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Acute Coronary Syndrome
Last Updated: March 27, 2006
Synonyms and related keywords:ACS, angina, myocardial ischemia, acute myocardialischemia, myocardial infarction, MI, coronary artery disease, coronary heart disease, heart
disease, chest pain, atherosclerotic plaques, variant angina, Prinzmetal angina, coronaryvasospasm, stable angina, unstable angina, hypertension, diabetes mellitus, smoking,
hypercholesterolemia, hyperlipidemia
AUTHOR INFORMATION Section 1 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
Author: Drew E. Fenton, MD, Emergency Physician, Department of Emergency
Medicine, St. Mary Medical Center
Coauthor(s):Brigitte M Baumann, MD, DTM & H, Assistant Professor, Head, Division
of Research, Department of Emergency Medicine, University of Medicine and Dentistryof New Jersey, Robert Wood Johnson Medical School; Sarah Stahmer, MD, Residency
Director, Associate Professor, Department of Emergency Medicine, University of
Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School
Drew E. Fenton, MD, is a member of the following medical societies: American Academy
of Emergency Medicine
Editor(s): Edward Bessman, MD, Chairman, Department of Emergency Medicine, JohnHopkins Bayview Medical Center; Assistant Professor, Department of Emergency
Medicine, Johns Hopkins University; Francisco Talavera, PharmD, PhD, Senior
Pharmacy Editor, eMedicine; Gary Setnik, MD, Chair, Department of Emergency
Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine,
Harvard Medical School; John Halamka, MD, Chief Information Officer, CareGroupHealthcare System, Assistant Professor of Medicine, Department of Emergency Medicine,
Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard MedicalSchool; and Jonathan Adler, MD, Attending Physician, Department of Emergency
Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard
Medical School
Disclosure
INTRODUCTION Section 2 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
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Background: The initial diagnosis of acute coronary syndrome (ACS) may be based
entirely on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are
due to myocardial ischemia, the underlying cause of which is an imbalance betweensupply and demand of myocardial oxygen.
Patients with ACS include those whose clinical presentations cover the following rangeof diagnoses: unstable angina, nonST-elevation myocardial infarction (NSTEMI), and
ST-elevation myocardial infarction (STEMI). This ACS spectrum concept is a usefulframework for developing therapeutic strategies.
Pathophysiology: Myocardial ischemia is most often due to atherosclerotic plaques,
which reduce the blood supply to a portion of myocardium. Initially, the plaques allow
sufficient blood flow to match myocardial demand. When myocardial demand increases,the areas of narrowing may become clinically significant and precipitate angina. Angina
that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest,
and without recent change in frequency or severity of activity that produce symptoms, is
called chronic stable angina. Over time, the plaques may thicken and rupture, exposing athrombogenic surface upon which platelets aggregate and thrombus forms. The patient
may note a change in symptoms of cardiac ischemia with a change in severity or ofduration of symptoms. This condition is referred to as unstable angina.
Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct
artery. Angiographic evidence of coronary thrombus formation may be seen in more than
90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. However, not every STEMI evolves
into a Q-wave MI; likewise, a patient with NSTEMI may develop Q waves.
The excessive mortality rate of coronary heart disease is primarily due to rupture andthrombosis of the atherosclerotic plaque. Inflammation plays a critical role in plaquedestabilization and is widespread in the coronary and remote vascular beds. Systemic
inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome.
Evidence indicates that platelets contribute to promoting plaque inflammation as well asthrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging,
providing an opportunity for intervention.
A less common cause of angina is dynamic obstruction, which may be caused by intense
focal spasm of a segment of an epicardial artery (Prinzmetal angina). Coronaryvasospasm is a frequent complication in patients with connective tissue disease. Other
causes include arterial inflammation and secondary unstable angina. Arterial
inflammation may be caused by or related to infection. Secondary unstable angina occurswhen the precipitating cause is extrinsic to the coronary arterial bed, such as fever,
tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who
experience secondary unstable angina have chronic stable angina as a baseline medical
condition.
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Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of
ACS and should be included in the differential diagnosis, especially when a younger
female or cocaine user is being evaluated. An early clinical suspicion of this disease isnecessary for a good outcome. Cardiology consultation should be obtained for
consideration for urgent percutaneous coronary intervention.
Although rare, pediatric and adult ACS may result from the following (see Myocardial
Infarction in Childhood):
ACS may occur with Marfan syndrome; Kawasaki disease; Takayasu arteritis; or
cystic medial necrosis with aortic root dilatation, aneurysm formation, and
dissection into the coronary artery.
Anomalous origin of the left coronary artery from the pulmonary artery mayoccur as unexplained sudden death in a neonate.
Coronary artery ostial stenosis may occur after repair of a transposition of the
great arteries in the neonatal period.
An aberrant left main coronary artery with its origin at the right sinus of Valsalvamay cause ACS, especially with exertion.
Traumatic myocardial infarction can occur in patients at any age.
Accelerated atherosclerosis is known to occur in cardiac transplant recipients on
immunosuppressive therapy.
Progeria
Irrespective of the cause of unstable angina, the result of persistent ischemia ismyocardial infarction (MI).
Frequency:
In the US: Although the exact incidence of ACS is difficult to ascertain, hospital
discharge data indicate that 1,680,000 unique discharges for ACS occurred in2001.
Internationally: In Britain, annual incidence of angina is estimated at 1.1 cases
per 1000 males and 0.5 cases per 1000 females aged 31-70 years. In Sweden,
chest pain of ischemic origin is thought to affect 5% of all males aged 50-57years. In industrialized countries, annual incidence of unstable angina is
approximately 6 cases per 10,000 people.
Mortality/Morbidity: When the only treatment for angina was nitroglycerin andlimitation of activity, patients with newly diagnosed angina had a 40% incidence of MIand a 17% mortality rate within 3 months. A recent study shows that the 30-day mortality
from ACS has decreased as treatment has improved, a statistically significant 47%
relative decrease in 30-day mortality among newly diagnosed ACS from 1987-2000. Thisdecrease in mortality is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and
coronary revascularization via medical intervention or procedures.
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Clinical characteristics associated with a poor prognosis include advanced age, male sex,
prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.
Sex: Incidence is higher in males among all patients younger than 70 years. This is due tothe cardioprotective effect of estrogen in females. At 15 years postmenopause, the
incidence of angina occurs with equal frequency in both sexes. Evidence exists thatwomen more often have coronary events without typical symptoms, which might explain
the frequent failure to initially diagnose ACS in women.
Age: ACS becomes progressively more common with increasing age. In persons aged
40-70 years, ACS is diagnosed more often in men than in women. In persons older than
70 years, men and women are affected equally.
CLINICAL Section 3 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
History:
Typically, angina is a symptom of myocardial ischemia that appears in
circumstances of increased oxygen demand. It usually is described as a sensationof chest pressure or heaviness that is reproduced by activities or conditions that
increase myocardial oxygen demand.
Not all patients experience chest pain. Some present with only neck, jaw, ear,
arm, or epigastric discomfort. Other symptoms, such as shortness of breath or severe weakness, may represent
anginal equivalents.
A patient may present to the ED because of a change in pattern or severity ofsymptoms. A new case of angina is more difficult to diagnose because symptoms
are often vague and similar to those caused by other conditions (eg, indigestion,
anxiety).
Patients may have no pain and may only complain of episodic shortness of breath,weakness, lightheadedness, diaphoresis, or nausea and vomiting.
Patients may complain of the following:
o Palpitations
o Pain, which is usually described as pressure, squeezing, or a burning
sensation across the precordium and may radiate to neck, shoulder, jaw,
back, upper abdomen, or either arm
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o Exertional dyspnea that resolves with pain or rest
o Diaphoresis from sympathetic discharge
o Nausea from vagal stimulation
o Decreased exercise tolerance
o Patients with diabetes and elderly patients are more likely to have atypical
presentations and offer only vague complaints, such as weakness, dyspnea,
lightheadedness, and nausea.
Stable angina
o Involves episodic pain lasting 5-15 minutes
o Provoked by exertion
o Relieved by rest or nitroglycerin
Unstable angina: Patients have increased risk for adverse cardiac events, such as
MI or death. Three clinically distinct forms exist, as follows:
o New-onset exertional angina
o Angina of increasing frequency or duration or refractory to nitroglycerin
o Angina at rest
Variant angina (Prinzmetal angina)
o Occurs primarily at rest
o Triggered by smoking
o Thought to be due to coronary vasospasm
Physical:
Physical examination results are frequently normal. If chest pain is ongoing, thepatient usually will lie quietly in bed and may appear anxious, diaphoretic, andpale.
Hypertension may precipitate angina or reflect elevated catecholamines due to
either anxiety or exogenous sympathomimetic stimulation.
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Hypotension indicates ventricular dysfunction due to myocardial ischemia,
infarction, or acute valvular dysfunction.
Congestive heart failure (CHF)
Jugular venous distention
o Third heart sound (S3)
o A new murmur may reflect papillary muscle dysfunction
o Rales on pulmonary examination, suggesting left ventricular (LV)
dysfunction or mitral regurgitation
o Presence of a fourth heart sound (S4), a common finding in patients with
poor ventricular compliance due to preexisting ischemic heart disease or
hypertension
Causes:
Atherosclerotic plaque is the predominant cause. Coronary artery vasospasm isless common.
Alternative causes of angina include the following:
o Ventricular hypertrophy due to hypertension, valvular disease, or
cardiomyopathy
o Embolic occlusion of the coronary arteries
o Hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders
o Cocaine and amphetamines, which increase myocardial oxygen demand
and may cause coronary vasospasm
o Underlying coronary artery disease, which may be unmasked by severe
anemia
o Inflammation of epicardial arteries
o Coronary artery dissection
Risk factors for ACS should be documented and include the following:
o Male gender
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o Diabetes mellitus (DM)
o Smoking history
o Hypertension
o Increased age
o Hypercholesterolemia
o Hyperlipidemia
o Prior cerebrovascular accident (CVA) - These patients constitute 7.5% of
patients with ACS and have high-risk features.
o Inherited metabolic disorders
o Methamphetamine use
o Occupational stress
o Connective tissue disease
DIFFERENTIALS Section 4 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
AnxietyAortic Stenosis
AsthmaCardiomyopathy, Dilated
Esophagitis
GastroenteritisHypertensive Emergencies
Myocardial Infarction
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Myocarditis
Pericarditis and Cardiac Tamponade
Pneumothorax, Iatrogenic, Spontaneous and PneumomediastinumPulmonary Embolism
WORKUP Section 5 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
Lab Studies:
Troponin I is considered the preferred biomarker for diagnosing myocardial
necrosis. Troponins have the greatest sensitivity and specificity in detecting MI,
and elevated serum levels are considered diagnostic of MI. They also haveprognostic value.
o For early detection of myocardial necrosis, sensitivity of troponin is
superior to that of the creatine kinaseMB (CK-MB). Troponin I isdetectable in serum 3-6 hours after an MI, and its level remains elevated
for 14 days.
o Troponin is a contractile protein that normally is not found in serum. It is
released only when myocardial necrosis occurs.
o Troponin should be used as the optimum biomarkers for the evaluation of
patients with ACS who have coexistent skeletal muscle injury.
Troponin T has similar release kinetics to troponin I and remains elevated for 14
days. False-positive results may occur in patients with renal failure. Minorelevations in troponin T also identify patients at risk for subsequent cardiac
events.
Elevated troponin levels may also point to minor myocardial injury due to other
causes. Zellweger et al described 4 patients with elevated troponin levels aftersupraventricular tachycardia without evidence of coronary artery disease and very
low risk scores for ACS. Similarly, Koller found that endurance athletes may
show elevated serum troponin levels in the absence of ACS.
CK-MB levels begin to rise within 4 hours after MI, peak at 18-24 hours, andsubside over 3-4 days. A level within the reference range does not exclude
myocardial necrosis.
o The upper limit of normal for CK-MB is 3-6% of total CK. A normal level
in the ED does not exclude the possibility of MI. A single assay in the EDhas a 34% sensitivity for MI. Serial sampling over periods of 6-9 hours
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increases sensitivity to approximately 90%. Serial CK-MB over 24 hours
detects myocardial necrosis with a sensitivity near 100% and a specificity
of 98%.
o Occasionally, a very small infarct will be missed by CK-MB; therefore,
troponin levels should be measured for patients suspected to have MI whohave negative results from serial CK-MB tests.
o One study looked at using the 2-hour delta (increase or decrease) of
cardiac markers as 1 of 6 criteria in making the diagnosis of ACS and MI.
According to one of the Erlanger criteria, an increase in the CK-MB level
of 1.5 ng/mL or greater or an increase of the cardiac troponin I level of 0.2ng/mL or greater over 2 hours in itself would allow one to make the
provisional diagnosis of ACS with a high degree of sensitivity and
specificity, even if the total levels were within the normal range. Patients
with recent MI were also identified by a decreasing curve of CK-MB.
Using this 2-hour delta of cardiac markers greatly reduces the number ofcases of MI and ACS that are overlooked in patients who are then
inappropriately discharged home.
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal
muscle, is released more rapidly from infarcted myocardium than troponin and
CK-MB and may be detected as early as 2 hours after MI. Myoglobin levels,
although highly sensitive, are not cardiac specific. They may be useful for earlydetection of MI when performed with other studies.
Cardiac markers should be used liberally to evaluate patients with prolonged
episodes of ischemic pain, with new changes on ECG, or with nondiagnostic ornormal ECGs in whom the diagnosis of ACS or MI is being considered.
Complete blood count is indicated to determine if anemia is a precipitant.
Transfusion with packed red blood cells may be indicated.
Chemistry profile: Obtain a basic metabolic profile, including a check of blood
sugar level, renal function, and electrolytes levels, for patients with new-onsetangina. Potassium and magnesium levels should be monitored and corrected.
Creatinine levels must be considered before using an angiotensin-converting
enzyme (ACE) inhibitor.
Other biochemical markers
o C-reactive protein (CRP) is a marker of acute inflammation. Patients
without biochemical evidence of myocardial necrosis but elevated CRP
level are at increased risk of an adverse event.
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o 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 ofadverse outcomes in patients with unstable angina.
In one study, patients presenting to the ED with suspected myocardial ischemiashowing higher levels of inflammatory cytokines were associated with an
increased risk of a serious cardiac event during the subsequent 3 months.However, the cytokines have limited ability to predict a serious adverse cardiac
event.
Erythrocyte sedimentation rate rises above reference range values within 3 daysand may remain elevated for weeks.
Serum lactase dehydrogenase level rises above the reference range within 24
hours of MI, reaches a peak within 3-6 days, and returns to the baseline within 8-
12 days.
Imaging Studies:
Chest radiograph may demonstrate complications of ischemia, such as pulmonary
edema, or provide clues to alternative causes of symptoms, such as thoracic
aneurysm or pneumonia.
Echocardiogram often demonstrates wall motion abnormalities due to ischemia. Itis of limited value in patients whose symptoms have resolved or in those with
preexisting wall motion abnormalities. However, echocardiogram may be useful
in identifying precipitants for ischemia, such as ventricular hypertrophy andvalvular disease.
Radionuclide myocardial perfusion imaging has been shown to have favorable
diagnostic and prognostic value in this setting, with an excellent early sensitivity
to detect acute myocardial infarction (MI) not achieved by other testingmodalities.
o A normal resting perfusion imaging study has been shown to have a
negative predictive value of more than 99% in excluding MI.Observational and randomized trials of both 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.o Perfusion imaging has also been used in risk stratification after MI 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 imagingof ACS. (See Myocardial Ischemia - Nuclear Medicine and Risk
Stratification.)
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Multislice spiral computed tomography (MSCT) is a new, noninvasive imaging
technique for detecting coronary artery disease. It allows direct visualization of
not only the lumen of the coronary arteries but also plaque within the artery. Afew studies are present in the literature with more underway that may eventually
allow MSCT angiography to determine in real-time presence or absence of
significant coronary artery stenosis or occlusion. This modality does not yet havea weight of evidence to allow its use in the ED as a standard of care to determine
or rule-out coronary artery disease.
Technetium-99m (99mTc) tetrofosmin single-photon emission computed
tomography (SPECT) is a useful method to exclude high-risk patients amongpatients with chest pain in the emergency department.
Resting cardiac magnetic resonance (MR) imaging has exhibited diagnostic
operating characteristics suitable for triage of patients with chest pain in the ED.
Performed urgently to evaluate chest pain, MR accurately detected a high fraction
of patients with ACS, including patients with enzyme-negative unstable angina.MR can identify wall thinning, scar, delayed enhancement (infarction), and wall
motion abnormalities (ischemia). Coronary artery assessment may be coupledwith MR angiography in the future.
Other Tests:
ECG is the most important ED diagnostic test for angina. It may show changes
during symptoms and in response to treatment, which would confirm a cardiac
basis for symptoms. It also may demonstrate preexisting structural or ischemicheart 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 episodesinclude the following:
o Transient ST-segment elevations (fixed changes suggest acute MI): In
patients with elevated ST segments, consider LV aneurysm, pericarditis,
Prinzmetal angina, early repolarization, and Wolff-Parkinson-Whitesyndrome as possible diagnoses.
o Dynamic T-wave changes (inversions, normalizations, or hyperacute
changes): In patients with deep T-wave inversions, consider also CNS
events or drug therapy with tricyclic antidepressants or phenothiazines.
o ST depressions that may be junctional, downsloping, or horizontal
o Diagnostic sensitivity may be increased by performing right-sided leads
(V4R), posterior leads (V8, V9), and serial recordings.
TREATMENT Section 6 of 10
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Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
Prehospital Care: Generally, patients transported with chest pain should initially bemanaged under the assumption that the pain is ischemic in origin. Prehospital
interventions should be guided by the nature of the presenting complaint, individual riskfactors, and associated symptoms (eg, breathing difficulty, hemodynamic instability,
appearance of ectopy). Airway, breathing, and circulation should be rapidly assessed withinstitution of CPR, ACLS-guided interventions, or other measures as indicated for the
unstable patient.
Obtain IV access.
Administer supplemental oxygen.
Aspirin may be given in the field, 162-325 mg PO.
Telemetry and prehospital ECG, if available, may be helpful in selectedcircumstances. Certain EMS systems have investigated protocols for prehospital
administration of thrombolytic therapy. This has not become a trend due tounproven benefit and due to the increase in availability of percutaneous coronary
intervention (PCI) in many medical centers as an alternative to thrombolysis for
STEMI.
Perform pulse oximetry.
Administer sublingual or aerosolized nitroglycerin if chest pain is ongoing and is
felt to be cardiac in origin.
Emergency Department Care: The ACS spectrum concept is a useful framework for
developing therapeutic strategies. Antithrombin therapy and antiplatelet therapy shouldbe administered to all patients with an ACS regardless of the presence or the absence of
ST-segment elevation. Patients presenting with persistent ST-segment elevation are
candidates for reperfusion therapy (either pharmacological or catheter based) to restoreflow promptly in the occluded epicardial infarct-related artery. Patients presenting
without ST-segment elevation are not candidates for immediate pharmacological
reperfusion but should receive anti-ischemic therapy and PCI when appropriate. "Time is
myocardium" is a dictum to be remembered as survival has been shown to correlate withtime to reperfusion in patients with acute MI. Many centers set goals for, and routinely
record, door-to-ECG, door-to-needle (thrombolytic therapy), or door-to-vascular access(for patients receiving PCI) times as measures of quality of care provided.
Goals of ED care are rapid identification of patients with STEMI, exclusion ofalternative causes of nonischemic chest pain, and stratification of patients with
acute coronary ischemia into low- and high-risk groups.
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Obtain IV access, administer supplemental oxygen, and provide telemetry
monitoring if these procedures have not already been accomplished in the
prehospital phase. In addition, obtain a 12-lead ECG as soon as possible afterarrival.
Complete a history and physical examination, with focus on risk factors forcoronary ischemia; onset, duration, and pattern of symptoms; and early
identification of complications of myocardial ischemia (eg, new murmurs, CHF).
Perform frequent reassessment of vital signs and symptoms in response to
administered therapies.
Serial ECGs and continuous ST segment monitoring may be useful.
Many EDs have an observation unit that may be an appropriate disposition for
patients who meet admission criteria.
Medical therapy as discussed inMedication.
Consultations: Cardiology or interventional cardiology consultation may be indicated
for patients with any of the following:
STEMI - Depending on the center, the patient may be a candidate for PCI and
immediate interventional cardiology consultation is indicated.
o Ongoing symptoms highly suggestive of acute coronary ischemia and
nondiagnostic ECG (eg, left bundle-branch block [LBBB])
o Ongoing symptoms refractory to aggressive medical therapy
o Hemodynamic instability
o Evidence of acute valvular dysfunction
o Shock
o Known severe aortic stenosis and ongoing symptoms
o Uncertainty of the diagnosis
MEDICATION Section 7 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
The goals of treatment are to preserve patency of the coronary artery, augment blood
flow through stenotic lesions, and reduce myocardial oxygen demand. All patients should
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receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive
aggressive medical intervention until signs of ischemia, as determined by symptoms and
ECG, resolve.
Drug Category: Antiplatelet agents -- Inhibit the cyclooxygenase system, decreasing the
level of thromboxane A2, which is a potent platelet activator. Antiplatelet therapy hasbeen shown to reduce mortality by reducing the risk of fatal strokes and fatal myocardial
infarctions.
Drug Name
Aspirin (Anacin, Ascriptin, Bayer Aspirin) -- Early
administration of aspirin in patients with AMI may reduce
cardiac mortality in first mo.
Adult Dose160-324 mg PO or chewed; suppository if patient is unableto take PO medications
Pediatric Dose Not established
ContraindicationsDocumented hypersensitivity; liver damage;hypoprothrombinemia; vitamin K deficiency; bleeding
disorders; asthma; children (2 g/d maypotentiate glucose-lowering effect of sulfonylurea drugs
Pregnancy D - Unsafe in pregnancy
Precautions
May cause transient decrease in renal function and
aggravate chronic kidney disease; avoid use in severe
anemia, history of blood coagulation defects, or patientstaking anticoagulants
Drug Category: Nitrates -- These agents oppose coronary artery spasm and reducemyocardial oxygen demand by reducing both preload and afterload.
Drug Name
Nitroglycerin (Nitro-Bid) -- Causes relaxation of the
vascular smooth muscle via stimulation of intracellularcyclic guanosine monophosphate production, causing adecrease in blood pressure.
Adult Dose 400 mcg SL or spray q5min, repeated up to 3 times
If symptoms persist, administer 5-10 mcg/min IV infusion
Dose should be titrated to reduce MAP by 10%, relievesymptoms, limit adverse effects of hypotension (>30%
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reduction in MAP or
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Drug Category: Anticoagulants -- These agents are used to prevent recurrence of clot
after a spontaneous fibrinolysis.
Drug Name
Heparin -- Augments activity of antithrombin III and
prevents conversion of fibrinogen to fibrin. Does not
actively lyse but is able to inhibit further thrombogenesis.Prevents recurrence of a clot after spontaneous fibrinolysis.
Adult Dose 80 U/kg IV bolus, followed by an infusion of 18 U/kg/h
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; diagnosed subacute bacterialendocarditis; active bleeding; history of heparin-induced
thrombocytopenia
Interactions
Digoxin, nicotine, tetracycline, and antihistamines may
decrease effects; NSAIDs, aspirin, dextran, dipyridamole,and hydroxychloroquine may increase heparin toxicity
PregnancyC - Safety for use during pregnancy has not been
established.
Precautions
Observe for prolonged or excessive bleeding at
venipuncture sites; some preparations contain benzylalcohol as a preservative; benzyl alcohol, used in large
amounts, has been associated with fetal toxicity (gasping
syndrome); use of preservative-free heparin isrecommended in neonates; use with caution in patients
diagnosed with shock or severe hypotension
Drug Category: Beta-adrenergic blockers -- These agents have antiarrhythmic andantihypertensive properties as well as the ability to reduce ischemia. They minimize the
imbalance between myocardial supply and demand by reducing afterload and wall stress.In patients with acute MI, they have been shown to decrease infarct size as well as short-
and long-term mortality, which is a function of their anti-ischemic and antiarrhythmic
properties.
Drug Name
Metoprolol (Lopressor) -- Selective beta1-adrenergicreceptor blocker that decreases the automaticity of
contractions.
During IV administration, carefully monitor blood pressure,
heart rate, and ECG. Goal of treatment is to reduce heartrate to 60-90 beats/min.
Adult Dose5 mg slow IV infusion q5min; to a maximum dose of 15 mg
or desired heart rate
Pediatric Dose Not established
Contraindications Documented hypersensitivity; uncompensated congestiveheart failure; bradycardia; asthma; cardiogenic shock; AV
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conduction abnormalities
Interactions
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium
salts, cholestyramine, and rifampin may decrease
bioavailability and plasma levels of metoprolol, possiblyresulting in decreased pharmacologic effects; toxicity of
metoprolol may increase with coadministration ofsparfloxacin, phenothiazines, astemizole (recalled from US
market), calcium channel blockers, quinidine, flecainide,
and contraceptives; metoprolol may increase toxicity of
digoxin, flecainide, clonidine, epinephrine, nifedipine,prazosin, verapamil, and lidocaine
PregnancyC - Safety for use during pregnancy has not been
established.
Precautions
Beta-adrenergic blockade may reduce signs and symptoms
of acute hypoglycemia and may decrease clinical signs of
hyperthyroidism; abrupt withdrawal may exacerbatesymptoms of hyperthyroidism, including thyroid storm;
monitor patients closely and withdraw the drug slowly;during IV administration, carefully monitor blood pressure,
heart rate, and ECG
Drug Name
Esmolol (Brevibloc) -- Excellent drug for use in patients at
risk for complications from beta-blockers, particularly
reactive airway disease, mild-to-moderate LV dysfunction,and peripheral vascular disease. Short half-life of 8 min
allows for titration to desired effect with ability to stop
quickly prn.
Adult Dose
Initial maintenance dose: 0.1 mg/kg/min IV; titrate inincrements of 0.05 mg/kg/min q10-15min to a total dose of
0.2 mg/kg/min
Optional loading dose: 0.5 mg/kg slow IV infusion
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; uncompensated congestiveheart failure; bradycardia; cardiogenic shock; AV
conduction abnormalities
Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium
salts, cholestyramine, and rifampin may decrease
bioavailability and plasma levels, possibly resulting in adecreased pharmacologic effect; conversely, cardiotoxicity
of sotalol may increase when coadministered withsparfloxacin, astemizole (recalled from US market),
calcium channel blockers, quinidine, flecainide, or
contraceptivesToxicity of sotalol increases when administered
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concurrently with digoxin, flecainide, acetaminophen,
clonidine, epinephrine, nifedipine, prazosin, haloperidol,
phenothiazines, or catecholamine-depleting agents
PregnancyC - Safety for use during pregnancy has not beenestablished.
Precautions
Do not use in cocaine-related ischemia; beta-adrenergic
blockade may decrease the signs and symptoms of acute
hypoglycemia and the clinical signs of hyperthyroidism;abrupt withdrawal may exacerbate symptoms of
hyperthyroidism, including thyroid storm; slowly withdraw
drug; closely monitor patients
Drug Category: Glycoprotein IIB/IIA inhibitors -- Glycoprotein (GP) IIb/IIIa antagonists
prevent the binding of fibrinogen, thereby blocking platelet aggregation. Studies to datesuggest that as a class, the addition of intravenous GP IIb/IIIa inhibitors to aspirin and
heparin improves both early and late outcomes, including mortality, Q-wave MI, need forrevascularization procedures, and length of hospital stay.
Currently, IIb/IIIb antagonists in combination with aspirin are considered standardantiplatelet therapy for patients at high risk for unstable angina. Adenosine diphosphate
(ADP) antagonists are not considered standard therapy but may be used in patients unable
to tolerate aspirin.
Drug Name
Abciximab (ReoPro) -- Chimeric human-murinemonoclonal antibody. Binds to receptor with high affinity
and reduces platelet aggregation by 80%. Inhibition of
platelet aggregation persists for up to 48 h after end ofinfusion.
Abciximab has been approved for use in
elective/urgent/emergent percutaneous coronaryintervention.
Adult Dose0.25 mg/kg bolus IV followed by an infusion of 0.125
mcg/kg/min; maximum 10 mcg/min for 12 h
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; bleeding diathesis;
thrombocytopenia (>100,000 cells/mcL); recent trauma;
intracranial tumor and/or hemorrhage; severe uncontrolledhypertension; history of vasculitis; cerebrovascular accident
within 2 years; active internal bleeding; intracranialhemorrhage; hemorrhagic stroke; severe HTN (systolic BP
>200 mm Hg, or diastolic BP >110 mm Hg); major surgical
procedure within the past mo
InteractionsToxicity increases with coadministration of anticoagulants,antiplatelets, and thrombolytics
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PregnancyC - Safety for use during pregnancy has not been
established.
Precautions
Bleeding complications may occur in patients 65
years, with history of GI disease, or recently receivedthrombolytic therapy; severe thrombocytopenia may occur
within first 24 h of usePatients receiving other drugs that affect hemostasis (eg,thrombolytics, NSAIDs, dipyridamole, ticlopidine,
clopidogrel)
Drug Name
Eptifibatide (Integrilin) -- Antagonist of the platelet GP
IIb/IIIa receptor, which reversibly prevents von Willebrand
factor, fibrinogen, and other adhesion ligands from bindingto the GP IIb/IIIa receptor. End effect is the inhibition of
platelet aggregation. Effects persist over duration of
maintenance infusion and are reversed when infusion ends.
Adult Dose
Unstable angina: 180 mcg/kg IV bolus, followed by acontinuous infusion of 2 mcg/kg/min until discharge or
surgery
Patients undergoing PCI: 135 mcg/kg IV bolus; administer before PCI, followed by a continuous infusion of 0.5
mcg/kg/min
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; severe hypertension (SBP
>200 mm Hg); active internal bleeding; history ofintracranial hemorrhage; intracranial neoplasm,
arteriovenous malformation, or aneurysm; acute pericarditis;
bleeding diathesis; trauma or stroke within previous 30 d;platelet count 2 mg/dL (for 180mcg/kg bolus and 2 mcg/kg/min infusion) or >4 mg/dL (for
135 mcg/kg bolus and 0.5 mcg/kg/min infusion)
History of bleeding diathesis within 30 d; intracranialhemorrhage; history of hemorrhagic stroke; severe HTN
(systolic BP >200 mm Hg, or diastolic BP >110 mm Hg);
major surgical procedure within the past mo
Interactions
When used with heparin and aspirin, an increase inbleeding, compared with using heparin and aspirin alone,
can occur
If using concurrently with other drugs that affect hemostasis
(eg, warfarin), closely monitor patients
PregnancyC - Safety for use during pregnancy has not been
established.
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Precautions
Most common complications encountered during therapy
with eptifibatide are bleeding events; caution in patients
with a platelet count 200 mm Hg, or diastolic BP >110 mm Hg);
major surgical procedure within the past mo
Interactions When used with heparin and aspirin, an increase in
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bleeding, compared with using heparin and aspirin alone,
can occur
If using concurrently with other drugs that affect hemostasis(eg, warfarin), closely monitor patients
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
Most common complications in therapy with tirofiban are
bleeding events; caution in patients with platelet counts
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combination of eptifibatide with enoxaparin appears to have a more potent antithrombotic
effect than that of eptifibatide and unfractionated heparin (UFH).
Drug Name
Enoxaparin (Lovenox) -- LMWH is produced by partial
chemical or enzymatic depolymerization of UFH. Binds to
antithrombin III, enhancing its therapeutic effect. Theheparin-antithrombin III complex binds to and inactivates
activated factor X (Xa) and factor II (thrombin). LMWHdiffers from unfractionated heparin by having a higher ratio
of antifactor Xa to antifactor IIa compared to UFH.
Adult Dose
1 mg/kg administered SC q12h in conjunction with oral
aspirin (100-325 mg/d); maximum antifactor Xa andantithrombin activities occur 3-5 h postadministration
Pediatric Dose Not established
ContraindicationsDocumented hypersensitivity; major bleeding;
thrombocytopenia
Interactions
Platelet inhibitors or oral anticoagulants (eg, dipyridamole,salicylates, aspirin, NSAIDs, sulfinpyrazone, ticlopidine)
may increase risk of bleeding
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
If thromboembolic event occurs despite LMWH
prophylaxis, discontinue drug and initiate alternate therapy;elevation of hepatic transaminases may occur but is
reversible; heparin-associated thrombocytopenia may occur
with fractionated LMWHs; 1 mg of protamine sulfate will
reverse effect of approximately 1 mg of enoxaparin ifsignificant bleeding complications develop
Drug Category:Direct thrombin inhibitors -- Hirudin is the prototype of direct thrombin
inhibitors. Hirudin binds directly to the anion binding site and the catalytic sites of
thrombin to produce potent and predictable anticoagulation.
Drug Name
Hirudin (Lepirudin, Refludan) -- When compared tounfractionated heparin in unstable angina trials, hirudin
demonstrated a modest short-term reduction in the
composite end point of death or nonfatal MI. Risk of
bleeding is increased modestly. Currently, hirudin isindicated only in patients unable to receive heparin because
of heparin-induced thrombocytopenia.
Adult Dose
0.4 mg/kg IV bolus over 15-20 s, followed by a continuousinfusion of 0.15 mg/kg/h; goal is to increase aPTT 1.5-2.5
times the control; adjust dosing in renal impairment
Pediatric Dose Not established
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Contraindications Documented hypersensitivity
Interactions
Intracranial bleeding may be life threatening following
concomitant thrombolytic therapy with rt-PA or
streptokinase
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
Associated with an increased need for transfusion
(compared to unfractionated heparin) and increased risk of
intracranial hemorrhage; no specific antidote exists; if life-threatening bleeding occurs, stop administration, determine
coagulation profiles, send T/S, and prepare for blood
transfusion
Drug Name
Bivalirudin (Angiomax) -- Used for anticoagulation in
unstable angina undergoing PTCA. Synthetic analogue ofrecombinant hirudin. Inhibits thrombin. Potential
advantages over conventional heparin therapy include more
predictable and precise levels of anticoagulation, activityagainst clot-bound thrombin, absence of natural inhibitors
(eg, platelet factor 4, heparinase), and continued efficacy
following clearance from plasma (because of binding to
thrombin).
Adult Dose
1 mg/kg IV bolus initially; followed by 2.5 mg/kg/h IV for 4
h; may administer additional IV infusion at 0.2 mg/kg/h (not
to exceed 20 h); administer with aspirin 325 mg/d
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; cerebral aneurysm;
intracranial hemorrhage, general uncontrollablehemorrhage, or active major bleeding
Interactions
Coadministration with antiplatelets (other than aspirin) or
other anticoagulants has not been evaluated fully, usecaution
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
Caution in renal impairment (adjust dose), recent surgery or
trauma, GI ulceration; risk of bleeding; may cause back
pain, nausea, headache, hypotension
Drug Category: Adenosine diphosphate receptor antagonists -- Two thienopyridines,ticlopidine and clopidogrel, are ADP antagonists that are approved for antiplatelet
activity. Both have irreversible antiplatelet activity but take several days to become
manifest. A potential additive benefit exists when ADP antagonists are used in
conjunction with aspirin.These drugs may be considered alternatives to aspirin in patients intolerant or allergic to
aspirin.
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Drug Name
Clopidogrel (Plavix) -- Generally preferred over ticlopidine
because it more rapidly inhibits platelets and appears to
have a more favorable safety profile.
Adult Dose 300 mg PO loading dose, followed by 75 mg PO qd
Pediatric Dose Not established
ContraindicationsDocumented hypersensitivity; active bleeding; peptic ulcer
or CNS hemorrhage
Interactions
Safety of concomitant use of heparin not established;
coadministration with NSAIDS is associated with increasedgastrointestinal bleeding
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
TTP has been reported rarely after use of Plavix; caution in
patients at risk of bleeding from trauma, surgery, or other
pathological conditions; caution in prolonged bleeding
time/liver disease
Drug Name
Ticlopidine (Ticlid) -- Beneficial effects were noted in
patients with UA after 2 wk of use in one randomized trial.
When compared to controls, ticlopidine use decreasedvascular deaths and nonfatal MIs.
Adult Dose 250 mg PO bid
Pediatric Dose Not established
Contraindications
Documented hypersensitivity; presence of neutropenia or
thrombocytopenia or a past history of either TTP or aplastic
anemia; hemostatic disorder or active bleeding; severe liver
impairment
Interactions
Effects may decrease with coadministration of
corticosteroids and antacids; toxicity increases when taken
concurrently with theophylline, cimetidine, aspirin, andNSAIDS
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions
Discontinue if absolute neutrophil count decreases to
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Patients with unstable angina and/or ECG changes should be admitted to a
telemetry bed. A certain subset of patients with stable angina may be treated as
outpatients with antianginal agents, but close follow-up is necessary.
Patients with symptoms refractory to aggressive medical treatment, shock,
suspected or known aortic stenosis, or new or worsening mitral regurgitation areat high risk. Management for these patients should include the following:
o Admission to an intensive care unit setting
o Cardiology consultation
Consideration for intra-aortic balloon pump (IABP) and early angiography to
delineate anatomy
Continue antiplatelet and antianginal medications initiated in the ED. Subsequent
dosing is determined by symptomatic response and tolerance of side effects.
The routine use of lidocaine as prophylaxis for ventricular arrhythmias in patients
with ACS is not indicated. In MI, it has been shown to increase mortality rates.
Lidocaine may be used for patients with complex ventricular ectopy or for
patients with hemodynamically significant, nonsustained, or sustained ventriculartachycardia.
Further Outpatient Care:
Patients with chronic stable angina may be considered for discharge after
occurrence of the following:
o Symptom duration is brief and identical to symptoms experienced in the
past.
o ECG is normal or unchanged.
o Patient has access to timely follow-up with a primary care physician.
When in doubt, admit. The usual reason for a patient with chronic stable angina topresent to the ED is a change in pattern or severity of symptoms, which makes
their angina unstable.
A recent study by Bartholomew et al may be helpful in making the decision to
admit or discharge. This prospective thrombolysis in myocardial infarction riskscore (TIMI-RS) used 7 variables in patients with suspected ACS: (1) age older
than 65, (2) 3 or more cardiac risk factors, (3) ST deviation, (4) aspirin use within
7 days, (5) 2 or more anginal events over 24 hours, (6) history of coronary
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stenosis, and (7) elevated troponin levels. Patients were contacted at 30 days and
data was collected concerning major adverse cardiac events.
o In patients presenting with chest pain, a higher TIMI-RS was associated
with an increase in major adverse cardiac events within 30 days. The
authors concluded that the 30-day event rate was 0% for a score of 1, 20%for a score of 2, 24% for a score of 3, 42% for a score of 4, 52% for a
score of 5, and 70% for a score of 6 or 7 (p < 0.0001).
o The TIMI-RS successfully differentiates early risk for major adverse
cardiac events in a general population presenting with symptoms
suggestive of ACS. A simple bedside calculation of the TIMI-RS providesrapid risk stratification, allowing facilitation of therapeutic decision-
making in patients with symptoms suggestive of ACS and may be helpful
with the patient's disposition.
In/Out Patient Meds:
Aspirin
o Use clopidogrel as a substitute for patients unable to take aspirin because
of a history of hypersensitivity or bleeding.
o Use a 300-mg loading dose, then 75 mg qd.
Nitrates
o Use topical or oral nitrates for those who are discharged or for those who
are stable inpatients.
o Intravenous infusion is preferable for those admitted with unstable
symptoms.
Beta-blockers
o Metoprolol and propranolol are excellent choices for inpatient and
outpatient management.
o Use esmolol for inpatient treatment, particularly those at risk for adverse
effects from beta-blockade.
Heparin: Use heparin for inpatient management of unstable angina. Some
preliminary data suggest that LMWH is a safe and effective alternative.
Significant clustering of recurrent ischemic events occurs within 24 hours after
cessation of both short-term UFH and enoxaparin treatment, and patients should
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be carefully monitored during that period. This early rebound may be prevented
by continuation of a fixed dose of enoxaparin.
Transfer:
Consider transfer only for particularly patients at particularly high risk and forthose who are being evaluated in a center without access to timely cardiac
catheterization, PTCA, or bypass.
High-risk criteria include the following:
o Symptoms refractory to medical management
o Hemodynamic instability, cardiogenic shock
o New or worsening mitral regurgitant murmur
o Known or suspected severe aortic stenosis
The risks of transferring these unstable patients must be carefully weighed against
the benefits of transfer.
Deterrence/Prevention:
Cessation of smoking
Assessment of lipid profile and dietary changes, where appropriate (Among
patients who have recently had an ACS, an intensive lipid-lowering statin regimenprovides greater protection against death or major cardiovascular events than astandard regimen [Cannon, 2004].)
Blood pressure control
Compliance with medications, particularly aspirin
Comprehensive risk assessment by primary care physician, including exercise
tolerance test (ETT) for individuals at high risk and identification of structuralheart disease (eg, left ventricular hypertrophy [LVH], aortic stenosis)
Complications:
Acute myocardial infarction
Cardiogenic shock
Ischemic mitral regurgitation
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Arrhythmias
o Supraventricular arrhythmias (rare complication of ischemia, may actually
precipitate ischemic events)
o Ventricular arrhythmias; simple and complex premature ventricularcontractions (PVCs), and nonsustained ventricular tachycardia (NSVT)
Atrioventricular nodal blockade
o Usually transient in setting of reversible ischemia
o Treatment guided by location of block and hemodynamic stability.
Ventricular rupture occurs in the interventricular septum or the LV free wall. Thisrepresents a catastrophic event with mortality rates greater than 90%. Prompt
recognition, stabilization, and surgical repair are crucial to any hope of survival.An echocardiogram usually will define the abnormality, and a right heartcatheterization may show an oxygenation increase with septal rupture.
Prognosis:
Patients with angina either go on to infarct or have their disease stabilized by
medical and/or interventional therapies. Patients with angina are a heterogeneous
group; therefore, prognosis varies with respect to stability of disease,demographics, comorbidity, and current intervention.
Patients with ACS with atrial fibrillation (AF) are associated with increased
morbidity and mortality (Mehta, 2003). Patients with ACS and DM, especially those with ST elevation, had increased in-
hospital mortality. Among patients with ACS and DM, those receiving insulin had
worse outcomes. Outcomes were similar for those on hypoglycemic medication oron diet alone (Hasdai, 2003).
In chronic stable angina, prognosis is generally excellent. Factors that have been
shown to impact prognosis include the following:
o Aspirin reduces progression to both nonfatal MI and cardiac death.
o Beta-blockers control anginal symptoms and reduce cardiac complicationsin patients with hypertension.
o PTCA and revascularization improve the prognosis in high-risk patients.
o Poor prognostic factors include male sex, diabetes, and hypertension.
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In unstable angina, prognosis is determined by the ability to control symptoms
acutely, preventing progression to AMI. Factors associated with a poorer
prognosis include the following:
o Evidence of myocardial necrosis, as determined by elevated troponin T
o Delays in angiography in patients at high risk (Early angiography allows
for triage to medical therapy, PTCA, or revascularization.)
Patient Education:
For patients being discharged home, emphasize the following:
o Timely follow-up with primary care physician
o Compliance with discharge medications, specifically aspirin and other
medications used to control symptoms
o Need to return to ED for any change in frequency or severity of symptoms
MISCELLANEOUS Section 9 of 10
Author Information Introduction Clinical Differentials Workup TreatmentMedicationFollow-upMiscellaneousBibliography
Medical/Legal Pitfalls:
Failure to consider the diagnosis - Groups at risk include the following:
o Women, particularly premenopausal
o Diabetics
o Elderly
o Patients with cocaine-related ischemia
Inadequate risk stratification in ED
Failure to administer aspirin as first-line therapy
Overcautious use of beta-blockers in ED
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