eMedicine Specialties > Emergency Medicine > Cardiovascular

Angina Pectoris

Author: Marc D Haber, MD, Assistant Professor, Department of Emergency Medicine, Baystate Medical Center, Tufts University School of Medicine; President of Young Physician Section, AAEM.
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
Contributor Information and Disclosures

Updated: Jun 15, 2009

Introduction

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 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.

Pathophysiology

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.

Conservative 2006 data show 733,000 acute coronary syndrome (ACS) discharges from hospitals.⁷

Mortality/Morbidity

In 2005, 1 in 5 deaths is from coronary heart disease (both angina and myocardial infarction).

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

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 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 7}  

Sex

Among Americans aged 40-74 years, the age-adjusted prevalence of angina pectoris (AP) was higher among women than men.⁷  Although 2005 CDC data suggest that men (5.5%) have a higher prevalence of angina and/or coronary heart disease than women (3.4%).⁸

Age

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

Statistics from American Heart Association (2008 Data) and Centers for Disease Control and Prevention.

Clinical

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.⁹

• 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.¹⁰

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.^11,12

Causes

See Pathophysiology.

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