pain (none of whom subsequently infarcted or died). Continuing symptoms were infrequent, and satisfaction was high, although 13% of patients had been revascularized. A significant number of patients required immediate admission and/or ultimate revascularization, but many more did not. The majority of these patients had non-coronary chest pain, and this diagnosis was substantiated by their excellent outcome and (in some cases) by further investigation.      

Clinical signs of pulmonary congestion predict outcome in patients with acute chest pain

BACKGROUND: Pulmonary congestion is associated with poor outcome in patients with acute coronary syndromes. In consecutive patients presenting with acute unexplained chest pain to a primary care facility, the prognostic impact of pulmonary congestion is indeterminate. Therefore, we assessed the predictive value of clinical signs of pulmonary congestion in patients presenting with acute chest pain to an emergency department with regard to the origin of the symptoms. METHODS: 1288 consecutive patients with acute chest pain were prospectively assessed for clinical signs of pulmonary congestion. The diagnosis was confirmed by chest radiography. The association of pulmonary congestion and short- and intermediate-term mortality in patients with coronary (n = 381) and non-coronary (n = 907) causes of chest pain was determined using multivariate Cox regression analysis. RESULTS: 108 (8%) patients had clinical signs of pulmonary congestion. Within the mean follow-up period of 23 months (SD 4) 67 patients died, mainly within the first 6 months. Of 108 patients with pulmonary congestion, 82 (76%) had coronary and 26 (24%) had non-coronary chest pain. Pulmonary congestion was independently associated with mortality in patients with coronary chest pain (hazard ratio 6.4, 95% confidence interval 2.5 to 16.1, p < 0.0001), both in patients with acute coronary syndromes or angina pectoris. However, in patients with non-coronary chest pain we observed no independent association of pulmonary congestion with outcome. CONCLUSION: Clinical signs of pulmonary congestion indicate an increased risk for poor outcome in patients with chest pain due to myocardial ischemia. Mortality of these patients is high, particularly in the first months after presentation. Therefore, hospital admission is warranted, including patients with angina pectoris, who otherwise may be candidates for early discharge.     

Serum markers in the emergency department diagnosis of acute myocardial infarction

No currently used cardiac-specific serum marker meets all the criteria for an "ideal" marker of AMI. No test is both highly sensitive and highly specific for acute infarction within 6 hours following the onset of chest pain, the timeframe of interest to most emergency physicians in making diagnostic and therapeutic decisions. Patients presenting to the ED with chest pain or other symptoms suggestive of acute cardiac ischemia therefore cannot make a diagnosis of AMI excluded on the basis of a single cardiac marker value obtained within a few hours after symptom onset. The total CK level is far too insensitive and nonspecific a test to be used to diagnose AMI. It retains its value, however, as a screening test, and serum of patients with abnormal total CK values should undergo a CK-MBmass assay. Elevation in CK-MB is a vital component of ultimate diagnosis of AMI, but levels of this marker are normal in one fourth to one half of patients with AMI at the time of ED presentation. The test is highly specific, however, and an abnormal value (particularly when it exceeds 5% of the total CK value) at any time in a patient with chest pain is highly suggestive of an AMI. There have been several improvements of CK-MB assay timing and subform quantification that appear highly useful for emergency physicians. Rapid serial CK-MB assessment greatly increases the diagnostic value of the assay in a timeframe suitable for ED purposes but unfortunately still misses about 10% of patients ultimately diagnosed with acute MI. Assays of CK-MB subforms have very high sensitivity, and, although unreliable within 4 hours of symptom onset, have excellent diagnostic value at 6 or more hours after chest pain begins. Automated test assays recently have become available and could prove applicable to ED settings. The cardiac troponins are highly useful as markers of acute coronary syndromes, rather than specifically of AMI, and abnormal values at any time following chest pain onset are highly predictive of an adverse cardiac event. The ED applicability of the troponins is severely limited, however, because values remain normal in most patients with acute cardiac events as long as 6 hours following symptom onset. Myoglobin appeared promising as a marker of early cardiac ischemia but appears to be only marginally more sensitive than CK-MB assays early after symptom onset and less sensitive than CK-MB at 8 hours or more after chest pain starts. Rapid serial myoglobin assessment, however, appears highly useful as an early marker of AMI. The marker has a very narrow diagnostic window. The clinician is left with several tests that are highly effective in correctly identifying patients with AMI (or at high risk for AMI), but none that can dependably exclude patients with acute coronary syndromes soon after chest pain onset. A prudent strategy when assessing ED patients with chest pain and nondiagnostic ECGs is to order CK-MB and troponin values on presentation in the hope of making an early diagnosis of AMI or unstable coronary syndrome. Although it is recognized that normal values obtained within 6 hours of symptom onset do not exclude an acute coronary syndrome, patients at low clinical risk and having normal cardiac marker tests could be provisionally admitted to low-acuity hospital settings or ED observation. After 6 to 8 hours of symptom duration has elapsed, the cardiac-specific markers are highly effective in diagnosing AMI, and such values obtained can be used more appropriately to make final disposition decisions. At no time should results of serum marker tests outweigh ECG findings or clinical assessment of the patient's risk and stability.