Definitions

graph TD
    CAD["Coronary Artery Disease (CAD)"]
    StableAngina["Chronic Stable Angina"]
    ACS["Acute Coronary Syndrome (ACS)"]
    UnstableAngina["Unstable Angina"]
    NSTEMI["NSTEMI"]
    STEMI["STEMI"]

    CAD --> StableAngina
    CAD --> ACS
    ACS --> UnstableAngina
    ACS --> NSTEMI
    ACS --> STEMI

Coronary artery disease

• Coronary artery disease (CAD): ischemic heart disease due to narrowing or blockage of coronary arteries, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand
• Stable CAD: a form of CAD in which patients are either asymptomatic or have stable or low-risk unstable angina; also used for patients with a history of MI whose symptoms are controlled with treatment

Chest pain and angina

Preferred terminology for types of chest pain

• 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

The following terms are no longer recommended for use in the 2021 AHA/ACC chest pain guidelines.

• 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

Epidemiology

Etiology

Pathophysiology

• Patients with CAD usually become symptomatic when the degree of coronary stenosis reaches ≥ 70%.

Clinical features

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

Diagnostics

Treatment

Approach

• All patients: pharmacotherapy for CAD
  • Start prevention of recurrent CAD, i.e., antiplatelet agents, statins, and management of comorbidities.
  • Start antianginal medication.

Pharmacotherapy for CAD

Antianginal drugs

• Goal: reduction of myocardial oxygen demand (MVO2)
• First-line agent: beta blockers
• Second-line agents: CCBs, nitrates, ranolazine
• Third-line agent: Consider ranolazine if beta-blockers, CCBs, and nitrates are ineffective or not tolerated.
  

Prevention of recurrence and/or progression

• Antiplatelet agents
• ACEIs or ARBs
• Beta blockers

Subtypes and variants

Vasospastic angina

Previously known as variant or Prinzmetal 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

Etiology

• Cigarette smoking; use of stimulants (e.g., cocaine, amphetamines), alcohol, or triptans
• Stress, hyperventilation, exposure to cold
• Common atherosclerotic risk factors (except smoking) do not apply to vasospastic angina.

Pathogenesis

• Hyperreactivity of coronary smooth muscle due to endothelial dysfunction & autonomic imbalance
  • Triggered by excess vagal tone, and they occur most commonly at night when vagal tone is at a peak.
  • Both acetylcholine and ergot alkaloids (eg, dihydroergotamine) provoke symptoms and may also aid in diagnosis, as follows:
    • Acetylcholine normally stimulates endothelial muscarinic receptors to cause vasodilation via increased release of nitric oxide. However, a deficiency of endothelial nitric oxide in affected patients causes increased vagal tone to instead trigger vasoconstriction and precipitate vasospastic symptoms.
    • Ergot alkaloids activate 5-HT2 serotonergic receptors to cause vasoconstriction. Normally, the vasoconstriction is somewhat offset by endothelial release of vasodilatory prostaglandins, but this response is lacking in affected patients due to endothelial dysfunction.

Clinical presentation

• Young age (<50)
• Minimal CAD risk factors (other than smoking)
• Recurrent chest discomfort
  • At rest or during sleep
  • Spontaneous resolution ≤15 min

Diagnosis

• ECG: ST-segment elevation during episode
• Coronary angiography: no CAD

Treatment

• Smoking cessation
• Avoid beta-blockers (particularly nonselective beta blockers), and other agents that induce vasoconstriction
  • Blockade of beta-2 receptors prevents smooth muscle cell relaxation and may cause additional vasoconstriction.
• First-line therapy: calcium channel blockers, e.g., verapamil, diltiazem, or nifedipine