Can myocardial infarction be rapidly identified in emergency department patients who have left bundle-branch block?

STUDY OBJECTIVES: Fibrinolytic therapy is recommended for patients who have chest pain and left bundle-branch block (LBBB). However, the presence of baseline ECG abnormalities makes early accurate identification of acute myocardial infarction (AMI) difficult. The predictive ability of clinical and ECG variables for identifying patients with LBBB and AMI has not been well studied. We sought to determine the prevalence and predictors of myocardial infarction among patients presenting to the emergency department with LBBB on the initial ECG who were evaluated for myocardial infarction. METHODS: All patients presenting to the ED were prospectively risk stratified on the basis of clinical and historical variables. ECGs from patients with LBBB were compared retrospectively with previously published criteria for identification of AMI. The ability of a new LBBB to predict AMI was also determined. RESULTS: Twenty-four (13%) of the 182 patients with LBBB had AMI. Clinical and historical variables were similar in patients with and without AMI. A new LBBB had a sensitivity of 42% and a specificity of 65%. The presence of concordant ST-segment elevation or depression had specificities and positive predictive values of 100%; however, sensitivities were only 8% and 17%, respectively. The best diagnostic criterion was the presence of concordant ST-segment elevation or depression on the ECG or an initially elevated creatine kinase MB (sensitivity, 63%; specificity, 99%). CONCLUSION: ECG criteria for identifying patients with AMI and LBBB identify only a small minority of patients with AMI. Treating all patients with LBBB and chest pain with fibrinolytics would result in treatment of a significant number of patients without AMI.

A nonischemic electrocardiogram does not always predict a small myocardial infarction: results with acute myocardial perfusion imaging.

BACKGROUND: A nonischemic electrocardiogram (ECG) in association with myocardial infarction (MI) indicates a small MI in some but not all cases. Myocardial perfusion imaging using technetium-99m sestamibi offers the ability to better characterize these "electrically silent" infarctions. METHODS: Patients considered low risk for myocardial infarction with a normal or nonischemic ECG (no significant ST elevation, ST depression, ischemic T-wave inversion, or left bundle branch block) underwent early emergency department perfusion imaging, followed by serial myocardial marker sampling. Risk area (defect size) was quantitated by use of a 50% threshold from multiple short-axis slices. RESULTS: A total of 87 patients with nonischemic ECGs had myocardial infarction (mean peak creatine kinase [CK] 710 +/- 720 U/L, range 111-3196 U/L). Peak CKs were lower in the 7 patients with negative perfusion imaging (420 +/- 290 U/L vs 730 +/- 740 U/L, P =.06). Mean risk area was 18% +/- 11% of the left ventricle (range 0%-62%) and was not significantly different among the different infarct-related arteries. Patients with normal ECGs had a similar risk area compared with other patients (16% +/- 12% vs 19 +/- 12%, P =.25). Coronary angiography was performed in 81 patients, with significant stenoses in 74 (91%) (37 one-vessel, 19 two-vessel, 18 three-vessel), with the infarct related artery most commonly the left circumflex (n = 32 [38%]). CONCLUSIONS: The ischemic risk area in patients with a nonischemic ECG was comparable to patients with inferior ST-elevation myocardial infarction found in previous studies. A nonischemic ECG does not predict a small ischemic risk area.

Rationale for the early clinical application of markers of ischemia in patients with suspected acute coronary syndromes.

Mandates for more rapid treatment of patients with acute myocardial infarction (AMI) are driving public education initiatives aimed at having patients present earlier in the course of their symptoms. This will make it less likely that markers of necrosis will provide the level of diagnostic sensitivity needed. In fact, the goal is to identify and treat these patients sooner in order to prevent necrosis from occurring. Given the limitations of the standard 12-lead ECG to detect ischemia, other technologies are being evaluated: the value of echocardiography and technetium-based myocardial perfusion imaging have been proven. However, the goal is to develop a simple, rapid-turn-around biochemical marker that can provide this same function, and clear progress is being made toward this end. Emergent, rapid restoration of blood flow via pharmacologic revascularization or primary percutaneous interventions can reduce morbidity and mortality when applied in the setting of acute myocardial injury seen on the ECG. Exciting new research suggests that the protection of myocytes against ischemic injury is possible if initiated early, which can limit cellular damage and improve clinical outcomes. Thus, the ability to rapidly detect ischemia will have profound therapeutic possibilities that could further reduce the morbidity and mortality associated with acute coronary syndrome.

Evaluation of the emergency department chest pain patient.

Patients presenting to the emergency department with chest pain are a common and perplexing problem. Because of the limitations of the initial evaluation, most patients are admitted, although many are found to have noncardiac causes of 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 electrocardiogram and use of newer myocardial markers of necrosis, such as mass assays for CK-MB as well as troponin T and troponin I. Use of acute rest myocardial perfusion imaging also has been shown to be a highly valuable technique for risk stratification of the intermediate- to low-risk chest pain patient.

Ability of troponin I to predict cardiac events in patients admitted from the emergency department.

OBJECTIVES: We sought to determine the predictive ability of troponin I (TnI) in a heterogeneous group of patients with chest pain admitted from the emergency department (ED) for exclusion of myocardial infarction (MI). BACKGROUND: Previous studies in high-risk patients demonstrated that troponin elevations are associated with increased cardiac events. Little information is available on its predictive ability in more heterogeneous, lower risk patients. METHODS: Consecutive patients admitted from the ED for possible MI underwent serial myocardial marker sampling of TnI and creatine kinase, CK-MB over an 8-h period. Patients with ST segment elevation were excluded. End points included MI, death, significant complications (e.g., cardiac or respiratory arrest, intra-aortic balloon pump, pulmonary artery catheter or pacemaker placement, revascularization or inotropic infusion) and significant disease. RESULTS: Events occurred in 513 (27%) of the 1,929 patients evaluated: MI in 175 (9.1%) and death in 34 (1.8%); an additional 248 patients (13%) without MI had complications, and 323 (17%) without MI had significant disease. Sensitivity of TnI for MI was high (96%). Patients without MI who were TnI-positive were more likely to have complications (43% vs. 12%) or significant disease (41% vs. 17%) as compared with those who were TnI-negative; however, the sensitivity of TnI for these two end points was low (14% and 21%, respectively). Predictive values were unchanged after excluding patients with ischemic electrocardiograms. CONCLUSIONS: Troponin I had a high sensitivity for MI when used as part of a rapid rule-in protocol; however, the sensitivity for other end points was low. Use of TnI alone failed to identify the majority of patients who had either significant disease or complications.

Clinical evaluation of the first medical whole blood, point-of-care testing device for detection of myocardial infarction.

BACKGROUND: Validation of whole blood, point-of-care testing devices for monitoring cardiac markers to aid clinicians in ruling in and ruling out myocardial infarction (MI) is necessary for both laboratory and clinical acceptance. METHODS: This study evaluated the clinical diagnostic sensitivity and specificity of the First Medical Cardiac Test device operated by nursing and laboratory personnel that simultaneously measures cardiac troponin I (cTnI), creatine kinase (CK) MB, myoglobin, and total CK on the Alpha Dx analyzer in whole blood for detection of MI. Over a 6-month period, 369 patients initially presenting to the emergency department with chest pain were evaluated for MI using modified WHO criteria. Eighty-nine patients (24%) were diagnosed with MI. RESULTS: In whole blood samples collected at admission and at 3- to 6-h intervals over 24 h, ROC curve-determined MI decision limits were as follows: cTnI, 0.4 microgram/L; CKMB, 7.0 microgram/L; myoglobin, 180 microgram/L; total CK, 190 microgram/L. Based on peak concentrations within 24 h after presentation, the following sensitivities (+/- 95% confidence intervals) were found: cTnI, 93% +/- 5.5%; myoglobin, 81% +/- 9.7%; CKMB, 90% +/- 6.3%; total CK, 86% +/- 7.5%. Sensitivities were maximal at >90% for both cTnI and CKMB at >12 h in MI patients, without differences between ST-segment elevation and non-ST-segment elevation MI patients. CONCLUSIONS: The First Medical point-of-care device provides cardiac marker assays that can be used by laboratories and clinicians in a variety of hospital settings for ruling in and ruling out MI.

Impact of the measurement of troponin on the triage, prognosis, and treatment of patients with chest pain.

There are several issues driving the rapid advancement in diagnostic technology for acute cardiac syndromes. First is safety, primarily the need to improve sensitivity in lower-risk patients presenting with symptoms suggestive of ischemia; second is fiscal, especially to reduce the cost for the evaluation of low-risk chest pain patients; and third is therapeutic, including the ability to effectively risk-stratify patients who may be candidates for more aggressive therapy.

National Academy of Clinical Biochemistry Standards of Laboratory Practice: recommendations for the use of cardiac markers in coronary artery diseases.

The Sixth Conference on the "Standards of Laboratory Practice Series", sponsored by the National Academy of Clinical Biochemistry (NACB), was held on August 4-5, 1998, at the Annual Meeting of the American Association for Clinical Chemistry, in Chicago, IL. An expert committee was assembled to write recommendations on the use of cardiac markers in coronary artery diseases. The NACB Committee prepared a preliminary draft of the guidelines, made them available on the World Wide Web (www.nacb.org), and distributed them before the presentations. The recommendations were divided into four areas: the use of markers in the triage of patients with chest pain, acute coronary syndromes, clinical applications other than acute myocardial infarction and research, and assay platforms and markers of acute myocardial infarction. The recommendations were revised and subsequently re-presented in part at the "Biomarkers in Acute Cardiac Syndromes Conference", sponsored by the Jewish Hospital Heart and Lung Institute, Louisville KY, on October 16-17, 1998. This report lists each recommendation, its scientific justification, and a summary of discussions from conference participants and reviewers. Approximately 100 individuals responded to various versions of these recommendations via direct correspondences, telephone calls to Committee members, electronic mail correspondence to the Committee Chairman, or oral questions and comments raised during one of the two conference presentations. Some of the recommendations were changed to reflect the consensus opinion. In cases in which there was no consensus, the Committee included pertinent discussion without necessarily changing the original recommendations. At times, the Committee members felt that although a particular recommendation might not be the current standard of care today, they anticipate that it likely will be adopted in the near future.

Myocardial perfusion imaging with technetium-99m sestamibi in patients with cocaine-associated chest pain.

STUDY OBJECTIVE: To describe the characteristics and outcome in patients presenting to the emergency department with chest pain associated with cocaine use, the majority of whom underwent early rest perfusion imaging. METHODS: From January 1994 to June 1996, 218 patients had 241 ED visits for evaluation of symptoms consistent with myocardial ischemia after cocaine use. High-risk patients (N=25) were admitted directly to the CCU for exclusion of myocardial infarction (MI). Moderate- to low-risk patients (N=216) were promptly injected with technetium-99m sestamibi in the ED and underwent gated myocardial perfusion imaging 60 to 90 minutes later. Moderate-risk patients were observed in the CCU, whereas low-risk patients with negative perfusion imaging results were discharged home directly from the ED. RESULTS: A diagnosis of MI was made in 6 patients, 4 of whom had ECG findings consistent with MI. Of the 216 patients who underwent perfusion imaging, 5 had positive study results, including 2 with MI. None of the 38 patients with negative results after perfusion imaging who were admitted to the CCU had a diagnosis of MI. Only 6 of the 67 patients undergoing stress perfusion imaging had reversible perfusion defects. At 30-day follow-up, there were no cardiac events in patients with negative results after rest perfusion imaging. CONCLUSION: Acute MI is infrequent in patients presenting with cocaine-associated chest pain. Positive results after rest perfusion imaging are uncommon, suggesting that myocardial ischemia is infrequently the cause of cocaine-associated chest pain. Early perfusion imaging may offer an effective alternative to routine CCU admission of patients with cocaine-related cardiac symptoms.

Comparison of myocardial perfusion imaging and cardiac troponin I in patients admitted to the emergency department with chest pain.

BACKGROUND: Identification of patients with acute coronary syndromes (ACS) among those who present to emergency departments with possible myocardial ischemia is difficult. Myocardial perfusion imaging with 99mTc sestamibi and measurement of serum cardiac troponin I (cTnI) both can identify patients with ACS. METHODS AND RESULTS: Patients considered at low to moderate risk for ACS underwent gated single-photon emission CT sestamibi imaging and serial myocardial marker measurements of creatine kinase-MB, total creatine kinase activity, and cTnI over 8 hours. Positive perfusion imaging was defined as a perfusion defect with associated abnormalities in wall motion or thickening. cTnI >/=2.0 ng/mL was considered abnormal. Among the 620 patients studied, 59 (9%) had myocardial infarction and 81 (13%) had significant coronary disease; of these patients, 58 underwent revascularization. Perfusion imaging was positive in 241 patients (39%), initial cTnI was positive in 37 (6%), and cTnI was >/=2.0 ng/mL in 74 (12%). Sensitivity for detecting myocardial infarction was not significantly different between perfusion imaging (92%) and cTnI (90%), and both were significantly higher than the initial cTnI (39%). Sensitivity for predicting revascularization or significant coronary disease was significantly higher for perfusion imaging than for serial cTnI, although specificity for all end points was significantly lower. Lowering the cutoff value of cTnI to 1.0 ng/mL did not significantly change the results. CONCLUSIONS: Early perfusion imaging and serial cTnI have comparable sensitivities for identifying myocardial infarction. Perfusion imaging identified more patients who underwent revascularization or who had significant coronary disease, but it had lower specificity. The 2 tests can provide complementary information for identifying patients at risk for ACS.

Early diagnosis of acute myocardial infarction in patients without ST-segment elevation.

Early identification of acute myocardial infarction (AMI) is necessary to initiate appropriate treatment. In patients presenting without ST-segment elevation, diagnosis is often dependent on the presence of elevated myocardial markers. This study examines the ability of serial MB mass alone and in combination with myoglobin in diagnosing AMI in patients without ST-segment elevation within 3 hours of presentation. In all, 2,093 patients were admitted and underwent serial marker analysis using myoglobin, creatine kinase (CK), and CK-MB at 0, 3, 6, and 8 hours. AMI was diagnosed by a CK-MB > or =8.0 ng/ml and a relative index (RI) (CK-MB x 100/total CK) > or =4.0. A total of 186 patients (9%) were diagnosed with AMI. The optimal diagnostic strategy was an elevated CK-MB + RI on the initial or 3-hour sample or at least a twofold increase in CK-MB without exceeding the upper range of normal over the 3-hour time period (sensitivity 93%, specificity 98%). The combination of an elevated CK-MB + RI or myoglobin on the initial or 3-hour sample had a sensitivity of 94%, although specificity was significantly lower, at 86%. Sensitivities and specificities after exclusion of the 242 patients with ischemic electrocardiographic changes were essentially unchanged. We conclude that most patients with AMI presenting with nondiagnostic electrocardiograms can be diagnosed within 3 hours of presentation.

Comparison between 2-dimensional echocardiography and myocardial perfusion imaging in the emergency department in patients with possible myocardial ischemia.

BACKGROUND: Accurate identification of patients at high risk for acute coronary syndromes among those seen in the emergency department (ED) with possible myocardial ischemia and nonischemic electrocardiograms is problematic. Both 2-dimensional echocardiography and myocardial perfusion imaging with technetium-99m sestamibi can identify patients at low and high risk; however, comparative studies are lacking. METHODS AND RESULTS: Patients initially considered at low or moderate risk for myocardial ischemia on the basis of the presenting history, physical examination, and electrocardiogram underwent both echocardiography and myocardial perfusion imaging within 4 hours of ED presentation. Positive echocardiography was defined as the presence of segmental wall motion abnormalities or moderate to severe global systolic dysfunction; positive perfusion imaging was defined as a perfusion defect in association with abnormal wall motion, thickening, or both. End points included MI, percutaneous transluminal coronary angioplasty, and positive stress perfusion imaging. Both imaging procedures were performed in the ED on 185 patients. Six patients had MI, and an additional 4 patients underwent percutaneous transluminal coronary angioplasty. Echocardiography and perfusion imaging were positive in all 10. Overall agreement between the 2 techniques was high (concordance 89%, kappa coefficient 0.74) in the 27 patients who had MI or underwent coronary angiography. For all patients, concordance was 89%, with a kappa coefficient of 0.66. CONCLUSIONS: Agreement between echocardiography and perfusion imaging with technetium-99m sestamibi is high when used in patients in the ED with possible myocardial ischemia. Both techniques identified patients at high risk who required admission and those who could be safely discharged directly from the ED.

Cost-effectiveness of cardiac troponin I in a systematic chest pain evaluation protocol: use of cardiac troponin I lowers length of stay for low-risk cardiac patients.

We evaluated several measures of clinical and fiscal interest to assess the effect of adding an automated cardiac troponin I (c-TnI) assay to our current cardiac panel, which consists of creatine kinase MB (CK-MB), myoglobin, total CK activity, and a calculated CK-MB relative index. Samples were collected on admission and at 3, 6, and 8 hours after admission as part of our diagnostic protocol. Our study was designed to collect data on a control group of patients, implement a change (i.e., c-TnI testing), and then measure the effect of the change on a test population having otherwise equivalent diagnostic and therapeutic pathways. We assessed differences in patient hospital and cardiac care unit length of stay (LOS), time to cardiac catheterization, and hospital and laboratory charges and costs. We found that adding c-TnI to our testing regimen decreased LOS for the large test population. Within this large test population, patients classified as low risk for acute myocardial infarction experienced statistically and clinically significant shorter LOS and lower total and variable hospital costs; for patients with unstable angina, there was an increase (though not statistically significant) in laboratory costs.

Value of acute rest sestamibi perfusion imaging for evaluation of patients admitted to the emergency department with chest pain.

OBJECTIVES: This study sought to determine the ability of early perfusion imaging using technetium-99m sestamibi to predict adverse cardiac outcomes in patients who present to the emergency department with possible cardiac ischemia and nondiagnostic electrocardiograms (ECGs). BACKGROUND: Evaluation of patients presenting to the emergency department with possible acute coronary syndromes and nondiagnostic ECGs is problematic. Accurate risk stratification is necessary to prevent serious adverse outcomes. Initial results suggest that early perfusion imaging using technetium-99m sestamibi enables reliable risk stratification. METHODS: Patients presenting to the emergency department with a low to moderate probability of acute coronary syndromes underwent rapid sestamibi injection with gated single-photon emission computed tomographic imaging. Studies showing perfusion defects with associated wall motion abnormalities were considered positive. RESULTS: A total of 532 consecutive patients underwent serial myocardial marker analysis and rest perfusion imaging. Of these patients, perfusion imaging was positive in 171 (32%). Positive perfusion imaging was the only multivariate predictor of myocardial infarction (MI) (p < 0.0001, odds ratio [OR] 33, 95% confidence interval [CI] 7.7 to 141) and was the most important independent predictor of MI or revascularization (p < 0.0001, OR 14, 95% CI 7.3 to 25), followed by diabetes (p < 0.01, OR 2.8, 95% CI 1.5 to 5.1), typical angina (p = 0.01, OR 2.1, 95% CI 1.2 to 3.7) and male gender (p = 0.03, OR 1.9, 95% CI 1.1 to 3.5). The sensitivity of positive perfusion imaging for MI was 93% (95% CI 77% to 98%), and for MI or revascularization it was 81% (95% CI 71% to 88%), with negative predictive values of 99% (95% CI 98% to 100%) and 95% (95% CI 92% to 97%), respectively. CONCLUSIONS: Positive rest perfusion imaging accurately identified patients at high risk for adverse cardiac outcomes, whereas negative perfusion imaging identified a low risk patient group. Early perfusion imaging allows for rapid and accurate risk stratification of emergency department patients with possible cardiac ischemia and nondiagnostic ECGs.

Evaluation of chest pain in the emergency department.

The evaluation of chest pain in the emergency setting should be systematic, risk based, and goal driven. An effective program must be able to evaluate all patients with equal thoroughness under the assumption that any patient with chest pain could potentially be having an MI. The initial evaluation is based on the history, a focused physical examination, and the ECG. This information is sufficient to categorize patients into groups at high, moderate, and low risk. Table 14 is a template for a comprehensive chest-pain evaluation program. Patients at high risk need rapid initiation of appropriate therapy: thrombolytics or primary angioplasty for the patients with MIs or aspirin/heparin for the patients with unstable angina. Patients at moderate risk need to have an acute coronary syndrome ruled in or out expediently and additional comorbidities addressed before discharge. Patients at low risk also need to be evaluated, and once the likelihood of an unstable acute coronary syndrome is eliminated, they can be discharged with further evaluation performed as outpatients. Subsequent evaluation should attempt to assign a definitive diagnosis while also addressing issues specific to risk reduction, such as cholesterol lowering and smoking cessation. It is well documented that 4% to 5% of patients with MIs are inadvertently missed during the initial evaluation. This number is surprisingly consistent among many studies using various protocols and suggests that an initial evaluation limited to the history, physical examination, and ECG will fail to identify the small number of these patients who otherwise appear at low risk. The solution is to improve the sensitivity of the evaluation process to identify these patients. It appears that more than simple observation is required, and at the present time, no simple laboratory test can meet this need. However, success has been reported with a number of strategies including emergency imaging with either radionuclides such as sestamibi or echocardiography. Early provocative testing, either stress or pharmaceutic, may also be effective. The added value of these tests is only in their use as part of a systematic protocol for the evaluation of all patients with acute chest pain. The initial evaluation of the patient with chest pain should always consider cardiac ischemia as the cause, even in those with more atypical symptoms in whom a cardiac origin is considered less likely. The explicit goals for the evaluation of acute chest pain should be to reduce the time to treat MIs and to reduce the inadvertent discharge of patients with occult acute coronary syndromes. All physicians should become familiar with appropriate risk stratification of patients with acute chest pain. Systematic strategies must be in place to assure rapid and consistent identification of all patients and the expedient initiation of treatment for those patients with acute coronary syndromes. These strategies should include additional methods of identifying acute coronary syndromes in patients initially appearing as at moderate or low risk to assure that no unstable patients are discharged. All patients should be followed up closely until the cardiovascular evaluation is completed and, when possible, a definitive diagnosis is determined. Finally, this must be done efficiently, cost-effectively, and in a manner that will result in an overall improvement in patient care.

Usefulness of the admission electrocardiogram for identifying the infarct-related artery in inferior wall acute myocardial infarction.

We analyzed the admission electrocardiogram in 109 patients with inferior wall acute myocardial infarction in an attempt to determine the infarct-related artery (IRA). The presence of ST depression in leads V1 or V2 had a high sensitivity for predicting the left circumflex artery as the IRA. The lack of ST depression in V1 or V2 had a high negative predictive value for excluding the left circumflex artery as the IRA.

Use of the combination of myoglobin and CK-MB mass for the rapid diagnosis of acute myocardial infarction.

Early identification of patients presenting with myocardial infarction (MI) is necessary for rapid initiation of treatment. Currently, MI has been diagnosed using the combination of the history, electrocardiogram (ECG), and biochemical markers of myocardial necrosis. Unfortunately, all lack sufficient sensitivity and specificity to confidently identify most patients with MI in a timely enough fashion to influence early intervention. Development of newer immunochemical assays for CK-MB mass and myoglobin have allowed for earlier, more rapid diagnosis; however, each has important limitations. The diagnostic sensitivity of CK-MB mass, myoglobin, and the combination of both were analyzed at the time of presentation (0 hours) and again 4 hours later in 101 patients admitted from the emergency department (ED) with possible MI. Twenty patients were subsequently diagnosed as having MI. The sensitivity of the initial ECG was 60%, compared with the sensitivities of the initial myoglobin and CK-MB mass of 70% and 30%, respectively. By 4 hours the sensitivity of myoglobin had increased to 85% and CK-MB mass to 90%. The combination of the initial myoglobin and CK-MB mass had a sensitivity of 85%. Combining these two markers, using both the initial and 4-hour samples, raised the sensitivity to 100%, with a specificity of 100% and negative predictive value of 100%. When patients with diagnostic ECGs were excluded, the sensitivity of the combination at 0 hours was 80% with a specificity of 84%, while the use of the 0- and 4-hour markers had a sensitivity and specificity of 100% and 100%, respectively. We conclude that the combination of CK-MB mass and myoglobin can rapidly diagnose or exclude MI in as short as 4 hours after ED presentation, and accuracy is not different in patients without diagnostic ECGs. Application of this strategy could potentially lead to more rapid intervention in patients with MI, while also allowing early identification of lower risk patients.