Harvey's Garden

Coronary artery disease

5 min read

Definitions

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

    CAD --> StableAngina
    CAD --> ACS
	CAD --> Variant
    ACS --> UnstableAngina
    ACS --> NSTEMI
    ACS --> STEMI
FeatureChronic Stable AnginaUnstable Angina (UA)NSTEMISTEMIVasospastic (Prinzmetal) Angina
PathophysiologyFixed >70% stenosisPlaque rupture, sub-occlusive thrombusPlaque rupture, sub-occlusive thrombusPlaque rupture, occlusive thrombusCoronary artery spasm
Chest PainPredictable, on exertion; lasts <20 minUnpredictable, at rest or crescendo patternProlonged, severe, at restProlonged, severe, crushing, at restEpisodic, at rest (often nocturnal)
Relieved by Rest/NTGYesOften notNoNoYes (spontaneously or w/ NTG)
ECG FindingsNormal at rest; ST depression on stressST depression / T-wave inversion (or normal)ST depression / T-wave inversion (or normal)ST Elevation (or new LBBB)Transient ST Elevation during pain
Cardiac BiomarkersNegativeNegativePositivePositiveNegative
Key ManagementMedical Tx (ASA, β-blocker, Statin), NTG prnAnticoagulation (Heparin), dual antiplatelet therapy (DAPT)Anticoagulation, DAPT; often early invasive strategy (PCI)Emergent Reperfusion (PCI <90min or Fibrinolysis)CCBs, Nitrates; AVOID non-selective β-blockers

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%.
FeatureStable PlaqueUnstable (Vulnerable) Plaque
Fibrous CapThick, strong, intactThin, weak, prone to rupture/erosion
Lipid CoreSmaller, less necroticLarger, highly necrotic, soft
InflammationLowHigh (active macrophages, MMPs)
Smooth MuscleMore, synthesizing collagenFewer, more apoptosis
Primary ProblemSlow development.
Allow the development of viable collateral vessels		Rupture/Erosion & Thrombosis
Clinical RiskStable Angina, ClaudicationAcute Coronary Syndromes (MI, UA), Stroke
Acute Event RiskLowerHigher

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

Stable Ischemic Heart Disease (SIHD)

  • Goal: Prevent future MI/death & control angina.
  • Medical Tx (Universal):
    • Antiplatelet: Aspirin (or Clopidogrel if allergic).
    • Statin: High-intensity (e.g., Atorvastatin) for ALL patients.
  • Symptom (Angina) Control:
    • 1st Line: Beta-blockers.
    • Acute Relief: Sublingual Nitroglycerin (NTG).
    • Add-on Tx: Calcium Channel Blockers (CCBs), long-acting nitrates.
  • Revascularization (PCI/CABG):
    • For refractory symptoms despite max medical Tx or high-risk anatomy (e.g., Left Main, 3-vessel disease).
    • CABG > PCI for diabetics and complex multi-vessel disease.

Acute Coronary Syndrome (ACS: UA, NSTEMI, STEMI)

  • Immediate Tx (All ACS):
    • DAPT: Aspirin + P2Y₁₂ inhibitor (e.g., Clopidogrel, Ticagrelor).
    • Anticoagulation: Heparin (UFH or LMWH).
    • High-Intensity Statin.
    • Symptom Control: NTG, Morphine, Beta-blockers (if stable).
  • STEMI-Specific Tx:
    • IMMEDIATE REPERFUSION.
    • PCI: Gold standard. Goal: door-to-balloon < 90 min.
    • Thrombolysis: If PCI is not available (>120 min away).
  • NSTEMI / UA-Specific Tx:
    • Risk Stratify (TIMI score).
    • High-risk: Early invasive strategy (angiography ± PCI).
    • Low-risk: Conservative medical management initially.

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

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