Chadwick D. Miller
This chapter discusses the features of low-probability, or possible, acute coronary syndrome (ACS). Patients classified into this group have no objective evidence of acute coronary ischemia or infarction: there is no characteristic electrocardiogram (ECG) ST-segment elevation or depression, and cardiac markers are not elevated.
Chest pain accounts for approximately 6 million ED visits annually. Only 15% to 25% of patients tested for ACS will have this condition.
ACS is a constellation of signs and symptoms resulting from an imbalance of myocardial oxygen supply and demand.
ACS can be further classified as unstable angina, ST-segment elevation myocardial infarction (STEMI), and non-ST-segment elevation myocardial infarction (NSTEMI).
Unstable angina (UA) is characterized by myocardial ischemia but not infarction; as a result, no elevation of biomarkers and no pathologic ST-segment elevation occur.
Acute myocardial infarction (AMI) occurs when myocardial tissue is devoid of oxygen and substrate for a sufficient period of time to cause myocyte death.
NSTEMI is characterized by biomarker elevation and no pathologic ST-segment elevation.
STEMI is characterized by ST-segment elevation and biomarker elevation, although biomarker elevation is not required at onset to make this diagnosis.
The vast majority of ACS is caused by intraluminal coronary arterial obstruction, usually associated with atherosclerosis.
Atherosclerotic plaques can slowly enlarge, leading to progressive exertional angina. Or, more commonly, plaques become unstable and rupture, leading to coronary artery thrombosis. If the thrombus is completely occlusive, STEMI occurs, but partial occlusion may result in intermittent angina, rest angina, or NSTEMI.
Plaque rupture is unpredictable and commonly occurs in plaques previously demonstrated to be “nonocclusive.”
A key determination by the emergency physician is whether to pursue further evaluation for possible ACS. From 3% to 6% of patients thought to have non-cardiac chest pain or a clear-cut alternative diagnosis, will have a short-term adverse cardiac event.
High-risk historical features include chest pain with any of the following descriptors: radiation to shoulders or arms, occurrence with exertion, pressure sensation, similarity to previous cardiac pain, or accompanying nausea or diaphoresis.
Low-risk historical features include pain that is pleuritic, positional, reproducible, and sharp or stabbing.
Patients with low-risk features, or without high-risk features, may still have a clinically significant risk of ACS. Therefore absence of high-risk, or presence of low-risk historical features should not solely be used to exclude ACS. The clinical features of patients with possible ACS are the same as discussed in Chapter 20.
A previous negative cardiac stress test should not prevent an appropriate evaluation for ACS in a patient with concerning history or ECG findings. Previous stress testing results cannot determine whether the patient’s current symptoms represent new ischemia from a recent plaque rupture.
Previous cardiac catheterization results can be of benefit in determining whether a patient should undergo stress testing after exclusion of myocardial infarction. It is unlikely that a patient with previously normal or near-normal coronary arteries has developed significant epicardial stenosis within 2 years of the procedure.
DIAGNOSIS AND DIFFERENTIAL
The evaluation of patients with possible ACS can be conceptualized into a primary and secondary assessment. The primary evaluation must detect patients with ST-segment elevation that require emergent revas-cularization and distinguish between patients with definite ACS, possible ACS, and those with symptoms that are definitely not ACS. Alternative causes of chest pain should be considered (see Chapter 19).
The primary evaluation should include a history, physical examination, ECG, chest radiography, and cardiac biomarkers if ACS remains in the differential diagnosis. Serial ECGs should be obtained in patients with ongoing symptoms. All available data are used to create a composite picture for decision making.
The pretest ACS probability below which further testing is not indicated is a subject of debate; current recommendations are in the 1% to 2% range.
At the conclusion of the primary evaluation, patients should be classified as having AMI, possible acute ischemia, or definitely not ischemia.
Patients with possible acute ischemia are further stratified into high, intermediate, and low risk for adverse events based on the pattern of symptoms, clinical features, and ECG findings (Table 22-1).
TABLE 22-1 Risk Stratification Scheme for Patients with Possible acute Coronary Syndrome
I. Acute myocardial infarction: immediate revascularization candidate
II. Probable acute ischemia: high risk for adverse events
Clinical instability, ongoing pain thought to be ischemic, pain at rest associated with ischemic ECG changes
III. Possible acute ischemia: intermediate risk for adverse events
History suggestive of ischemia with absence of high-risk features, and any of the following:
Pain at rest, new onset of pain, crescendo pattern of pain, ischemic pattern on ECG not associated with pain (may include ST depression < 1 mm or T-wave inversion > 1 mm)
IV. Possible acute ischemia: low risk for adverse events
History not strongly suggestive of ischemia, ECG normal, unchanged from previous, or nonspecific changes
V. Definitely not ischemia: very low risk for adverse events
Clear objective evidence of non-ischemic symptom etiology, ECG normal, unchanged from previous, or nonspecific changes, clinician estimate of ACS probability < 2%
The TIMI risk score may inform risk assessment decision making, but this score should not be used as the sole determinant as to whether a patient is above or below the testing threshold.
The secondary assessment can be conducted in an observation unit or in the inpatient arena. This assessment should exclude both components of ACS, AMI, andUA.
AMI is excluded through the use of serial tro-ponin measurements to detect myocardial necrosis. Serum troponin levels can take as long as 8 hours from the time of infarction to become elevated. Therefore, a cardiac biomarker approach should take into account the time from symptom onset, and generally should include multiple measurements. A traditional approach is to obtain troponin measurements at the time of arrival and 6 to 8 hours after arrival. An interim 3 to 4 hour measurement may be added depending on clinical circumstances.
Normal serial myocardial marker measurements reduce the likelihood of AMI but do not exclude UA, which if diagnosed still puts the patient at high risk for a subsequent adverse cardiac event. Therefore, patients with possible ACS should undergo some form of objective cardiac testing.
Objective cardiac testing defines either the patient’s coronary anatomy, cardiac function, or both.
Common cardiac testing modalities include stress electrocardiography, stress echocardiography, resting and/or stress nuclear imaging, stress cardiac magnetic resonance imaging (MRI), and computed tomography coronary angiography (CTCA).
Most patients undergo cardiac testing during the hospitalization associated with the ED presentation. Outpatient testing is an option for low-risk patients in whom AMI has been excluded. This option is most useful in reliable patients presenting to a facility where a mechanism exists to arrange this testing.
Selection of an objective cardiac testing strategy needs to take into account the modalities available at each institution. The first determination is whether stress testing or coronary imaging with CTCA is desired.
The most promising application of CTCA is the exclusion of coronary disease in low-risk patients, and its use in this population is supported in the 2007 ACC/AHA Guidelines. At this time, it appears that in patients likely to have, or known to have coronary atherosclerosis, a functional assessment with stress testing is preferable.
If a stress testing approach is desired, the method of stress (exercise or pharmacologic) should be determined based on ability to exercise; those who cannot walk receive pharmacologic stress.
Options for the method of cardiac assessment during stress testing include ECG, nuclear imaging, echocardiography, or MRI-based strategies. Selection from these strategies is often based on institutional expertise and equipment availability. Decision making is informed by matching pretest disease probability with imaging modality sensitivity; radiation exposure risks are also included in decision making.
ECG-based exercise treadmill testing is the least costly and most widely available modality, but has the lowest sensitivity (68%) of the imaging options; it should not be used in patients with high pretest probability for disease. Further, ECG-based exercise treadmill testing should not be used in patients with abnormal baseline ECGs due to difficulties in interpretation.
Stress echocardiography has the advantages of no radiation exposure, improved sensitivity (80%), and wide availability.
Nuclear imaging, also widely available, allows assessment of myocardial perfusion and has high accuracy. However, it is associated with radiation exposure and delays in readying radio-isotopes.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
While testing is ongoing for possible ACS, patients should receive aspirin 160 to 325 milligrams PO, and nitroglycerin 0.4 milligrams spray or sublingual.
If symptoms continue, administer anti-ischemic therapy using β-blockers (metoprolol 25–50 milligrams PO in the first 24 hours) and/or morphine sulfate 1 to 5 milligrams IV. There are several contraindications to β-blockade; they include heart failure, low cardiac output, heart blocks, active reactive airway disease, tachycardia, and hypotension (see Chapter 20, Acute Coronary Syndrome, for further details).
There are other adjunctive treatment options for patients at intermediate risk. The decision to administer these medications should be institution-specific, balanced with the patient’s bleeding risk and potential benefit, and determined through multidis-ciplinary discussions. These options include: (1) dual antiplatelet therapy: a common regimen is clopidog-rel 300 to 600 milligrams PO in addition to aspirin, (2) anti-thrombin therapy: common regimens are heparin 60 units/kg IV bolus (maximum bolus 4000 units) 12 units/kg/h IV infusion (maximum infusion 1000 units/h) or enoxaparin 1 milligrams/kg SC every 12 hours.
Patients with negative serial cardiac markers, without diagnostic ECG changes, and who have normal objective cardiac testing are unlikely to have ACS as a cause of their symptoms.
Consideration should be given to alternative life-threatening causes with further evaluation conducted as appropriate.
Those with positive cardiac markers, diagnostic ECG changes, or diagnostic testing supporting ACS are admitted to the hospital for cardiology care.
Those with nondiagnostic testing should be handled on a case-by-case basis and most should be discussed with a cardiologist.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th edition., see Chapter 55, “Low Probability Acute Coronary Syndromes,” by Chadwick D. Miller.