The role of cardiac troponin t and other new biochemical markers in evaluation and risk stratification of patients with acute chest pain syndromes

Background and hypothesis: Increased serum creatinine kinase (CK) and CK-MB enzyme levels have been used for years to detect myocardial infarction (MI). However, serum myoglobin and CK-MB mass or protein levels may indicate MI earlier; cardiac troponin T is the most specific marker of myocardial injury and it can detect even minor myocardial necrosis. The diagnostic and prognostic utility of the traditional and new markers of cardiac injury in the emergency evaluation of patients with acute chest pain syndromes were therefore compared. Methods: One hundred and fifteen consecutive patients with an acute coronary syndrome, and 64 controls recruited during the same period, were examined. The time elapsed from onset of symptoms to blood collection was recorded. Cardiac markers were measured in specimens collected upon arrival (0 h), and 2 and 5–9 h, and later in cases of longer observation. The major cardiac events occurring up to 40 months after the index examination were recorded. Results: cTnT levels provided unique information: they were the most specific indicators of myocardial damage and identified unstable angina patients at high risk of future major events. Up to 6 h after the onset of chest pain, the new markers were elevated more frequently than the traditional ones and permitted earlier MI recognition. The worst prognosis (nonfatal myocardial infarction or death) was noted in subjects with chest pain at rest within 48 h before the index examination and elevated cTnT levels. Conclusions: The new markers, particularly cardiac troponin T, offer considerable advantages and they should be more widely used in the diagnosis and risk stratification of acute coronary syndromes.     

Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician

BACKGROUND: Over the past 2 decades, the 12-lead electrocardiogram has attained special significance for the diagnosis and triage of patients with chest pain because timely detection of myocardial injury and a rapid assessment of myocardium at risk proved pivotal to implementing effective reperfusion therapies during acute myocardial infarction. However, this wealth of information could still be underutilized by clinicians who may restrict their diagnostic quest in patients with chest pain to the more classic electrocardiographic signs. METHODS: The medical literature on electrocardiographic manifestations of acute myocardial infarction was extensively reviewed. RESULTS: The widespread utilization of both coronary angiography and methods to determine myocardial function and metabolism in patients with acute myocardial infarction over the last 10 years has provided the means for rigorous comparisons with electrocardiographic information. We summarize these electrocardiographic signs and patterns in terms of their relevance to the clinician to help reduce the incidence of "nondiagnostic electrocardiograms" and improve timely decision-making. CONCLUSIONS: The electrocardiogram continues to be an invaluable tool in the initial evaluation of patients with chest pain. The plethora of data currently available on electrocardiographic changes correlating with myocardial injury allows clinicians to make faster and better decisions than ever before.     

Diagnosis of myocardial injury by biochemical markers: problems and promises

The role of biochemical markers in the diagnosis of acute coronary syndromes has increased considerably in the past decade. The World Health Organization previously defined acute myocardial infarction as a combination of at least 2 of 3 components: symptoms consistent with acute myocardial infarction, electrocardiogram changes diagnostic of acute myocardial infarction, and an enzyme pattern with classic rise and fall. Measurement of creatine kinase and its MB fraction by various assays was the gold standard for the diagnosis. Troponins are more specific and sensitive markers for myocardial injury, and their increasing utilization has resulted in a broadening of the definition of acute myocardial infarction to incorporate high-risk acute coronary syndromes. Previously, traditional enzyme evaluation left patients with small amounts of cellular death undiagnosed; these patients were categorized as having unstable angina or, worse, noncardiac chest pain. Newer markers now identify these patients as a subgroup at high risk for cardiac death or cardiac events. Newer therapeutic interventions and a more invasive strategy have been shown to improve outcomes in this high-risk subgroup. Increased specificity has also reduced the number of patients who undergo extensive, expensive, and invasive evaluations for noncardiac syndromes due to false elevations of traditional markers. This article comprehensively reviews the evolution of biochemical markers for the diagnosis of acute myocardial infarction, addressing their promise for improving delivery of care and outcomes and their technical and diagnostic pitfalls.     

Myocardial perfusion imaging in acute coronary syndromes: potential use in decision making for emergent revascularization

We report two cases of patients presenting to the emergency department with chest pain who had low risk electrocardiographic findings. Myocardial perfusion imaging (MPI) revealed a significant area of decreased uptake suggestive of acute transmural infarction. In both cases, biochemical markers later confirmed the diagnosis of myocardial infarction. Cardiac catheterization revealed a large area at risk which was then treated with percutaneous intervention. As MPI is increasingly utilized in the acute evaluation of chest pain, it may serve as a useful adjunct in selecting patients who may benefit from emergent cathertization and revascularization.     

Clinical policy: critical issues in the evaluation and management of adult patients presenting with suspected acute myocardial infarction or unstable angina. American College of Emergency Physicians

This clinical policy focuses on critical issues in the evaluation and management of patients with acute myocardial infarction or unstable angina. A MEDLINE search for articles published between January 1993 and December 1998 was performed using combinations of the key words chest pain, acute myocardial infarction, unstable angina, thrombolytics, primary angioplasty, 12-lead ECG, ST-segment monitoring, cardiac serum markers, and chest pain centers. Subcommittee members and expert peer reviewers also supplied articles with direct bearing on the policy. This policy focuses on 5 areas of current interest and/or controversy: (1) ECG eligibility criteria for fibrinolytic therapy, (2) role of primary angioplasty in patients with acute myocardial infarction, (3) use of serum markers to diagnose acute myocardial infarction, (4) serial 12-lead ECGs during the initial evaluation, and (5) chest pain evaluation units. Recommendations for patient management are provided for each of these 5 topics based on strength of evidence (Standards, Guidelines, Options). Standards represent patient management principles that reflect a high degree of clinical certainty; Guidelines represent patient management principles that reflect moderate clinical certainty; and Options represent other patient management strategies based on preliminary, inconclusive, or conflicting evidence, or based on panel consensus. This guideline is intended for physicians working in hospital-based emergency departments or chest pain evaluation units.     

Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction

OBJECTIVE: To investigate the clinical features, electrocardiographic findings, and hospital course in patients admitted with acute chest pain temporally related to cocaine use. DESIGN: Retrospective data analysis. SETTING: A 485-bed county hospital. PATIENTS: One hundred and one consecutive patients with cocaine-related chest pain admitted to the hospital to rule out myocardial infarction. MEASUREMENTS AND MAIN RESULTS: The quality of the chest pain frequently suggested myocardial ischemia. Dyspnea was common (56%). The onset of chest pain occurred during cocaine use in 21% of patients, within 1 hour of use in 37%, and after 1 hour of use in 42%. Admission electrocardiographic findings were interpreted as normal in 32% of patients; as acute myocardial injury in 8%; as early repolarization variant in 32%; as left ventricular hypertrophy in 16%; and as "other" in 12%. Forty-three percent of patients had ST-segment elevation meeting the electrocardiographic criteria for use of thrombolytic therapy, but such elevation was usually due to the early repolarization variant. The initial total creatine kinase was elevated more than 3.3 mu kat/L (200 U/L) in 43% of patients, and an elevated total creatine kinase was recorded at some time during the hospital course in 47% of patients. The creatine kinase MB fraction was less than 0.02 in all patients. Myocardial infarction was ruled out in all patients. No patient experienced in-hospital cardiovascular complications. CONCLUSION: The quality of acute chest pain related to cocaine use is indistinguishable from that experienced in acute myocardial ischemia. Abnormal or normal variant electrocardiographic findings are common in patients with chest pain related to cocaine use, but nevertheless the incidence of acute myocardial infarction is low. The ST-segment and T-wave changes can mimic acute myocardial injury and are most likely normal findings in young black men that can be readily recognized in the emergency department. Most of these patients do not require admission to an intensive care unit.     

急性心肌梗塞再灌注损伤临床表现及分析

目的:对急性心肌梗塞(AMI)再灌注后出现的特殊临床表现进行分析。方法:对50例AMI患者静脉溶栓后冠状动脉造影(显示为TIMI血流3级)的资料进行分析。结果:再灌注后有48例胸痛迅速缓解,有2例患者在再灌注后胸痛突然加重;有44例患者出现心律失常;40例出现一过性低血压;8例出现一过性ST段抬高。结论:冠脉血管再通后绝大部分患者胸痛迅速缓解,但大多有心律失常发生,一过性低血压,少数患者可出现ST段一过性胸痛加重;故溶栓后应进行持续心电图和血压监测。     

Usefulness of Combining Necrosis and Platelet Markers in Triaging Patients Presenting with Chest Pain to the Emergency Department

Background: Myocardial injury and platelet activation play important roles in the pathogenesis of unstable coronary syndromes. We sought to determine whether the combined measurement of platelet and necrosis markers would improve risk stratification, and yield higher diagnostic utility in patients presenting to the emergency department with chest pain. Methods and Results: Platelet and soluble P-selectin together with myoglobin, creatine kinase, CK-MB fraction, and troponin I were measured from the autologous samples in 122 consecutive patients. Statistical analysis revealed strong Spearman correlation coefficients (0.141–0.412; p<0.001) between platelet expression of P-selectin and plasma levels of necrosis markers. Platelet P-selectin and necrosis markers were independent predictors (c-index>0.7) for acute myocardial infarction, while plasma P-selectin exhibited random distribution. Elevated soluble P-selectin and myoglobin were the most valuable in identifying patients with congestive heart failure. None of the markers were useful for triaging chest pain patients with unstable angina. Analysis of incremental gains (Chi-squares) reveals that with respect to platelet P-selectin, myoglobin adds 50%% to AMI diagnostic value, and creatine kinase yields an additional 20%% in triaging these patients. The diagnostic value of soluble P-selectin is substantially (72%%) increased by myoglobin measurements, and enhanced even further (44%%) by adding cardiac troponin I for identifying heart failure patients among the chest pain population. Conclusion: Simultaneous determination of platelet and necrosis markers improve the early diagnosis of acute myocardial infarction and congestive heart failure among patients with chest pain presenting into the Emergency Department. Well controlled clinical trials are needed to prove the advantage of combining platelet and necrosis data over presently used techniques in emergency medicine.     

Acute myocardial infarction in hemoglobin SC disease

Although there are reports of myocardial infarction (MI) in patients with sickle cell diseases, an antemortem diagnosis of acute MI in a patient with compound heterozygous hemoglobin SC disease has not been reported. Herein, we present a patient with hemoglobin SC who suffered an acute MI. She had typical chest pain for myocardial ischemia, associated with ST elevations on the electrocardiogram (EKG) and elevations of cardiac injury markers diagnostic of infarction. The patient was treated with conventional therapies for acute coronary syndrome and also emergent red blood cell exchange. Interestingly, coronary angiography was completely normal in this patient. Potential mechanisms and management for acute MI in patients with sickle cell disease are discussed.     

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.     

A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction--the MEMO study

OBJECTIVES: To compare the analgesic effect of metoprolol and morphine in patients with chest pain due to suspected or definite acute myocardial infarction after initial treatment with intravenous metoprolol. DESIGN: All patients, regardless of age, admitted to the coronary care unit at Uddevalla Central Hospital due to suspected acute myocardial infarction were evaluated for inclusion in the MEMO study (metoprolol-morphine). The effects on chest pain and side-effects of the two treatments were followed during 24 h. Pain was assessed by a numerical rating scale. RESULTS: A total of 265 patients were randomized in this prospective double-blind study and 59% developed a confirmed acute myocardial infarction. In both treatment groups, there were rapid reductions of pain intensity. However, in the patient group treated with morphine, there was a more pronounced pain relief during the first 80 min after start of double-blind treatment. The side-effects were few and were those expected from each therapeutic regimen. During the first 24 h, nausea requiring anti-emetics was more common in the morphine-treated patients. CONCLUSION: In suspected acute myocardial infarction, if chest pain persists after intravenous beta-adrenergic blockade treatment, standard doses of an opioid analgesic such as morphine will offer better pain relief than increased dosages of metoprolol.     

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.     

An evaluation of cocaine-induced chest pain

STUDY OBJECTIVE: To determine if enzymatic evidence of acute myocardial injury is present in patients complaining of chest pain after cocaine use when the ECG is normal or nondiagnostic. DESIGN: Serial ECG and creatinine kinase (CK) and CK isoenzymes (CK-ISO) determinations were performed at time of emergency department presentation and every six hours over 12 hours on individuals complaining of chest pain within six hours of last cocaine use. SETTING: ED of an urban tertiary care center. TYPE OF PARTICIPANTS: Forty-two individuals with a mean age of 28.5 years. INTERVENTIONS: Patients with positive CK-ISOs were admitted immediately to formally rule out myocardial infarction. Patients developing ECG changes during observation period also were admitted even if CK-ISOs were normal. Patients with unchanged ECGs and normal CK-ISOs were discharged after 12 hours of observation. RESULTS: Eight patients (19%) had elevated CK and CK-ISO values at presentation. Two of these patients had elevated values on three sequential determinations and were believed to have sustained acute myocardial infarction. Six patients had elevated CK and CK-ISOs at presentation only. ECGs remained normal or nondiagnostic in all patients. CONCLUSIONS: Enzymatic evidence of acute myocardial injury may occur in patients who develop chest pain after cocaine use and have normal or nondiagnostic ECGs. This injury may reflect acute infarction or transient ischemia. Single or serial normal or nondiagnostic ECGs do not rule out ischemia or injury in this group of patients.     

Combining different biochemical markers of myocardial ischemia does not improve risk stratification in chest pain patients compared to troponin I alone

OBJECTIVE: Early evaluation of patients with chest pain is important not only for the detection of acute myocardial infarction (AMI) but also for identification of patients at high risk for future cardiac events. A multimarker strategy applying results of early measurements of different biochemical markers of cardiac necrosis in combination may improve risk prediction in chest pain patients. METHODS: Rapid measurements of troponin I (TnI), creatine kinase MB and myoglobin were performed in 191 consecutive patients with chest pain and a non-diagnostic electrocardiogram for AMI. The prognostic value of these markers and different multimarker strategies was evaluated and compared. RESULTS: Ten (5.2%) patients died during follow-up, which for eight (4.2%) patients was due to cardiac causes. Myocardial reinfarctions occurred in 17 (6.8%) patients. TnI was most predictive for cardiac mortality (TnI>or=0.1 microg/l, 10.7% event rate compared with TnI<0.1 microg/l, 0%, P<0.001) and myocardial reinfarction (14.9% compared with 1.7%, P<0.001). The other markers and multimarker strategies had a lower capacity for predicting adverse events apart from myoglobin and the combination of TnI or myoglobin regarding the endpoint of total mortality. CONCLUSION: The combinations of different markers were prognostically non-superior compared to TnI, which thus, should be preferred as a biochemical marker for risk stratification in patients with chest pain.     

Utility of echocardiography for the early assessment of patients with nondiagnostic chest pain

A two-dimensional (2D) echocardiogram was recorded shortly after admission in 46 patients with nondiagnostic chest pain. Eighteen patients were studied during chest pain and 28 were studied following the resolution of chest pain. Of the 18 patients studied during chest pain, six of the eight patients who had a regional wall motion abnormality (RWMA) evolved an acute infarction and the remaining two patients had evidence of significant coronary artery disease. Only 1 of 10 patients without a RWMA evolved an infarction and none had significant coronary artery disease. Of the 28 patients studied following the resolution of chest pain, 8 of the 10 patients with a RWMA evolved an acute infarction and one patient had evidence of significant coronary artery disease, whereas of 18 patients without a RWMA, none evolved an acute infarction and five had evidence of significant coronary artery disease. These data suggest that in patients presenting with nondiagnostic chest pain, an early assessment of regional wall motion by 2D echocardiography can reliably differentiate patients with myocardial ischemia or early infarction from patients with nonischemic chest pain when performed during an episode of chest pain; can also identify those patients with early acute myocardial infarction, even when performed following the resolution of chest pain; but is not useful for the detection of patients with significant coronary artery disease without infarction when performed following the resolution of chest pain.     

Myocardial infarction induced by vincristine in patients with Hodgkin's lymphoma. Description of 2 cases and review of the literature

Five patients with lymphoma and Vincristine induced myocardial infarction are described in the medical literature. We report two new cases, in whom an anterior myocardial infarction developed few hours after the second administration of the drug. In the reported cases a strict cause-to-effect relationship between the drug and acute myocardial infarction seems indicated by: the striking temporal coincidence between Vincristine administration and onset of chest pain; the additional myocardial infarctions in patients in whom the treatment was continued after the first event; the nearly constant absence of important coronary risk factors and the young age of the patients, making preexisting coronary atherosclerosis unlikely. The mechanism for the described association is still unknown: the possible causes are discussed.     

Accuracy of computer-interpreted electrocardiography in selecting patients for thrombolytic therapy. MITI Project Investigators

A prehospital computer-interpreted electrocardiogram (ECG) was obtained in 1,189 patients with chest pain of suspected cardiac origin during an ongoing trial of prehospital thrombolytic therapy in acute myocardial infarction. Electrocardiograms were performed by paramedics 1.5 +/- 1.2 h after the onset of symptoms. Of 391 patients with evidence of acute myocardial infarction, 202 (52%) were identified as having ST segment elevation (acute injury) by the computer-interpreted ECG compared with 259 (66%) by an electrocardiographer (p less than 0.001). Of 798 patients with chest pain but no infarction, 785 (98%) were appropriately excluded by computer compared with 757 (95%) by an electrocardiographer (p less than 0.001). The positive predictive value of the computer- and physician-interpreted ECG was, respectively, 94% and 86% and the negative predictive value was 81% and 85%. Prehospital screening of possible candidates for thrombolytic therapy with the aid of a computerized ECG is feasible, highly specific and with further enhancement can speed the care of all patients with acute myocardial infarction.     

Acute myocardial infarction in a patient with normal coronary arteries--a case report

A case of a 72-year-old female who was admitted for elective dual-chamber pacemaker implantation, is presented. A few hours after the procedure the patient developed chest pain with ST-segment elevation in ECG and a significant increase in the troponin I level. An acute myocardial infarction was diagnosed. Urgent coronary angiography revealed normal coronary arteries without spasm. Possible causes of acute myocardial infarction following pacemaker implantation are discussed.     

Prognosis and thallium-201 scintigraphy in patients admitted with chest pain without confirmed acute myocardial infarction

Exercise and rest thallium scintigraphy and exercise electrocardiography were performed after discharge in 158 patients aged less than 76 years admitted with chest pain in whom a suspected diagnosis of acute myocardial infarction had not been confirmed. During a follow up of 12-24 months (median 14 months) there were 10 cardiac events--that is, non-fatal acute myocardial infarction or cardiac deaths. Transient thallium defects and abnormal ST response (that is ST segment deviation or uninterpretable ST segment) during exercise were correlated significantly with an unfavourable prognosis. One hundred and four patients with neither of these characteristics were at lower risk of a cardiac event than the 19 patients with both of these characteristics. The percentages of patients in these two groups without a cardiac event after one year were 98.1 and 78.8 respectively. Thallium scintigraphy, alone or in combination with exercise electrocardiography, can be used to identify groups at high and low risk of future cardiac events, in patients with chest pain in whom acute myocardial infarction is suspected but not found.