Acute Coronary Syndrome: Coronary Vasospasm

Basics

Description

  • Spontaneous episodes of chest pain due to coronary artery vasospasm in the absence of increase in myocardial oxygen demand in either normal or diseased coronary vessels
  • Also known as Prinzmetal angina or variant angina, originally described in 1959
  • Most common in younger patients and men
  • Usually occurs in patients without cardiac risk factors or coronary artery disease
  • Risk factors:
    • Smoking (up to 75% of cases)
    • Hypertension
    • Hypercholesterolemia
    • Diabetes mellitus
    • Cocaine use

Etiology

  • Abnormal vasodilator function in coronary arteries typically endothelial in origin
  • High prevalence of microvascular and epicardial vessel involvement
  • Defined by 3 types
    • Focal: Localized, often at or near a site of stenosis of a single artery
    • Multifocal: 2 or more segments of the same artery
    • Multivessel: Involving different coronary arteries
  • Unopposed α sympathetic stimulation
  • Sympathetic stimulation by endogenous hormones may cause vasoconstriction.
  • Conversely, also associated with increased vagal tone or withdrawal from vagal tone as proven with acetylcholine provocative testing
  • Hypersensitivity of coronary arteries due to mediators of vasoconstriction
  • Endothelial dysfunction possibly from genetic mutations in nitric oxide synthase
  • Newer research suggests potential increase ρ-kinase activity in smooth muscle cells

Diagnosis

Signs and Symptoms

  • Chest pain:
    • Retrosternal
    • Radiates to neck, jaw, left shoulder, or arm
    • Occurs at rest
    • Occurs more frequently at night or in the morning
  • Palpitations
  • Presyncope or syncope
  • Associated with migraine headaches and Raynaud disease in a minority of patients
  • May occur during cold weather or stress
  • May be prolonged in duration compared to typical angina
  • May be elicited by hyperventilation
  • May be elicited by exercise
  • Circadian pattern, typically at night or early morning

History
May mimic angina, occurrences in the early morning should raise suspicion for vasospasm, but also ask about relationship to stress, exercise, and cold weather

Physical Exam
Physical exam is typically nondiagnostic.

Essential Workup

  • Must include an ECG
  • Use of other tests depends on history.

Diagnostic Tests and Interpretation

  • ECG:
    • Transient ST-segment elevation is characteristic, is typically quite pronounced
    • Often with reciprocal changes
    • May be followed by ST depression or T-wave inversion
    • May have associated dysrhythmia during coronary spasm
    • Heart block with right coronary artery spasm
    • Ventricular tachycardia with LAD spasm
    • In rare cases can present with sudden death during prolonged vasospasm period

Lab
  • Troponin
  • CK/CKMB fraction
  • Toxicology screen:
    • Helpful if cocaine is suspected as etiology of chest pain

Imaging
  • CXR:
    • May be helpful to rule out other etiologies such as pneumonia, pneumothorax, or aortic dissection
  • Noninvasive coronary imaging (nuclear perfusion, coronary CTA, coronary MR):
    • Typically only helpful when combined with provocative testing

Diagnostic Procedures/Other
  • Exercise stress testing:
    • Usually not helpful, but can help define those with true ischemic disease
  • Noninvasive provocative hyperventilation
    • Highly specific, moderately sensitive, tends to favor those with increased disease activity
    • Paired with either EKG or EKG plus perfusion imaging
  • Holter monitor:
    • Can be helpful in silent cases or dysrhythmia
  • Coronary angiography:
    • Mild atherosclerosis is often the norm
    • Provocative test with acetylcholine is the gold standard

Differential Diagnosis

  • Angina pectoris
  • Anxiety and panic disorders
  • Aortic dissection
  • Cocaine chest pain
  • Esophageal rupture
  • Esophageal spasm
  • Esophagitis
  • GERD
  • Mitral valve prolapse
  • Musculoskeletal chest pain
  • MI
  • Peptic ulcer disease
  • Pericarditis
  • Pneumothorax
  • Pulmonary embolism
  • Takotsubo cardiomyopathy

Treatment

Pre Hospital

Treat as any other acute coronary syndrome.

Initial Stabilization/Therapy

  • IV access
  • Oxygen
  • Cardiac monitoring
  • Vital signs and oxygen saturation

Ed Treatment/Procedures

  • All patients with chest pain in which cardiac ischemia is a consideration should receive an aspirin upon arrival to the ED:
    • Paradoxically may increase severity of Prinzmetal angina due to inhibition of biosynthesis of naturally occurring coronary vasodilator—prostacyclin
  • Nitroglycerin should still be administered and usually will help relieve both ischemic and vasospastic chest pain.
  • A trial of calcium-channel blockers is indicated if clinical history is consistent with coronary vasospasm.
  • Heparin and β-blockers are not helpful in true coronary vasospasm:
    • β-blockers may be detrimental due to unopposed α-mediated vasoconstriction and should be avoided in suspected cocaine chest pain.

Medication

  • Aspirin: 325 mg PO
  • Diltiazem: 30–60 mg PO (immediate release)
  • Nitroglycerin, either:
    • 0.4 mg sublingual
    • 10–20 μg/min IV USE NON-PVC tubing, titrating to effect
    • 1–2 in of nitro paste
  • Verapamil: 40–80 mg PO (immediate release)

First Line
Diltiazem/verapamil:
  • >40% of patients will have recurrence of vasospastic angina despite calcium-channel blocker therapy
Long-acting nitrates
Second Line
  • α-blocking agents
  • Statin therapy
  • Percutaneous intervention with stenting of fixed lesions in area of vasospasm controversial; can lead to spasm in other areas of coronary tree
  • Pacemaker placement for patients with recurrent syncope or AV nodal block from vasospastic angina

Ongoing Care

Disposition

Admission Criteria
  • New-onset chest pain
  • Rule-in with positive biochemical markers or provocative testing
  • Rule-in with positive biochemical markers or stress testing
  • Many patients previously admitted to the hospital can now be effectively evaluated in a chest pain observation unit or clinical decision unit

Discharge Criteria
  • Stable (chronic chest pain)
  • Negative ischemic workup

Follow-Up Recommendations

Cardiology follow up within 7 days of ED evaluation

Pearls and Pitfalls

  • 95% survival at 5 yr
  • Typical patient will have no traditional coronary risk factors other than smoking.
  • Calcium-channel blockers are 1st-line therapy.
  • 30–40% of patients are refractory to treatment and will have repeat episodes.
  • May present as STEMI, however true infarction is almost always relegated to patient with pre-existing coronary atherosclerotic disease
  • β-blockers can lead to worsening of vasospasm due to unopposed α vasoconstriction.
  • Patients with prolonged vasospasm can present with ST elevation MI, ventricular arrhythmias, and sudden death.

Additional Reading

  • Crea F, Lanza GA. New light on a forgotten disease: vasospastic angina. J Am Coll Cardiol. 2011;58(12):1238–1240.  [PMID:21903057]
  • Krim NR, Narasimhan S, Monrad ES. Severe multivessel coronary vasospasm presenting as acute ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2012;60(15):1429.  [PMID:23036628]
  • Lanza GA, Careri G, Crea F. Mechanisms of coronary artery spasm. Circulation. 2011;124(16):1774–1782.  [PMID:22007100]
  • Moukarbel GV, Weinrauch LA. Disruption of coronary vasomotor function: the coronary spasm syndrome. Cardiovasc Ther. 2012;30(2):e66–e73.  [PMID:20946324]
  • Ong P, Athanasiadis A, Borgulya G, et al. 3-year follow-up of patients with coronary artery spasm as cause of acute coronary syndrome: the CASPAR (coronary artery spasm in patients with acute coronary syndrome) study follow-up. J Am Coll Cardiol. 2011;57(2):147–152.  [PMID:21211685]

See Also

  • ACS Unstable Angina
  • ACS Myocardial Infarction

Codes

ICD-9

  • 411.1 Intermediate coronary syndrome
  • 413.1 Prinzmetal angina

ICD-10

  • Angina pectoris with documented spasm
  • Acute ischemic heart disease, unspecified

SNOMED

  • 87343002 Prinzmetal angina (disorder)
  • 394659003 Acute coronary syndrome (disorder)

Authors

John W. Hardin
Shamai A. Grossman


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