Epidemiology

Etiology

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

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.

Previously known as variant or Prinzmetal 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

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.

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.