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    Vasospastic Angina (Coronary Artery Vasospasm)


    Last Reviewed on Jun 07, 2022
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    By Joe Finkler,Manjot Kahlon


    • Vasospastic angina (also called VSA, Prinzmetal’s angina or Variant Angina), is a syndrome that is characterized by spontaneous episodes of rest angina, not correlated with exertion, and which responds promptly to short-acting nitrates.
    • Caused by coronary artery vasospasms: constriction of arterial smooth muscle wall which reduces blood flow through the vessel, causing transmural ischemia.
    • Prevalence may be higher in Japanese populations.
    • Most common triggers: exposure to cold weather, Valsalva maneuver, hyperventilation, and recreational drug use such as cocaine, especially when used concurrently with cigarette smoking.
    • Average survival is 89-97% at 5 years, but mortality is greater for patients with both VSA and coronary artery obstruction.
    • Patients with prolonged vasospasm can present with sudden death and potentially life-threatening complications such as myocardial infarction and arrhythmias.
    • Other vasospastic disorders, such as Raynaud phenomenon and migraine headache, tend to co-occur with VSA in a small subset of patients.

    Diagnostic Process

    Diagnostic criteria for VSA– according to the Coronary Vasomotor Disorders International Study Group (COVADIS):

    • Nitrate-responsive angina with at least 1 of the following:
      • Rest angina, especially between night and early morning.
      • Marked diurnal variation in exercise tolerance (reduced in morning.)
      • Hyperventilation can trigger an episode.
      • Calcium channel blockers (but not beta-blockers) suppress episodes.
    • ECG showing transient ischemic changes during a spontaneous episode, including any of the following in at least 2 contiguous leads:
      • ST-segment elevation
      • ST-segment depression
      • New negative U waves
    • Angiography showing transient total or subtotal coronary artery occlusion (> 90% constriction.)
    • Definitive VSA: diagnosed if the patient has nitrate-responsive angina and either criteria 2 or 3 above fulfilled.
    • Suspected VSA: diagnosed if the patient only has nitrate-responsive angina.

    Provocative spasm testing:

    • Gold standard approach, although rarely performed.
    • Indicated if patient has history and/or symptoms suspicious of VSA but no documented episode.
    • Involves use of a pharmacologic stimulus (acetylcholine or ergonovine) or non-pharmacologic stimulus (hyperventilation or cold pressure testing).
    • Positive provocative test for VSA must show the stimulus to induce all the following:
      • Reproduction of the usual chest pain.
      • Ischemic ECG changes.
      • ≥ 90% vasoconstriction on angiography.

    Clinical pitfalls:

    • ECG is usually normal between episodes of coronary vasospasm, therefore, ambulatory ECG monitoring is recommended to detect episodes of ST-changes if the diagnosis is still being considered.
    • Toxicology screen may be helpful if recreational drug use is suspected as the etiology.

    Recommended Treatment

    Initial stabilization:

    • IV access, oxygen, cardiac monitoring, vital signs and oxygen saturation.

    First-line therapy:

    • Calcium channel blockers (CCBs): diltiazem, verapamil and amlodipine
      • Long-acting nifedipine may be used, however, patients must be monitored for potential side effects such as severe hypotension and reflex tachycardia.
    • Combination of long-acting nitrates with CCBs is recommended in patients who remain symptomatic despite treatment with CCBs
      • Long-acting nitrates: effective in alleviating symptoms, but less desirable as a first-line approach due to potential nitrate tolerance.

    Other treatment options:

    • Statins: shown to be effective in preventing coronary vasospasms.
    • Sublingual nitroglycerin: effective in reducing duration of each episode, thereby decreasing the likelihood of myocardial infarction and arrhythmias associated with VSA.
    • Percutaneous coronary intervention (PCI): not routinely indicated however, may be helpful if there is underlying obstructive coronary disease that is thought to potentially trigger the spasm.

    Drugs to avoid:

    • Avoid beta-blockers as they may exacerbate vasospasms through unopposed alpha-adrenergic vasoconstriction.
    • In patients with co-occurring migraine, avoid use of triptans for acute management.
    • Aspirin should be used with caution as high doses inhibit the production of prostacyclin (endogenous vasodilator), thereby possibly aggravating the vasospasm.

    Quality Of Evidence?


    Studies have shown calcium channel blocker therapy to be associated with positive outcomes in patients with VSA, however, this evidence comes largely from observational studies, rather than randomized controlled trials. There are several randomized trials that have shown nitrates to be an effective treatment for reducing the frequency of angina in patients with VSA.


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