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Acute Coronary Syndrome Workup

  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD  more...
 
Updated: Sep 09, 2015
 

Approach Considerations

Guidelines

Guidelines released by the European Society of Cardiology (ESC) in August 2011 for the management of non-ST-segment elevation ACSs recommend GRACE or a similar scoring system to score the risk of an ischemic event in the short-to-mid term. The guidelines state that bleeding risk can be stratified using the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) risk score.[2]

In 2015, the American College of Cardiology/American Heart Association (ACC/AHA) released the guidelines recommendations on the workup of non-ST-elevation ACSs to assist in maximizing patient outcomes, including the following[18] :

  • Patients with chest pain or other symptoms suggesting acute coronary syndromes (ACS) should have 12-lead electrocardiography (ECG) performed and evaluated within 10 min of arrival at an emergency facility, and serial ECGs should be performed to detect ischemic changes.
  • Serial cardiac troponin I or T levels (using a contemporary assay) should be obtained at presentation and at 3-6 hours after symptom onset. Risk scores can help assess prognosis.
  • In patients with symptoms consistent with ACS without objective evidence of myocardial ischemia (nonischemic ECG and normal cardiac troponin levels), noninvasive imaging is reasonable before emergency department discharge or within 72 hours after discharge.

As previously mentioned, stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmias) increases demands on the heart. In such cases, the diagnosis of acute myocardial infarction can be made if workup reveals the typical rise and fall of biochemical markers of myocardial necrosis along with either the development of pathologic Q waves or the presence (on ECG or in the setting of a coronary intervention) of ischemic ST-segment changes. (However, the presence of ischemic symptoms can be substituted for the Q-wave or ST-segment evidence.)[3]

Non–ST-segment elevation myocardial infarction (NSTEMI) is distinguished from unstable angina by elevated levels of cardiac enzymes and biomarkers of myocyte necrosis. Differentiation is generally based on 3 sets of biomarkers measured at 6- to 8-hour intervals after the patient's presentation to the ED. The current definition of NSTEMI requires a typical clinical syndrome plus elevated troponin (or creatine kinase isoenzyme MB [CK-MB]) levels to over 99% of the normal reference (with a coefficient of variation of < 10% for the assay). Given this definition, nearly 25% of patients who were previously classified as having unstable angina now fulfill the criteria for NSTEMI.

Measure cardiac enzyme levels at regular intervals, starting at admission and continuing until the peak is reached or until 3 sets of results are negative. Biochemical biomarkers (demonstrated in the image below) are useful for diagnosis and prognostication.

This plot shows changes in cardiac markers over ti This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.

Of note, cardiac-specific troponins are not detectable in the blood of healthy individuals; therefore, they provide high specificity for detecting injury to cardiac myocytes. These molecules are also more sensitive than CK-MB for myocardial necrosis and therefore improve early detection of small myocardial infarctions. Although blood troponin levels increase simultaneously with CK-MB levels (about 6 h after the onset of infarction), they remain elevated for as long as 2 weeks. As a result, troponin values cannot be used to diagnose reinfarction. New methods of detecting troponins in the blood can measure levels as low as 0.1-0.2 ng/mL.

Keller et al suggest that among patients with suspected acute coronary syndrome, highly sensitive troponin I assay (hsTnI) or contemporary troponin I assay (cTnI) determination 3 hours after admission for chest pain may facilitate early rule-out of acute myocardial infarction. A serial change in hsTnI or cTnI levels from admission (using the 99th percentile diagnostic cutoff value) to 3 hours postadmission may aid in early diagnosis of acute myocardial infarction.[19]

Minor elevations in these molecules can be detected in the blood of patients without ACS in the setting of myocarditis (pericarditis), sepsis, renal failure, acute congestive heart failure (CHF), acute pulmonary embolism, or prolonged tachyarrhythmias.

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Electrocardiography

ECGs should be reviewed promptly. Involve a cardiologist when in doubt.

Recording an ECG during an episode of the presenting symptoms is valuable. Transient ST-segment changes (>0.05 mV) that develop during a symptomatic period and that resolve when the symptoms do are strongly predictive of underlying CAD and have prognostic value. Comparison with previous ECGs is often helpful.

Alternative causes of ST-segment and T-wave changes are left ventricular aneurysm, pericarditis, Prinzmetal angina, early repolarization, Wolff-Parkinson-White syndrome, and drug therapy (eg, with tricyclic antidepressants, phenothiazines).

In the emergency setting, ECG is the most important ED diagnostic test for angina. It may show changes during symptoms and in response to treatment, confirm a cardiac basis for symptoms. It also may demonstrate preexisting structural or ischemic heart disease (left ventricular hypertrophy, Q waves). A normal ECG or one that remains unchanged from the baseline does not exclude the possibility that chest pain is ischemic in origin. Changes that may be seen during anginal episodes include the following:

  • Transient ST-segment elevations
  • Dynamic T-wave changes - Inversions, normalizations, or hyperacute changes
  • ST depressions - May be junctional, downsloping, or horizontal

In patients with transient ST-segment elevations, consider LV aneurysm, pericarditis, Prinzmetal angina, early repolarization, and Wolff-Parkinson-White syndrome as possible diagnoses. Fixed changes suggest acute myocardial infarction.

When deep T-wave inversions are present, consider the possibility of central nervous system (CNS) events or drug therapy with tricyclic antidepressants or phenothiazines as the cause.

Diagnostic sensitivity may be increased by performing right-sided leads (V4 R), posterior leads (V8, V9), and serial recordings.

ECGs from 2 patients are shown below.

A 50-year-old man with type 1 diabetes mellitus an A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and electrocardiogram (ECG) changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.
A 62-year-old woman with a history of chronic stab A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.

In difficult cases with nondiagnostic ECGs, such as those involving a left bundle-branch block, early imaging is useful to assess wall-motion abnormalities.

An important use of noninvasive imaging is to classify a patient has having NSTEMI or true STEMI.

The Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction (OCCULT-MI) trial compared the 80-lead (80L) mapping system to standard 12-lead (12L) ECG. The study concluded that the 80L body surface mapping technology detected more patients with MI or ACS than the 12L ECG, while still maintaining a high degree of specificity.[20]

A study by Damman et al examined information from 5,420 patients from the Fragmin and Fast Revascularization During Instability in Coronary Artery Disease (FRISC II), Invasive Versus Conservative Treatment in Unstable Coronary Syndromes (ICTUS), and Randomized Intervention Trial of Unstable Angina 3 (RITA-3) patient-pooled database. The study found that admission ECG characteristics had long-term prognostic value for cardiovascular death or myocardial infarction. Quantitative ECG characteristics showed no incremental discrimination compared with qualitative data.[21]

A 5-year follow-up of patients with non–ST-elevation acute coronary syndrome from these 3 trials found no link between a procedure-related MI and long-term cardiovascular mortality. However, long-term mortality substantially increased after a spontaneous MI.[22]

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Measurement of CK-MB Levels

CK-MB, the isoenzyme specific to the heart muscle, was the principal biomarker of cardiac injury until troponin supplemented it.

In the setting of myocardial infarction, plasma CK-MB concentrations typically rise about 4-6 hours after the onset of chest pain. They peak within 12-24 hours and return to baseline levels within 24-48 hours. Serial measurements obtained every 6-8 hours (at least 3 times) are warranted until peak values are determined.

The area under the concentration-time curve for CK-MB created with serial measurements of blood enzyme levels provides a reliable estimate of the size of the infarct.

Clinical settings other than ACS, such as trauma, heavy exertion, and skeletal muscle disease (eg, rhabdomyolysis), may elevate CK-MB values.

Determination of subforms of CK-MB (CK-MB2 that is more specific to heart muscle) may improve the sensitivity of this test.

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Measurement of Troponin levels

The troponins are regulatory proteins found in skeletal and cardiac muscle. The 3 subunits that have been identified include troponin I (TnI), troponin T (TnT), and troponin C (TnC). The genes that code for the skeletal and cardiac isoforms of TnC are identical; thus, no structural difference exists between them. However, the skeletal and cardiac subforms for TnI and TnT are distinct, and immunoassays have been designed to differentiate between them. This explains the cardiospecificity of the cardiac troponins. Skeletal TnI and TnT are structurally different. No cross-reactivity occurs between skeletal and cardiac TnI and TnT with the current assays.

The cardiac troponins are sensitive, cardiospecific, and provide prognostic information for patients with ACS. They have become the cardiac markers of choice for patients with ACS.

Early studies on the release kinetics of the cardiac troponins indicated that they were not early markers of myocardial necrosis. The early generation troponin assays yielded positive results within 4-8 hours after symptom onset, similar in timing to the release of CK-MB; however, they remained elevated for as long as 7-10 days post-myocardial infarction.

Initial studies on the cardiac troponins revealed a subset of patients with rest unstable angina in whom CK-MB levels were normal but who had elevated troponin levels. These patients had higher adverse cardiac event rates (acute myocardial infarction, death) within the 30 days after the index admission and a natural history that closely resembled patients with NSTEMI. The table below outlines many of the initial studies on troponins in ACS.

Use of cardiac markers in the ED. Studies on tropo Use of cardiac markers in the ED. Studies on troponins in ACS.

As previously mentioned, an elevated troponin level also enables risk stratification of patients with ACS and identifies patients at high risk for adverse cardiac events (ie, myocardial infarction, death) up to 6 months after the index event.[7, 8]

In a study by Antman et al, the initial TnI level on admission in patients with ACS correlated with mortality at 6 weeks. CK-MB levels, although sensitive and specific for the diagnosis of acute myocardial infarction, were not predictive of adverse cardiac events and had no prognostic value.[7] The relationship between TnI levels and risk of cardiac events and mortality is demonstrated in the graphs below.

Use of cardiac markers in the ED. Troponin I level Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event ra Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.

Data from a meta-analysis indicated that an elevated troponin level in patients without ST-segment elevation is associated with a nearly 4-fold increase in cardiac mortality rate. For the composite end point of acute myocardial infarction or death, an elevated troponin level was associated with an odds ratio of 3.3.[23]

The TIMI IIIB, GUSTO IIa, GUSTO IV ACS, and Fragmin During Instability in Coronary Artery Disease (FRISC) trial all demonstrated a direct correlation between the level of TnI or TnT and the adverse cardiac event rate and mortality rate in ACS.[7, 24, 25, 26, 27] These studies confirmed the use of the cardiac troponins TnI and TnT in risk stratification and therapeutic decision making.

Studies by Ohman et al and Stubbs et al revealed that an elevated troponin level at baseline was an independent predictor of mortality even in patients with chest pain and acute myocardial infarction with ST-segment elevation who were eligible for reperfusion therapy.[24, 28]

With the introduction of increasingly sensitive and precise troponin assays, up to 80% of patients with acute myocardial infarction will be found to have an elevated troponin within 2-3 hours of ED arrival. With this improved clinical performance in cardiac troponin assays, the so-called rapidly rising cardiac biomarkers, such as myoglobin or CK-MB isoforms, have little clinical utility.[29, 30, 31, 32] In a prospective multicenter study, patients with ACS who and presented with acute chest pain to the ED were followed for 12 months. The study found that patients with normal high-sensitivity cardiac troponin T (hs-cTnT) levels at presentation have low mortality rates but an increased rate of acute myocardial infarction during the subsequent 360 days.[33]

As a result, some authorities have called for a troponin standard alone and recommend eliminating CK-MB.[34]

Many patients with acute myocardial infarction present with equivocal ECG patterns, making prehospital ECG diagnosis difficult. A study by Sorensen et al suggests prehospital TnT testing may improve diagnosis in patients with chest pain transported by ambulance.[35] When quantitative TnT was measured at hospital arrival in 958 patients after 8 and 24 hours, a diagnosis of acute myocardial infarction was established in 208 of 258 patients with increased TnT levels, showing prehospital TnT testing is feasible with a high success rate. Prehospital implementation of quantitative tests, with lower detection limits, may identify most patients with acute myocardial infarction irrespective of ECG changes.

The 2007 American College of Cardiology (ACC) guidelines for NSTEMI recommend that serial troponins be obtained for a definitive rule out at baseline and 6-9 hours later. To establish the diagnosis of acute myocardial infarction, only 1 elevated level above the established cutoff is required. The demonstration of a rising or falling level is needed to distinguish persistently elevated troponin levels (eg, in some patients with renal failure) from those patients with acute myocardial infarction.[36]

If myocardial injury is suspected despite negative cardiac-specific troponin findings, additional, sensitive laboratory assays are indicated.[37]

Patients with suspected ACS who test negative for troponin and copeptin can be safely discharged from the hospital without further testing, according to a recent study, the Biomarkers in Cardiology 8 (BiC-8) trial. Copeptin, a marker of severe hemodynamic stress, can be detected immediately in acute myocardial infarction.[38] The study involved 902 patients at low to intermediate risk of ACS; half of the patients were treated with standard care, and the other 451 patients underwent a copeptin assay. In the latter group, patients with a positive copeptin test, defined as a level of 10 pmol/L or greater, were treated with standard ACS care, while patients with a copeptin level below 10 pmol/L were discharged into ambulant care, including an outpatient visit within 72 hours. In the 451 patients tested for troponin and treated with standard care, the 30-day rate of major adverse cardiovascular events was 5.5%, compared with 5.46% in the 451 patients tested for troponin and copeptin (a statisticallyinsignificant difference).[38]

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Measurement of Myoglobin Levels

Myoglobin is not cardiac specific, but it may be detected as early as 2 hours after myocardial necrosis starts. However, myoglobin results should be supplemented with other, more specific cardiac biomarkers, such as CK-MB or troponin.

Myoglobin values have a high negative predictive value when blood is sampled in the first 4-8 hours after onset.

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Complete Blood Count Determination

The CBC count helps in ruling out anemia as a secondary cause of ACS. Leukocytosis has prognostic value in the setting of acute myocardial infarction.

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Basic Metabolic Panel

Obtain a basic metabolic profile, including a check of blood glucose level, renal function, and electrolytes levels, for patients with new-onset angina. Close monitoring of potassium and magnesium levels is important in patients with ACS because low levels may predispose them to ventricular arrhythmias. Routine measurement of serum potassium levels and prompt correction are recommended.

Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor and particularly if cardiac catheterization is considered. Use of N -acetylcysteine and adequate hydration can help prevent contrast material–induced nephropathy.[39]

Other useful metabolic profiles include amylase and lipase.

A study by Charpentier et al suggests that a serum glucose level of more than 140 mg/dL is associated with non-ST elevation ACS in patients admitted to an ED for chest pain. However, when this level of blood glucose is added to the conventional diagnostic tools, the result is only a small increase in the ability to classify ACS.[40]

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New Biomarkers

levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP) are elevated in acute MI and provide predictive information for risk stratification across the spectrum of ACS.[41, 42] However, a single, low BNP level obtained within 4 hours of a patient presenting to the ED does not identify the patient as low-risk for 30-day acute myocardial infarction or death.[43]

In the future, a combination of levels of troponin (a biomarker for myocardial necrosis), NT-pro-BNP (an indicator of elevated LV end-diastolic pressure and wall stress), and C-reactive protein (CRP, an estimate of the extent of systemic inflammation) may prove useful for predicting the outcome of patients with ACS.

Routine measurement of BNP and CRP levels in patients with ACS is not warranted at this time.

Interleukin-6 is the major determinant of acute-phase reactant proteins in the liver, and serum amyloid A is another acute-phase reactant. Elevations of either of these can be predictive in determining increased risk of adverse outcomes in patients with unstable angina.

Cavusoqlu et al suggests that elevated baseline levels of plasma interleukin-10 are associated with long-term adverse outcomes in patients with ACS.[44]

Several other biomarkers with variable sensitivity and specificity have been investigated, including sCD40 ligand, myeloperoxidase, pregnancy-associated plasma protein-A, choline, placental growth factor, cystatin C, fatty acid binding protein, ischemia modified albumin, chemokines ligand-5 and -18 (mediators of monocyte recruitment induced by ischemia), angiogenin, SCUBE1 (a novel platelet protein), and others.[45, 46] In a study that included 107 patients presenting to an emergency department with chest pain, ischemia modified albumin was not found to have superior sensitivity and specificity over traditional biomarkers, with a sensitivity of 0.86 and specificity of 0.49.[47]

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Chest Radiography

Chest radiography helps in assessing cardiomegaly and pulmonary edema, or it may reveal complications of ischemia, such as pulmonary edema. It may also provide clues to alternative causes of symptoms, such as thoracic aneurysm or pneumonia (which can be a precipitating cause of ACS).

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Echocardiography

Echocardiograms may play an important role in the setting of ACS. Regional wall-motion abnormalities can be identified with this modality, and echocardiograms are especially helpful if the diagnosis is questionable.

An echocardiogram can also help in defining the extent of an infarction and in assessing overall function of the left and right ventricles. In addition, an echocardiogram can help to identify complications, such as acute mitral regurgitation, LV rupture, and pericardial effusion.

Absence of segmental wall-motion abnormality on echocardiography during active chest discomfort is a highly reliable indicator of a nonischemic origin of symptoms, although echocardiography is of limited value in patients whose symptoms have resolved or who have pre-existing wall-motion abnormalities.

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Myocardial Perfusion Imaging

Radionuclide myocardial perfusion imaging has been shown to have favorable diagnostic and prognostic value in the emergent setting, with an excellent early sensitivity in the detection of acute myocardial infarction not found in other testing modalities.

A normal resting perfusion imaging study has been shown to have a negative predictive value of more than 99% in excluding myocardial infarction. Observational and randomized trials of rest and stress imaging in the ED evaluation of patients with chest pain have demonstrated reductions in unnecessary hospitalizations and cost savings compared with routine care.

Perfusion imaging has also been used in risk stratification after myocardial infarction and for measurement of infarct size to evaluate reperfusion therapies. Novel "hot spot" imaging radiopharmaceuticals that visualize infarction or ischemia are currently undergoing evaluation and hold promise for future imaging of ACS.

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Cardiac Angiography

Cardiac catheterization helps in defining coronary anatomy and the extent of a patient’s disease.

Patients with cardiogenic shock, intractable angina (despite medication), severe pulmonary congestion, or right ventricular (RV) infarction should immediately undergo cardiac catheterization. (Cardiogenic shock is defined as a systolic BP of less than 90 mm Hg in the presence of organ hypoperfusion.)

For high-risk patients with ACS without persistent ST elevation, angiography with glycoprotein IIb/IIIa inhibition has been recommended. The earlier that coronary angiography is performed, the lower the risk of recurrent ischaemia.[48] This also shortens the hospital stay for those patients.

Most patients benefit from angiography when they have a TIMI (Thrombolysis in Myocardial Infarction) risk score of less than 3 points (see the Table below).

Table. TIMI Risk Score for Unstable Angina and NSTEMI[49] (Open Table in a new window)

Characteristic Risk Score
History
Age ≥65 years 1
At least 3 risk factors for coronary heart disease 1
Previous coronary stenosis ≥50% 1
Use of aspirin in previous 7 days 1
Presentation
At least 2 anginal episodes in the previous 24 hours 1
ST-segment elevation on admission ECG 1
Elevated levels of serum biomarkers 1
Total Score 0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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Computed Tomography Coronary Angiography and CT Coronary Artery Calcium Scoring

Dual-source 64-slice CT scanners can do a full scan in 10 seconds and produce high-resolution images that allow fine details of the patient's coronary arteries to be seen. This technology allows for noninvasive and early diagnosis of CAD and thus earlier treatment before the coronary arteries become more or completely occluded. It permits direct visualization of not only the lumen of the coronary arteries but also plaque within the artery. Dual-source 64-slice CT scanning is being used with intravenous (IV) contrast to determine if a stent or graft is open or closed.

CT coronary artery scoring is emerging as an attractive risk stratification tool in patients who are low risk for ACS. This imaging modality exposes the patient to very little radiation (1-2 msV). No contrast is needed, and the study does not have a requirement for heart rate.[50]

The CAPTURE study, a randomized diagnostic trial, compared the efficacy a comprehensive cardiothoracic CT examination in the evaluation of patients presenting to the emergency department with undifferentiated acute chest discomfort or dyspnea.[51] Comprehensive cardiothoracic CT scanning was reasonable, with a similar diagnostic yield to dedicated protocols, but it did not reduce the length of stay, rate of subsequent testing, or costs. The “triple rule out” protocol might be helpful in the evaluation of select patients, but these findings suggest that it should not be routinely used with the expectation that it will improve efficiency or reduce resource use.

Another study of the usefulness of CT for reducing hospital admission rates found that coronary computed tomographic angiography (CCTA) appears to allow safe, expedited discharge from the ED of low-to-intermediate-risk patients who would otherwise be admitted.[52]

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Other Techniques

Optical coherence tomography (OCT), palpography, and virtual histology are being studied for use in identifying vulnerable plaques.

Noninvasive whole-blood test prior to coronary angioplasty may be useful for assessing obstructive CAD in patients without diabetes.[53]

Stress cardiac magnetic resonance imaging (MRI) in an observation unit setting has shown to reduce the medical costs, compared with inpatient care, for patients who present with emergent, non-low-risk chest pain, without missing acute coronary syndrome.[54]

The CAPTURE study, a randomized diagnostic trial, compared the efficacy a comprehensive cardiothoracic CT examination in the evaluation of patients presenting to the emergency department with undifferentiated acute chest discomfort or dyspnea.[55] Comprehensive cardiothoracic CT scanning was reasonable, with a similar diagnostic yield to dedicated protocols, but it did not reduce the length of stay, rate of subsequent testing, or costs. The “triple rule out” protocol might be helpful in the evaluation of select patients, but these findings suggest that it should not be routinely used with the expectation that it will improve efficiency or reduce resource use.

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Contributor Information and Disclosures
Author

David L Coven, MD, PhD Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Director, Cardiology Outpatient Clinic, St Luke’s Site, Attending Physician, Department of Medicine, Division of Cardiology, St Luke’s-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society of Echocardiography, Association of Subspecialty Professors, American College of Cardiology, American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.

Arun Kalyanasundaram, MD, MPH Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society of General Internal Medicine, Southern Medical Association, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

Craig T Basson, MD, PhD Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and electrocardiogram (ECG) changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.
A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg and heart rate = 98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.
This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.
Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Use of cardiac markers in the ED. Studies on troponins in ACS.
Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.
Use of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.
Table. TIMI Risk Score for Unstable Angina and NSTEMI [49]
Characteristic Risk Score
History
Age ≥65 years 1
At least 3 risk factors for coronary heart disease 1
Previous coronary stenosis ≥50% 1
Use of aspirin in previous 7 days 1
Presentation
At least 2 anginal episodes in the previous 24 hours 1
ST-segment elevation on admission ECG 1
Elevated levels of serum biomarkers 1
Total Score 0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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