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This topic is from AHA Clinical Cardiac Consult About our sources

Angina, Prinzmetal's Variant Angina Reviewed 11/2010

Don O. Rowe, Nanette K. Wenger
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BASICS

  • Description
  • Epidemiology
  • Risk Factors
  • General Prevention
  • Pathophysiology
  • Etiology
  • Associated Conditions

DIAGNOSIS

  • History
  • Physical Exam
  • Tests
  • Differential Diagnosis

TREATMENT

  • Medication (Drugs)
  • Additional Treatment
  • Surgery
  • In-patient Considerations

ONGOING CARE

  • Follow-Up Recommendations
  • Diet
  • Patient Education
  • Prognosis
  • Complications
The following is an excerpt....
BASICS
Description
  • Variant angina is characterized by a transient, abrupt, marked reduction in the luminal diameter of an epicardial coronary artery which leads to symptomatic myocardial ischemia.
  • ST-segment elevation rapidly returns to baseline with relief of symptoms.
  • Exercise tolerance commonly preserved.
  • Symptoms often occur in early morning hours.
  • Most commonly occurs in right coronary artery, but can occur in left, and, less commonly, in coronary artery bypass grafts.
  • Synonym(s): Prinzmetal angina, cardiac syndrome X (angina pectoris with normal coronary arteries)
  • System(s) affected: Cardiovascular
Epidemiology
  • Patients younger than those with exertional angina
  • Other than tobacco use, classic cardiovascular risk factors uncommon
  • Associated with other vasospastic disorders
  • Substance abuse an important risk factor
  • Female predominance
Incidence
  • Exact incidence unknown ...

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Figure 24-5. Pathophysiology of anginal syndromes. A. Normal coronary arteries are widely patent, the endothelium functions normally, and platelet aggregation is inhibited. B. In stable angina, atherosclerotic plaque and inappropriate vasoconstriction (caused by endothelial damage) reduce the vessel-lumen diameter, and hence decrease coronary blood flow. C. In unstable angina, rupture of the plaque triggers platelet aggregation, thrombus formation, and vasoconstriction. Depending on the anatomic site of plaque rupture, this process can progress to non-Q wave (non-ST elevation) or Q wave (ST elevation) myocardial infarction. D. In variant angina, atherosclerotic plaques are absent, and ischemia is caused by intense vasospasm.Credit: Figure 24-5: Adapted with permission from Lilly LS, ed. Pathophysiology of Heart Disease, 2nd ed. Baltimore: Williams & Wilkins, 1998:141, Figure 6.5.
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