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Angina Pectoris in Emergency Medicine

  • Author: Marc D Haber, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
 
Updated: Feb 18, 2015
 

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, including the following:

  • 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 with spasm on angiography.
  • Cardiac syndrome X occurs when a patient has all of the symptoms of angina pectoris without coronary artery disease or spasm.
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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]

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Epidemiology

Frequency

United States

An average of 3.4 million US adults older than 40 years experience angina each year. Between 2007 and 2010, there were a total of 2.3 million office visits per year for angina.[7]

About 635,000 US adults with have a new coronary event (MI or CHD death), with an estimated 300,000 experiencing recurrent events.[7]

Conservative 2010 data show 625,000 acute coronary syndrome (ACS) discharges from hospitals.[7]

Mortality/Morbidity

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

The majority of coronary attacks are NOT preceded by long-standing angina pectoris (AP) (only 18%).[7]

Morbidity/mortality

Cardiovascular diseases, including heart disease and stroke, account for more than onethird (33.6%) of all U.S. deaths.[7]

Coronary heart disease is the single greatest killer of American men and women.[7]

In 2010, the total costs of cardiovascular diseases in the United States were estimated to be $444 billion, with treatment of these diseases accounting for about $1 of every $6 spent on US healthcare.[7]

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.

Race

The Centers for Disease Control and Prevention (CDC) note that the prevalence of angina and/or coronary heart disease is highest and increasing 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.[8, 9]

Sex

Among US adults aged 40-59 years and 80 years and older, the age-adjusted prevalence of angina pectoris (AP) is higher among women than men; in those aged 60-79 years, it is higher men than women.[7]

Age

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

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Contributor Information and Disclosures
Author

Marc D Haber, MD Assistant Professor, Department of Emergency Medicine, Tufts University School of Medicine; Clinical Associate of Radiology, Baystate Medical Center; Past President of Young Physician Section, AAEM

Marc D Haber, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Radiology, Radiological Society of North America, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas A Brunell, MD, MA, FACEP, FAAEM Director, Emergency Medicine Education, St Francis Hospital and Medical Center; Assistant Professor of Traumatology and Emergency Medicine, University of Connecticut Medical Center

Thomas A Brunell, MD, MA, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Massachusetts Medical Society, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Jerry R Balentine, DO, FACEP, FACOEP Vice President, Medical Affairs and Global Health, New York Institute of Technology; Professor of Emergency Medicine, New York Institute of Technology College of Osteopathic Medicine

Jerry R Balentine, DO, FACEP, FACOEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, American College of Osteopathic Emergency Physicians, American Association for Physician Leadership, American Osteopathic Association

Disclosure: Nothing to disclose.

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