AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Angina pectoris (AP) represents the clinical syndrome occurring when myocardial oxygen demand exceeds supply. The term is derived from Latin; the literal meaning is "the choking of the chest;" angere, meaning "to choke" and pectus, meaning "chest." The first English-written account of recurrent angina pectoris was by English nobleman Edward Hyde, Earl of Clarendon. He described his father as having, with exertion, "a pain in the left arm…so much that the torment made him pale".¹ The first description of angina as a medical disorder came from William Heberden. Heberden, a prodigious physician, made many noteworthy contributions to medicine during his career. He presented his observations on "dolor pectoris" to the Royal College of Physicians in 1768. Much of his classic description retains its validity today.²

Angina pectoris has a wide range of clinical expressions. The symptoms most often associated to angina pectoris are substernal chest pressure or tightening, frequently with radiating pain to the arms, shoulders, or jaw. The symptoms may also be associated with shortness of breath, nausea, or diaphoresis. Symptoms stem from inadequate oxygen delivery to myocardial tissue. No definitive diagnostic tools that capture all patients with angina pectoris exist. This, combined with its varied clinical expression, makes angina pectoris a distinct clinical challenge to the emergency physician. The disease state can manifest itself in a variety of forms:

• Stable angina pectoris is classified as a reproducible pattern of anginal symptoms that occur during states of increased exertion.
• Unstable angina pectoris (UA) manifests either as an increasing frequency of symptoms or as symptoms occurring at rest.
• Prinzmetal angina or variant angina occurs as a result of transient coronary artery spasms. These spasms can occur either at rest or with exertion. Unlike stable or unstable angina, no pathological plaque or deposition is present within the coronary arteries that elicits the presentation. On angiography, the coronary arteries are normal in appearance.
• Cardiac syndrome X occurs when a patient has all of the symptoms of angina pectoris without coronary artery disease or spasm.

Pathophysiology

The past 2 decades has greatly expanded our overall understanding of the pathophysiology of myocardial ischemic syndromes. The primary dysfunction in angina pectoris is decreased oxygen delivery to myocardial muscle cells. The 2 predominant mechanisms by which delivery is impaired appear to be coronary artery narrowing and endothelial dysfunction. Any other mechanism that affects oxygen delivery can also precipitate symptoms.

Extracardiac causes of angina include, but are by no means limited to, anemia, hypoxia, hypotension, bradycardia, carbon monoxide exposure, and inflammatory disorders.³ The end result is a shift to anaerobic metabolism in the myocardial cells. This is followed by a stimulation of pain receptors that innervate the heart. These pain receptors ultimately are referred to afferent pathways, which are carried in multiple nerve roots from C7 through T4. The referred/radiating pain of angina pectoris is believed to occur because these afferent pathways also carry pain fibers from other regions (eg, the arm, neck, and shoulders).

Coronary artery narrowing

Coronary artery narrowing appears to be the etiology of cardiac ischemia in the preponderance of cases. This has clinical significance when atherosclerotic disease diminishes or halts blood flow through the coronary arterial circulation, interfering with normal laminar blood flow. The significance of even a small change in the diameter of a blood vessel can be profound. The Poiseuille law predicts this outcome—the rate of flow is decreased exponentially by any change in the radius of the lumen. As with a smaller pediatric airway, even relatively minute changes in diameter have dramatic consequences in flow rates. Thus, when a lumen is narrowed by one fifth, the flow rate is decreased by about one half. This predicts that even a small change in a coronary artery plaque size can affect the oxygenation through that vessel's territory.

The epicardial vessel, where atherosclerosis often takes place, has the capacity to dilate via autoregulatory mechanisms to respond to increased demand. Angina occurs as this compensatory mechanism is overwhelmed either by large plaques (typically considered 70% or greater obstruction) or by significantly increased myocardial demand.⁴

Endothelial factors

Endothelial factors also play an important role in angina pectoris. During sympathetic stimulation, the endothelium is subjected to mediators of both vasoconstriction and vasodilatation. Alpha-agonists (catecholamines) directly cause vasoconstriction, while endothelial nitrous oxide synthase creates nitrous oxide (NO), which counteracts this constricting force via vasodilatation. 

In the diseased coronary artery, NO production is reduced or absent. In this setting, the catecholamine drive can overwhelm the autoregulatory mechanisms. In addition, the endothelium of the plaque-laden artery may, in itself, be dysfunctional. This limits the ability of the intra-arterial endothelium to produce mediators, which, in a healthy artery, would protect against further vasoconstriction, assist dilatation, and provide protection from platelet aggregation. Small lesions in these vessels may produce incompletely obstructing aggregates of platelets. This would further impede flow through the affected vessel.⁴

In the diseased heart, these 2 factors, coronary artery narrowing and endothelial dysfunction, synergistically result in reduced oxygen delivery to the myocardium. The net result is angina pectoris.

Extrinsic factors

Extrinsic factors can also play a role in specific circumstances. The oxygen-carrying capacity of blood is based on a number of factors. The most important of which is the amount of hemoglobin. Any alteration in the ability of blood to carry oxygen can precipitate angina. Anemia of any degree can result in anginal symptoms. Given a scenario where demand is increased, such as climbing a flight of stairs, increased stress, or even sexual intercourse, the anginal symptoms may appear.⁵ Abnormal hemoglobin, such as methemoglobin, carboxyhemoglobin, or any of a number of hemoglobinopathies, creates an environment at greater risk for precipitating angina.

Other extrinsic factors that affect hemoglobin formation, such as lead poisoning or iron-deficiency states, also lead to a similar decrease in oxygen-carrying capacity. Any mechanism that impedes oxygen delivery to the red blood cells has a similar effect. Therefore, any number of pulmonary causes, such as pulmonary embolism, pulmonary fibrosis or scarring, pneumonia, or congestive heart failure, can exacerbate angina. A decreased oxygen environment, such as travel to a higher elevation, has similar consequences due to the decrease in concentration of atmospheric oxygen.

Variant angina

The etiology of variant angina is currently not well understood. Research suggests that inflammatory mediators may result in focal coronary artery vasospasm. Another possibility is that perfusion is decreased through microvascular circulation. Spasm or intermittent narrowing of this microscopic lumen may result in transient areas of hypoperfusion and oxygen deprivation.⁶

Syndrome X

Syndrome X is the triad of angina pectoris, a positive ECG stress test result, and a normal coronary angiogram. The pathophysiology of this disease is not well understood. Many theories exist as to the underlying pathology. Decreased oxygenation of the underlying myocardium may be the result of impaired vasodilatation, dysfunctional smooth muscle cells, poor or deficient microvascular circulation, or even structural problems on a cellular level (eg, an inappropriately functioning sodium ion channel).⁶

Frequency

United States

An estimated 6,500,000 people in the United States experience angina pectoris.

Each year 400,000 new cases of angina pectoris develop.

Mortality/Morbidity

More than 479,000 people died from coronary heart disease (both angina and myocardial infarction) in 2003.

The estimated direct and indirect cost for Americans with coronary heart disease in 2006 was $142.5 billion.

Race

The Centers for Disease Control and Prevention (CDC) note that the prevalence of angina and/or coronary heart disease is highest in Hispanics followed by whites and black non-Hispanics (5%, 4.2%, 3.7%, respectively). This information includes the 50 US states, the District of Columbia, Puerto Rico, and the US Virgin Islands.⁷

Sex

According to National Health and Nutrition Examination Survey (NHANES) data, the age-adjusted prevalence of self-reported angina appears to be higher in woman than in men. Although 2005 CDC data suggest that men (5.5%) have a higher prevalence of angina and/or coronary heart disease than women (3.4%).⁷

Age

The incidence of new and recurrent angina increases with age but then declines at around 85 years.

Statistics from American Heart Association and Centers for Disease Control and Prevention.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Classically, angina presents as substernal chest discomfort that occurs with exertion, but it also may occur at rest. The discomfort is frequently described as a pressure or heaviness. Other commonly used adjectives for anginal pain include dull, aching, or squeezing. Pain may radiate to one or both arms, to one or both shoulders, or to the neck or jaw. Symptoms are highly variable. The entity cannot be expected to present with the classic triad of chest pressure with exertion radiating to the left arm. The diversity of disease expression is likely related to a patient's age, sex, race, and culture.

The caveat is to have a high index of suspicion for the disease. Many factors influence the expression of anginal symptoms. Familiar terms such as anginal equivalent and atypical chest pain are frequently used in these cases. In addition, systemic diseases, such as diabetes mellitus or chronic pain syndromes, may alter presenting anginal symptoms; while other diseases, such as prior cerebral vascular accident or dementia, may limit the patient's reporting of symptoms. A pain-free variant of angina—sometimes referred to as silent chest pain—also exists. These patients can present with complaints of shortness of breath, nausea, altered mentation, or abdominal pain.⁸

• Chest discomfort quality
• • Pain
  • Pressure
  • Squeezing
  • Dullness
  • Burning
  • Heaviness
  • Absent chest discomfort (eg, dyspnea, vomiting, altered sensorium)
• Location (often diffuse to any location of C7-T4 dermatomes)
• • Retrosternal or substernal
  • Inframammary
  • Left sided
  • Right sided
  • Upper abdominal
  • Shoulder, neck, arm
  • Teeth, jaw, lower face (above C7 unclear etiology)
  • Back, scapular region
• Radiation
• • Unilateral or bilateral arms
  • Unilateral or bilateral shoulders
  • Back
  • Neck
  • Jaw, ear, or lower face
• Temporal
• • Onset to maximum discomfort is progressive.
  • • With exertion (with or without increasing frequency)
    • At rest
  • Alleviation to relief is progressive.
  • Alleviation mediators
  • • Oxygen
    • Nitroglycerin
    • Reduction of stressful activity
    • Pain medication
    • Placebo effect (eg, "GI cocktail")
• Severity
• • Mild to severe (1/10 to >10/10)
  • "Like my heart pain" - Patients in the emergency department (ED) may refer to the pain as being consistent with prior heart pains.

Physical

The physical examination may reveal signs of a hyperadrenergic state. One might observe tachycardia, tachypnea, hypertension, and/or diaphoresis. In addition, ischemia may lead to the presence of crackles due to the loss in contractility with subsequent pulmonary edema or a reduction in the S₁ intensity.⁹

That said, no definitive examination findings suggest angina. Much of the information obtained from the physical examination may suggest other comorbidities that place the patient at higher risk for anginal symptoms (eg, chronic obstructive pulmonary disease [COPD], tachycardia, pale conjunctiva). Therefore, the physical examination is necessary to qualify the patient's current physical state and comorbidities. In this manner, the emergency physician obtains a baseline physical examination. Also, as mentioned, comorbid illnesses that affect the patient's level of cardiac, pulmonary, and circulatory function can be assessed.

As with many presentations to the emergency department, the physical examination in angina pectoris also serves as a marker for response to therapy. Important comorbidities that can be identified on physical examination include aortic stenosis, gastrointestinal bleeding, and airway obstruction. Unfortunately, no examination findings are pathognomonic for angina pectoris. In addition, no physical examination findings rule out the disease state.

Of note, while the reproducibility of chest wall pain with palpation may lower the likelihood of angina, this alone cannot rule out angina or myocardial infarction.^{10, 11}

Causes

See Pathophysiology.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Abdominal aortic aneurysm
Anxiety disorders
Aortic dissection
Boerhaave syndrome
Biliary colic
Cardiomyopathy, hypertrophic
Cholecystitis
Coronary artery atherosclerosis
Coronary artery vasospasm
Gastric ulcers
Gastritis, acute
Gastroesophageal reflux disease
Hiatal hernia
Hypercholesterolemia, familial
Hypercholesterolemia, polygenic
Hypertension
Hyperventilation syndrome
Isolated coronary artery anomalies
Kawasaki disease
Panic disorder
Peptic ulcer disease
Pericardial effusion
Pericarditis, acute
Pleurodynia
Pneumothorax
Polyarteritis nodosa
Pott disease (tuberculous spondylitis)
Pulmonary hypertension, primary
Pulmonary hypertension, secondary
Scleroderma
Takayasu arteritis
Tietze syndrome
Varicella-zoster virus anemia
Esophageal spasm
Pneumonia with pleural involvement

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• CBC (anemia, leukocytosis may suggest an alternative diagnosis)
• BUN and creatinine level, if intravenous contrast is anticipated
• Electrolyte levels are of virtually no value unless the patient is on a diuretic and concern for an abnormality exists.
• Cardiac enzyme levels, if positive may suggest non–ST-segment elevation myocardial infarction (NSTEMI); negative results do not rule out ischemia
• Coagulation studies, if anticoagulation or antiplatelets are anticipated
• Type and screen, if surgery or transfusions are considered

Imaging Studies

• Chest radiography is used to rule out an alternative diagnosis or contributing factors (eg, pneumothorax [PTX], pneumonia [PNA], congestive heart failure); it is also used to evaluate the aorta prior to anticoagulant administration.
• CT of the chest may be considered for evaluation of aortic or pulmonary disease; if evaluating the aorta include the abdominal aorta. Of note, the forthcoming "triple rule out CT scan" exposes the patient to an exorbitantly high dose of radiation and should only be used in certain circumstances.
• Nuclear imaging
• • V/Q (PE evaluation)
  • Resting Sestamibi (In the appropriate clinical setting, a normal study in a patient with ongoing chest pain may rule out myocardial ischemia.¹²
• ECG
• • Results may be normal or show signs of ischemia.
  • Main use is to establish a baseline and R/O acute ST-segment elevation myocardial infarction (STEMI).

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

Often, patients with angina pectoris rest or lie down to alleviate the pain. If the patient is not naive to cardiac disease, he or she may have access to nitroglycerin. Often, the patient uses nitroglycerin at home to palliate his or her symptoms. A patient who has known stable angina often is able to report what exacerbates the condition and what (as well as how often) is a "normal" number of tablets for him or her to use prior to alleviation of anginal symptoms. Patients are often instructed by their physicians that the use of more than 3 tablets of nitroglycerin necessitates a higher level of care (eg, calling for an ambulance). Some patients are instructed to take aspirin as well. A knowledgeable patient who reports a change in the pattern or presentation of his or her symptoms should be suspected as having worsening or unstable angina. However, any patient who presents to the ED with symptoms of angina should be assessed promptly for signs of acute myocardial infarction (AMI).

Most prehospital care for angina pectoris consists of administering nitroglycerin, oxygen, and aspirin. The ability to obtain a prehospital ECG is becoming more prevalent.

Emergency Department Care

In the ED, the patient who complains of chest discomfort needs to be immediately assessed for AMI as well as other high-risk diagnoses (eg, aortic dissection, pulmonary embolism). Vital in this assessment is an early ECG and a rapid history and physical examination. Should this initial encounter not reveal a definitive diagnosis, then a more focused history and physical examination needs to be performed. Serial ECGs, especially in the setting of changing symptoms, is imperative. Labeling the ECGs with the patient's level of pain is often useful. A consecutive series of ECGs taken when a patient is having "10/10" pain, "3/10" pain, and "0/10" pain may yield valuable information that would not be readily apparent with an isolated cardiogram. Continuous telemetry monitoring is recommended for higher-risk patients.¹³

• The patient who presents with chest pain is presumed to have underlying clinically significant cardiac pathology (ie, unstable angina or NSTEMI).
• • The initial treatment consists of administration of oxygen, aspirin, nitroglycerin, morphine, and a beta-blocker. Given an altered, yet nondiagnostic ECG and no contraindications, further treatment with heparin (low-molecular weight or unfractionated), clopidogrel, or other antiplatelet agents may be initiated. Most often, an additional marker (eg, an elevated serum troponin, myoglobin, or CPK level) will be used prior to antiplatelet therapy.
  • For persistent symptoms unresponsive to initial therapy, glycoprotein inhibitors can be considered. These appear to demonstrate an additional benefit in the patient population who will be undergoing cardiac catheterization (PCI).¹⁴ Persistent pain, in spite of this treatment, suggests either AMI or an alternative diagnosis. In the case of AMI, angioplasty or thrombolytics should be administered if available and not contraindicated. The American College of Cardiology offers an excellent evidenced-based online treatment resource (see American College of Cardiology Clinical Statements/Guidelines).
• Atypical presentations of angina, unfortunately, are often diagnosed retrospectively. This subset of patients is identified either when their condition progresses to STEMI or through elevated serum marker levels or cardiac dysrhythmia (often ventricular tachycardia or fibrillation). It cannot be understated that the variance of expression of angina pectoris makes it imperative that the clinician have a high level of suspicion for the disease. Little value exists in relying on a constancy of expression or on ECG, history, or physical examination alone for making the diagnosis. Angina pectoris should be considered as well as an extensive differential diagnosis, in just about any patient who presents to the ED with chest pain with or without other nonspecific complaints.
• Syndrome X and Prinzmetal angina are not diagnosed in the ED, but the patient's medical records or primary care physician may be helpful in recognizing these disorders.
• Admission is indicated for patients with unstable angina.

Consultations

In the setting of unstable angina or AMI, consultation with a cardiologist is warranted.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goal of all of the following medications is either to improve myocardial oxygen and glucose supply or to reduce myocardial oxygen and glucose demand.

The use of thrombolytics in unstable angina and NSTEMI are not useful and potentially harmful. They should be reserved for use in STEMI when indicated.¹⁵ (For more information, see American College of Cardiology Clinical Statements/Guidelines.)

Drug Category: Anti-platelet agents

These agents inhibit platelet aggregation.

Drug Category: Vasodilators

These agents relieve chest discomfort by improving myocardial oxygen supply, which, in turn, dilate epicardial and collateral vessels, improving blood supply to the ischemic myocardium.

Drug Category: Analgesics

These agents reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.

Drug Category: Beta-adrenergic blockers

This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand, secondary to elevations in heart rate and inotropy.

Drug Category: Calcium channel blockers

When beta-blockade is contraindicated in the setting of continuing angina, a nondihydropyridine calcium antagonist (eg, verapamil, diltiazem) may be used as initial therapy in the absence of severe LV dysfunction or other contraindications (see ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction).

Drug Category: Anticoagulants

Anticoagulants interfere with platelet aggregation and clot formation thus reducing arterial clot burden and promoting continued myocardial oxygen and glucose delivery. These agents do not digest present clots, they help prevent secondary formation during and after spontaneous fibrinolysis. Often, the decision of when and which anticoagulant to use is decided jointly by the emergency physician and cardiologist.

Drug Category: Platelet aggregation inhibitors

These agents block the GP IIb/IIIa receptor on platelets. Once the platelet is activated, these receptors change configuration, facilitating fibrinogen and ligand binding. GP IIb/IIIa receptor binding of fibrinogen is the final step leading to platelet aggregation. Thus, these agents stymie platelet aggregation.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients with angina pectoris who are admitted for alternative reasons do not routinely require telemetry monitoring.
• Low-risk, pain-free patients who are admitted with nondiagnostic ECGs and negative cardiac marker results, often do not require telemetry monitoring as inpatients.
• Patients admitted with UA/NSTEMI will likely undergo percutaneous transluminal coronary angioplasty (PTCA) if clinically indicated. If catheterization is not available, hospital transfer is suggested.

Further Outpatient Care

• Any discharged patient with suspected angina should have close primary or cardiology follow-up care.

Transfer

• Transfer of the high-risk patient to an active catheterization center is recommended. This may be done from the inpatient setting after the patient has been stabilized in the ED.

Complications

• Complications may occur from the progression of the patient's underlying disease or from failure to intervene. Unfortunately, even the testing for underlying disease (eg, stress testing, angiography) can lead to complications including progression to myocardial infarction and renal failure. The risks and benefits of testing and treatment must be determined for and discussed with each patient.

Prognosis

• The prognosis of each patient is dependent upon individual factors and the progression of their underlying disease.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• As previously stated, there is no standard presentation of angina. One must be vigilant for anginal equivalents, such as breathlessness or diaphoresis, in all subgroups of patients.
• No amount of testing can routinely be performed in the emergency department setting to definitively rule out angina as the cause of a patient's chest pain or suspected anginal equivalent.
• Reproducible chest wall pain is found in roughly 10% of all cases of AMI.¹⁶
• Missed MIs account for approximately 10% of malpractice claims against emergency physicians and 24% of payout.^{17, 18}

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Clarendon E. The Life of Edward, Earl of Clarendon. Oxford at the Clarendon Press; 1827:18.
2. Jay V. The legacy of William Heberden. Arch Pathol Lab Med. Dec 2000;124(12):1750-1. [Medline].
3. Kelemen MD. Angina pectoris: evaluation in the office. Med Clin North Am. May 2006;90(3):391-416. [Medline].
4. Maseri A, Crea F, Kaski JC, Davies G. Mechanisms and significance of cardiac ischemic pain. Prog Cardiovasc Dis. Jul-Aug 1992;35(1):1-18. [Medline].
5. Servoss SJ, Januzzi JL, Muller JE. Triggers of acute coronary syndromes. Prog Cardiovasc Dis. Mar-Apr 2002;44(5):369-80. [Medline].
6. Yang EH, Lerman A. Management of the patient with chest pain and a normal coronary angiogram. Cardiol Clin. Nov 2005;23(4):559-68, viii. [Medline].
7. Centers for Disease Control and Prevention. Prevalence of heart disease--United States, 2005. MMWR Morb Mortal Wkly Rep. Feb 16 2007;56(6):113-8. [Medline]. [Full Text].
8. Almeda FQ, Kason TT, Nathan S, Kavinsky CJ. Silent myocardial ischemia: concepts and controversies. Am J Med. Jan 15 2004;116(2):112-8. [Medline].
9. Clarke WB, Austin SM, Shah PM, Griffin PM, Dove JT, McCullough J, et al. Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. Circulation. Mar 1978;57(3):593-8. [Medline].
10. Goodacre S, Locker T, Morris F, Campbell S. How useful are clinical features in the diagnosis of acute, undifferentiated chest pain?. Acad Emerg Med. Mar 2002;9(3):203-8. [Medline].
11. Tierney WM, Roth BJ, Psaty B, McHenry R, Fitzgerald J, Stump DL, et al. Predictors of myocardial infarction in emergency room patients. Crit Care Med. Jul 1985;13(7):526-31. [Medline].
12. Udelson JE, Beshansky JR, Ballin DS, Feldman JA, Griffith JL, Handler J, et al. Myocardial perfusion imaging for evaluation and triage of patients with suspected acute cardiac ischemia: a randomized controlled trial. JAMA. Dec 4 2002;288(21):2693-700. [Medline].
13. Chen EH, Mills AM. Is it necessary to admit low-risk patients with suspected acute coronary syndrome to inpatient telemetry beds?. Ann Emerg Med. Nov 2005;46(5):440-4. [Medline].
14. Kou V, Nassisi D. Unstable angina and non-ST-segment myocardial infarction: an evidence-based approach to management. Mt Sinai J Med. Jan 2006;73(1):449-68. [Medline].
15. Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia. Circulation. Apr 1994;89(4):1545-56. [Medline].
16. Rouan GW, Lee TH, Cook EF, Brand DA, Weisberg MC, Goldman L. Clinical characteristics and outcome of acute myocardial infarction in patients with initially normal or nonspecific electrocardiograms (a report from the Multicenter Chest Pain Study). Am J Cardiol. Nov 15 1989;64(18):1087-92. [Medline].
17. Karcz A, Korn R, Burke MC, Caggiano R, Doyle MJ, Erdos MJ, et al. Malpractice claims against emergency physicians in Massachusetts: 1975-1993. Am J Emerg Med. Jul 1996;14(4):341-5. [Medline].
18. Rogers JT. Risk Management in Emergency Medicine. 1985:4-6.
19. American College of Cardiology, American Heart Association Task Force. ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction. Available at http://www.acc.org/qualityandscience/clinical/guidelines/unstable/incorporated/III_hospital.htm#III_.
20. American College of Cardiology, American Heart Association Task Force. ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction. 2004. Available at http://www.acc.org/qualityandscience/clinical/guidelines/stemi/Guideline1/index.htm.
21. American Heart Association, American Stroke Association. Heart Disease and Stroke Statistics --2006 Update. Available at http://www.americanheart.org/downloadable/heart/1136308648540Statupdate2006.pdf.
22. Kaski JC, Rosano GM, Collins P, Nihoyannopoulos P, Maseri A, Poole-Wilson PA. Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study. J Am Coll Cardiol. Mar 15 1995;25(4):807-14. [Medline].

Article Last Updated: Nov 27, 2007