Coronary artery disease

Last updated: June 7, 2022

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Coronary artery disease (CAD) is a condition that is most commonly caused by atherosclerosis and the subsequent reduction in blood supply to the myocardium, resulting in a mismatch between myocardial oxygen supply and demand. Acute retrosternal chest pain (angina) is the cardinal symptom of CAD. Other symptoms include dyspnea, dizziness, anxiety, and nausea. Patients with stable CAD may have stable angina or be asymptomatic, while severe ischemia may lead to acute coronary syndrome, including myocardial infarction (MI). Stable CAD can be diagnosed using cardiac stress testing, nonstress cardiac imaging, and/or coronary catheterization. The management of stable CAD involves secondary prevention of atherosclerosis (e.g., smoking cessation, and treatment of diabetes mellitus, hypertension, and dyslipidemia), antiplatelet agents, antianginal medication (e.g., beta blockers), and, in severe cases, revascularization (e.g., percutaneous transluminal coronary angioplasty).

This article provides an overview of CAD as well as diagnostic and treatment options for patients with stable CAD. Atherosclerosis and acute coronary syndrome (including MI) are discussed in separate articles.

  • CAD is the leading cause of death in the US and worldwide. [1]
  • The lifetime risk of coronary artery disease at age 50 is approx. 50% for men and 40% for women. [2]

Epidemiological data refers to the US, unless otherwise specified.

Plaque formation and coronary artery stenosis [3][4]

Myocardial oxygen supply-demand mismatch [5]

An increased heart rate reduces oxygen supply and increases oxygen demand.

Effect of vascular stenosis on resistance to blood flow [6]

  • The resistance to blood flow within the coronary arteries is calculated using the Poiseuille equation: R = 8Lη/(πr4), where R = resistance to flow, L = length of the vessel, η = viscosity of blood, and r = radius of the vessel.
  • Provided the length of the vessel and viscosity of blood remain constant; , the degree of resistance can be calculated using the simplified formula: R 1/r4

Vascular stenosis increases vascular resistance significantly. For example, a 50% reduction in radius results in a 16-fold increase in resistance: R ≈ 1/(0.5 x r)4 = [1/(0.5 x r)]4 = (2/r)4 = 16/r4.

Myocardial ischemia [5]

Coronary steal syndrome

Coronary steal syndrome should not be confused with coronary-subclavian steal syndrome.

Chronic ischemic heart disease


Angina is the cardinal symptom of CAD. Patients with CAD usually become symptomatic when the degree of coronary stenosis reaches ≥ 70%.

  • Typically retrosternal chest pain or pressure
    • Pain may radiate to the left arm, neck, jaw, epigastric region, or back.
    • Pain is not affected by body position or respiration.
    • No chest wall tenderness
    • May gradually increase in intensity
    • May present as gastrointestinal discomfort
    • May be absent, especially in geriatric and diabetic patients. [7]
  • Dyspnea
  • Dizziness, palpitations
  • Restlessness, anxiety
  • Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)

Stable angina

  • Symptoms are reproducible/predictable
  • Symptoms often subside within minutes with rest or after administration of nitroglycerin
  • Common triggers include mental/physical stress or exposure to cold

Vasospastic angina


  • Angina caused by transient coronary spasms (usually due to spasms occurring close to areas of coronary stenosis)
  • Not affected by exertion (may also occur at rest)
  • Typically occurs early in the morning [8]

Epidemiology [9]

  • Highest prevalence in the Japanese population (especially young women)
  • Average age of onset: 50 years


Diagnosis [11][12]

The goal of diagnostic testing is to detect transient ischemic changes and/or coronary artery spasm during anginal episodes, as well as concomitant coronary artery stenosis. Specialist consultation is advised. [12]

Diagnostic criteria for vasospastic angina [11][12]
Criteria Description
Typical clinical features
  • Spontaneous angina with a rapid response to short-acting nitrates and ≥ 1 of the following:
    • Occurrence at rest (especially at night or early morning)
    • Precipitated by hyperventilation
    • Responsive to treatment with CCBs (but not beta blockers)
    • Reported lower exercise tolerance in the morning
Transient ischemic ECG changes
Coronary spasm on angiography

Noninvasive bedside coronary artery spasm provocation testing can lead to significant adverse effects and even death. Provocative testing to diagnose vasospastic angina should only be attempted by a specialist, and usually only during coronary angiography. [11]

Treatment [12][15]

Complications [12][13]

Prolonged coronary artery spasms can lead to MI or fatal arrhythmias. [12]


  • 5-year survival rate is > 90% (with treatment). [18]
  • The persistence of symptoms is common.

This approach is consistent with 2012 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Task Force guidelines on the diagnosis of patients with stable ischemic heart disease (IHD), as well as the 2013 ACCF/AHA appropriate use criteria for the detection and risk assessment of stable IHD. Recommendations focus on patients with chronic stable angina. For patients with acute symptoms, see “Risk stratification for ACS.” [19][20]

Approach [19]

Clinical assessment of symptomatic patients to predict the probability of CAD is used to help determine the need for further diagnostic tests and guide the selection of the best initial diagnostic test.

Patients with chest pain or anginal equivalents should be evaluated for CAD. Other indications include newly diagnosed heart failure, arrhythmia, and syncope.

Resting ECG [19]

Resting ECG results are usually normal in patients with stable CAD.

This is one of several possible methods for estimating the pretest probability of CAD. See also “Chest pain” and “Risk stratification of ACS” for approaches to in patients with acute symptoms.

  • Pretest probability of CAD takes the following into consideration:
    • The patient's age and sex
    • Type of chest pain [20]
      • Typical angina fulfills all of the following criteria:
        • Retrosternal chest pain of characteristic nature and duration (e.g., transient retrosternal pressure)
        • Provoked by exertion or emotional stress
        • Relieved by rest and/or nitroglycerin
      • Atypical angina: fulfills only two of the aforementioned criteria
      • Nonanginal chest pain: fulfills one or none of the aforementioned criteria
    • The likelihood of an alternate diagnosis that explains the symptoms (see “Differential diagnoses of chest pain”).
Determining pretest probability of CAD [20][23]
Estimated PTP Clinical presentation
Very low (< 5%)

Low (5–10%)

Intermediate (10–90%)
High (> 90%)
Other factors that independently increase PTP [20]

Decision algorithm [19][20][21]

  • Consider specialist consultation for decisions regarding further diagnostic testing.
  • Indications and choice of testing are determined by the following:
    • Pretest probability of CAD
    • The patient's ability to exercise [19]
    • ECG interpretability
    • Contraindications to specific testing modalities
    • Test availability
  • For patients with a low or very low probability of CAD further testing should be considered on an individual basis.
Approach to further diagnostics based on PTP of CAD [20]
PTP Able to exercise with interpretable ECG Unable to exercise or uninterpretable ECG
Very low (< 5%)
  • Further testing is often unnecessary.
Low (5–10%)
Intermediate (10–90%)
High (> 90%)
For patients able to exercise with an uninterpretable ECG (regardless of PTP): Consider cardiac exercise stress test with imaging, e.g., echocardiography, or myocardial perfusion imaging

Cardiac stress testing is most useful for patients with an intermediate pretest probability of CAD; ischemic changes during testing allow for reclassification of patients into a high probability of CAD, while a normal test makes the probability of CAD low.

Further diagnostic testing may be unnecessary in individuals with a very low pretest probability of CAD. [20]

Noninvasive testing

Cardiac stress testing [19][20][24][25][26]

The goal is to detect evidence of stress-induced ischemia.

Comparison of cardiac stress tests [19][21][24]
Test characteristics Cardiac exercise stress test Cardiac pharmacological stress test
Specific criteria for test termination Clinical

Achievement of 85% of the patient's estimated maximum heart rate, no exaggerated BP response, and no ST-segment abnormalities during exercise stress testing confer a low probability of CAD (i.e., a normal test). [28]

Nonstress cardiac imaging [19]

  • Coronary CT angiography (CCTA): can visualize anatomic CAD [29]
    • Indications
    • Supportive findings [30]
      • Calcified or noncalcified plaques
      • The degree and extent of coronary stenosis can be measured and is usually reported using CAD-RADS.
  • Coronary artery calcium (CAC) scoring: measures the amount of calcification in the coronary arteries [20]
    • Rarely used to assess for CAD in symptomatic patients; usually reserved for asymptomatic patients (see “Diagnostics” in “Lipid disorders”)
    • Consider in patients with a low pretest probability of CAD to rule out the disease.

Invasive testing (coronary angiography) [19][31]

Patients with acute chest pain and other concerning clinical findings (e.g., hypotension) or ECG changes that are suggestive of acute coronary syndrome (e.g., new heart blocks or arrhythmias) should undergo cardiac catheterization.

See “Differential diagnosis of chest pain.”

The differential diagnoses listed here are not exhaustive.

The following recommendations are consistent with the 2012 ACCF/AHA Task Force guidelines on the management of patients with stable IHD, and with its 2014 focused update. [19][31]

Approach [19]

The goal of treatment is to reduce cardiovascular morbidity and mortality, improve ischemic symptoms, and maintain quality of life.

All patients with CAD should receive education on risk factor reduction, as well as treatment with antiplatelet agents and antianginal medications

Pharmacotherapy for CAD

Pharmacotherapy for CAD has two main therapeutic goals, secondary prevention for CAD and symptomatic relief with antianginal treatment. Specific indications and potential effects should be taken into account before prescribing the different drug classes.

Antianginal drugs

Effects of antianginal medications
Parameters that impact MVO2 Beta blockers Nitrates Combination of a beta blocker and a nitrate

Blood pressure

Heart rate

↑ (reflectory)

Unchanged or slightly ↓
Inotropy (contractility) ↑ (reflectory) Unchanged
Ejection time Unchanged
End-diastolic volume Unchanged or ↑ Unchanged or slightly ↓
Overall effect on MVO2 ↓↓

Overview of pharmacotherapeutic agents for CAD

Pharmacotherapy for CAD [19]
Therapeutic goal Drug class Example agents Specific indications and effects
Secondary prevention Antiplatelet agents
  • Recommended for all patients with CAD
Secondary prevention and antianginal treatment Beta blockers
Antianginal treatment CCBs
Metabolic modulators
  • Ranolazine

Beta blockers are used both to reduce the risk of MI and death (secondary prevention) and for symptom relief (antianginal treatment) in patients with CAD.

Revascularization for stable CAD [19][32]

Decisions regarding revascularization are complex and should be made with a multidisciplinary team of specialists (e.g., interventional cardiologists, cardiac surgeons) on an individual basis. See “Acute coronary syndrome” for revascularization indications of patients with acute symptoms.

The choice of revascularization technique should take into account patient preference, coronary anatomy, left ventricular function, prior history of revascularization, and the presence of concomitant chronic conditions.

Revascularization is harmful in patients who do not meet anatomical or physiological criteria for intervention, e.g, patients with 1-vessel disease without proximal LAD stenosis.

  • Prognostic factors
  • Stable angina
    • Annual mortality rate: up to 5% [19]
    • 25% of patients will develop acute MI within the first 5 years. [41]
    • High-grade stenosis is associated with an unfavorable prognosis.

Primary prevention of CAD

Similar to other atherosclerotic cardiovascular diseases: See “ASCVD prevention.”

Secondary prevention of CAD

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