Coronary artery disease

Last updated: November 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).

For the diagnostics and management of acute chest pain, see “Acute coronary syndrome” and “Chest pain.” See also “Atherosclerosis” and “Myocardial infarction.”

Coronary artery disease

Chest pain and angina

Preferred terminology for types of chest pain [1][2][3]

  • Cardiac chest pain: likely associated with cardiac ischemia based on symptoms (e.g., central, retrosternal, squeezing, exertional).
  • Possible cardiac chest pain: may be associated with cardiac ischemia based on symptoms (e.g., stabbing, tearing, ripping, burning).
  • Noncardiac chest pain: unlikely associated with cardiac ischemia based on symptoms (e.g., positional, fleeting).

Historical terminology for types of chest pain [1][2][3]

The following terms are no longer recommended for use in the 2021 AHA/ACC chest pain guidelines. [1][2][3]

  • 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
  • CAD is the leading cause of death in the US and worldwide. [4]
  • The lifetime risk of coronary artery disease at age 50 is approx. 50% for men and 40% for women. [5]

Epidemiological data refers to the US, unless otherwise specified.

Plaque formation and coronary artery stenosis [6][7]

Myocardial oxygen supply-demand mismatch [8]

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

Effect of vascular stenosis on resistance to blood flow [9]

  • 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 [8]

Coronary steal syndrome

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

Chronic ischemic heart disease

Angina

  • Paroxysmal attacks of retrosternal chest discomfort, tightness, or pressure due to myocardial ischemia.
  • Most commonly occurs in individuals with coronary heart disease.
  • Triggers include exertion or stress, which results in increased myocardial oxygen demand.
  • 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 is not affected by body position or respiration.
    • No chest wall tenderness
    • May gradually increase in intensity
    • May be absent, especially in geriatric and diabetic patients. [10]

Stable angina

  • Symptoms are reproducible/predictable and severity, frequency, and threshold for reproduction of symptoms do not change.
  • Symptoms often subside within minutes with rest or after administration of nitroglycerin
  • Common triggers include physical/mental stress or exposure to cold

Anginal equivalents [1][11]

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

The following recommendations are consistent with the 2012 and 2013 American Heart Association (AHA) guidelines for the management of stable ischemic heart disease (IHD) and the 2021 AHA chest pain guidelines. They focus on patients with chronic stable angina and no history of CAD. For patients with acute symptoms, see “Diagnostics” in “Acute coronary syndrome.” [1][2][12]

New onset chest pain, pain at rest, and increasing frequency or severity of pain are symptoms of unstable angina.

Symptomatic patients without known CAD [2][2][12]

Initial evaluation

Additional evaluation [2]

Perform the following according to the pretest probability of CAD: [13]

Either cardiac stress testing or CCTA can be used to risk stratify patients with intermediate to high PTP of obstructive CAD. [2]

Additional diagnostic testing is not routinely recommended for patients with a low pretest probability of obstructive CAD. [2]

Asymptomatic patients

Resting ECG [12]

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

The 2021 AHA chest pain guidelines recommend using validated scores published within the past 10 years to predict the pretest probability of obstructive CAD. [2]

Pretest probability of obstructive CAD by age, sex, and symptoms

Pretest probability of obstructive CAD causing suspected cardiac symptoms [2]
Age Men Women
Chest pain Dyspnea Chest pain Dyspnea
30–39 Low Low Low Low
40–49 Intermediate Low Low Low
50–59 Intermediate Intermediate Low Low
60–69 Intermediate Intermediate Intermediate Intermediate
≥ 70 High Intermediate Intermediate Intermediate

Interpretation

  • Low: ≤ 15%
  • Intermediate: 16%–50%
  • High: > 50%

Other factors that independently increase PTP [1]

Overview

Cardiac stress testing [1][2][12][15][16][17]

Description

  • The goal is to detect evidence of stress-induced ischemia.
  • Heart rate is monitored throughout the study [18]
  • 12-lead ECG is used for monitoring throughout the study.

Indications [19]

Types of stress induction

Modalities and diagnostic endpoints

Evidence of stress-induced ischemia
Modality Findings
ECG

Echocardiography

  • Changes in global left ventricular function during or after stress
  • New or worsening wall motion abnormalities
Myocardial perfusion scan (e.g., SPECT, PET)
CMR
  • New wall motion abnormality or perfusion abnormality

General criteria for test termination

Some clinical and ECG criteria vary between exercise stress tests and pharmacological stress tests (see “Comparison of cardiac stress tests” for details). General criteria include the following:

  • A diagnostic endpoint is reached (preferred). [13][18][19]
  • A target heart rate threshold is achieved (i.e., if no diagnostic endpoint is reached)
  • Significant cardiac arrhythmia
  • Technical issues with patient monitoring
  • Patient request

Test preparation

Comparison of cardiac stress tests [1][2][12][13][15]
Test characteristics Cardiac exercise stress test Cardiac pharmacological stress test
Procedure
  • Stress is induced by exercise on a treadmill or bicycle.
  • Duration varies by protocol (e.g., Bruce protocol). [19]
  • Metabolic equivalents (METs): A measure of energy expenditure used to estimate exercise tolerance. [17]
    • 1 MET = 3.5 mL O2/kg/minute
    • Approx. 5 METs are required to fulfill everyday activities, such as climbing a flight of stairs.

Typical modalities [1]

Contraindications
Specific criteria for test termination Clinical
ECG

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). [19]

Cardiac anatomic testing [12]

Coronary angiography [12][22]

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, 2014, and 2021 American Heart Association (AHA) guidelines on the management of patients with stable IHD and coronary artery revascularization. [12][22][25]

Approach [12]

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 [12]
Therapeutic goal Drug class Example agents Specific indications and effects
Secondary prevention Antiplatelet agents
  • Recommended for all patients with CAD
ACEIs or ARBs
Secondary prevention and antianginal treatment Beta blockers
Antianginal treatment CCBs
Nitrates
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 [12][25]

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.

  • Prognostic factors
  • Stable angina
    • Annual mortality rate: up to 5% [12]
    • 25% of patients will develop acute MI within the first 5 years. [33]
    • 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

Vasospastic angina

Description

  • 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 [35]

Epidemiology [36]

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

Etiology

Diagnosis [11][38]

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. [11]

Diagnostic criteria for vasospastic angina [11][38]
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. [38]

Treatment [11][41]

Complications [11][39]

Prolonged coronary artery spasms can lead to MI or fatal arrhythmias. [11]

Prognosis

  • 5-year survival rate is > 90% (with treatment). [44]
  • The persistence of symptoms is common.

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