Coronary Artery Vasospasm Workup

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Eric H Yang, MD   more...
 
Updated: Apr 19, 2012
 

Laboratory Studies

Evaluation of the standard hematology, serum chemistry, and lipid profiles is appropriate for excluding anemia, infection, primary platelet disorders, renal failure, hyperglycemia, electrolyte abnormalities, and dyslipidemia. Serial measurement of cardiac enzyme and troponin levels should be performed to assess for evidence of ischemia.

Magnesium levels may be checked; magnesium deficiency can heighten sensitivity to acetylcholine- and hyperventilation-induced spasm. Magnesium supplementation may be a potentially useful therapy.[5]

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Perfusion Imaging and Echocardiography

Myocardial perfusion imaging may be helpful in ruling out obstructive atherosclerotic disease between episodes of coronary artery vasospasm. During episodes, myocardial perfusion imaging may help identify and quantify ischemia and localize it to the culprit artery.

Standard transthoracic echocardiography should be considered to evaluate for stigmata of other causes of nonexertional chest pain (eg, pericarditis or abnormalities of the aorta). Preliminary data suggest a potential role for hyperventilation and cold-pressor stress echocardiography as a noninvasive means for detecting coronary artery vasospasm, though this method may not be as sensitive as using intracoronary acetylcholine as the provocative agent.[31]

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Electrocardiography and Monitoring

Transient ST-segment elevation on electrocardiography (ECG) is a characteristic finding in patients with variant angina,[5] but it may only be present during symptomatic episodes and typically resolves completely within minutes. However, in more severe cases, ST elevation may be followed by T-wave inversions for hours to days.[32] During recovery, U-wave inversions may be present, particularly in lead V5.[33]

Many episodes of coronary artery vasospasm are brief and may be asymptomatic; however, ST-segment changes may be detected by ambulatory electrocardiography, which may allow for more accurate characterization of the frequency and duration of attacks.

Severe vasospastic angina may result in heart block or potentially fatal ventricular arrhythmias. Inpatient telemetry monitoring serves an important role in acutely ill patients. In outpatients, Holter monitoring may facilitate detection of nonsustained arrhythmias.

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Angiography

Coronary angiography may reveal focal spasm of a coronary artery; when coupled with typical symptoms, ECG changes, and even ventricular dysfunction, this spasm may be pathognomonic for the condition.

Most patients with variant angina and documented coronary artery vasospasm have some angiographic evidence of atherosclerotic coronary artery disease (CAD), which is typically mild. Focal spasm more commonly occurs within 1 cm of an angiographically apparent obstruction. If minimal or no angiographic evidence of CAD is found in a patient who has recently had angina at rest with transient ST-segment elevation, variant angina is the more likely diagnosis, and further testing is unnecessary.

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Provocative Testing

Provocative testing is infrequently used in clinical practice but may facilitate identification of patients with coronary artery vasospasm.

The most commonly used provocative agent is ergonovine maleate, an ergot alkaloid that stimulates both alpha-adrenergic and serotonergic receptors, exerting a direct constrictive effect on vascular smooth muscle. Normal coronary arteries respond to ergonovine maleate with a mild diffuse spasm, whereas abnormal arteries may respond with an intense focal spasm. Acetylcholine and hyperventilation have also been used to provoke spasm.

Intravenous (IV) administration of incremental doses of methylergonovine, starting at 0.05 mg and increasing to a maximum of 0.40 mg, is both sensitive and specific, and there is an inverse relation between the dose required to provoke spasm in the laboratory and the frequency of spontaneous episodes experienced by the patient.

To ensure a valid test, nitrates and calcium antagonists must be withdrawn for at least 48 hours before testing. The intracoronary route of administering methylergonovine is preferable for provocation of spasm and affords the opportunity to evaluate the left and right coronary circulations separately. Small dosing increments (ie, 5-10 µg) are used, with the total dose not to exceed 50 µg.

Intracoronary nitrates should be readily available. Complication rates during provocative testing are relatively low with either ergonovine or acetylcholine, provided that intracoronary nitrates are on hand for use to relieve induced spasms.[34]

Absolute contraindications to provocative testing with methylergonovine include the following:

  • Pregnancy
  • Severe hypertension
  • Severe left ventricular dysfunction
  • Moderate-to-severe aortic stenosis
  • High-grade left main coronary stenosis
  • Significant stenoses in epicardial coronary vessels

Relative contraindications include the following:

  • Uncontrolled or unstable angina
  • Uncontrolled ventricular arrhythmia
  • Recent MI
  • Advanced coronary disease
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Contributor Information and Disclosures
Author

Stanley S Wang, MD, JD, MPH  Clinical Cardiologist, Austin Heart South; Director of Legislative Affairs, Austin Heart; Director, Sleep Disorders Center at Heart Hospital of Austin; Assistant Professor of Medicine (Adjunct), University of North Carolina School of Medicine

Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Sleep Medicine, American College of Cardiology, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, American Stroke Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital, University of North Carolina at Chapel Hill School of Medicine

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Gregory J Dehmer, MD Director, Division of Cardiology, Scott & White Healthcare; Professor of Medicine, Texas A&M Health Science Center College of Medicine

Gregory J Dehmer, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

References

  1. Prinzmetal M, Kennamer R, Merliss R. A variant form of angina pectoris. Am J Med. 1959;27:375-388.

  2. Maseri A, Severi S, Nes MD, et al. "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol. Dec 1978;42(6):1019-35. [Medline].

  3. Yasue H, Omote S, Takizawa A, Nagao M, Miwa K, Tanaka S. Circadian variation of exercise capacity in patients with Prinzmetal's variant angina: role of exercise-induced coronary arterial spasm. Circulation. May 1979;59(5):938-48. [Medline].

  4. Yasue H, Nakagawa H, Itoh T, Harada E, Mizuno Y. Coronary artery spasm--clinical features, diagnosis, pathogenesis, and treatment. J Cardiol. Feb 2008;51(1):2-17. [Medline].

  5. Ajani AE, Yan BP. The mystery of coronary artery spasm. Heart Lung Circ. Feb 2007;16(1):10-5. [Medline].

  6. Yasue H, Touyama M, Kato H, Tanaka S, Akiyama F. Prinzmetal's variant form of angina as a manifestation of alpha-adrenergic receptor-mediated coronary artery spasm: documentation by coronary arteriography. Am Heart J. Feb 1976;91(2):148-55. [Medline].

  7. Yasue H, Horio Y, Nakamura N, Fujii H, Imoto N, Sonoda R, et al. Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm. Circulation. Nov 1986;74(5):955-63. [Medline].

  8. Kaneda H, Taguchi J, Kuwada Y, Hangaishi M, Aizawa T, Yamakado M, et al. Coronary artery spasm and the polymorphisms of the endothelial nitric oxide synthase gene. Circ J. Apr 2006;70(4):409-13. [Medline].

  9. Nishijima T, Nakayama M, Yoshimura M, Abe K, Yamamuro M, Suzuki S, et al. The endothelial nitric oxide synthase gene -786T/C polymorphism is a predictive factor for reattacks of coronary spasm. Pharmacogenet Genomics. Aug 2007;17(8):581-7. [Medline].

  10. Egashira K, Katsuda Y, Mohri M, Kuga T, Tagawa T, Shimokawa H, et al. Basal release of endothelium-derived nitric oxide at site of spasm in patients with variant angina. J Am Coll Cardiol. May 1996;27(6):1444-9. [Medline].

  11. Nakano T, Osanai T, Tomita H, Sekimata M, Homma Y, Okumura K. Enhanced activity of variant phospholipase C-delta1 protein (R257H) detected in patients with coronary artery spasm. Circulation. Apr 30 2002;105(17):2024-9. [Medline].

  12. Stern S, Bayes de Luna A. Coronary artery spasm: a 2009 update. Circulation. May 12 2009;119(18):2531-4. [Medline].

  13. Adlam D, Azeem T, Ali T, Gershlick A. Is there a role for provocation testing to diagnose coronary artery spasm?. Int J Cardiol. Jun 22 2005;102(1):1-7. [Medline].

  14. Harding MB, Leithe ME, Mark DB, Nelson CL, Harrison JK, Hermiller JB, et al. Ergonovine maleate testing during cardiac catheterization: a 10-year perspective in 3,447 patients without significant coronary artery disease or Prinzmetal's variant angina. J Am Coll Cardiol. Jul 1992;20(1):107-11. [Medline].

  15. Bertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FA, Delforge MR, Carre AG, et al. Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography. Circulation. Jun 1982;65(7):1299-306. [Medline].

  16. Sueda S, Kohno H, Fukuda H, Ochi N, Kawada H, Hayashi Y, et al. Frequency of provoked coronary spasms in patients undergoing coronary arteriography using a spasm provocation test via intracoronary administration of ergonovine. Angiology. Jul-Aug 2004;55(4):403-11. [Medline].

  17. Sueda S, Kohno H, Oshita A, Fukuda H, Kondou T, Yano K, et al. Coronary abnormal response has increased in Japanese patients: Analysis of 17 years' spasm provocation tests in 2093 cases. J Cardiol. May 2010;55(3):354-361. [Medline].

  18. Bory M, Pierron F, Panagides D, Bonnet JL, Yvorra S, Desfossez L. Coronary artery spasm in patients with normal or near normal coronary arteries. Long-term follow-up of 277 patients. Eur Heart J. Jul 1996;17(7):1015-21. [Medline].

  19. Mayer S, Hillis LD. Prinzmetal's variant angina. Clin Cardiol. Apr 1998;21(4):243-6. [Medline].

  20. Selzer A, Langston M, Ruggeroli C, Cohn K. Clinical syndrome of variant angina with normal coronary arteriogram. N Engl J Med. Dec 9 1976;295(24):1343-7. [Medline].

  21. Pristipino C, Beltrame JF, Finocchiaro ML, Hattori R, Fujita M, Mongiardo R, et al. Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction. Circulation. Mar 14 2000;101(10):1102-8. [Medline].

  22. Bott-Silverman C, Heupler FA Jr. Natural history of pure coronary artery spasm in patients treated medically. J Am Coll Cardiol. Aug 1983;2(2):200-5. [Medline].

  23. Mishra PK. Variations in presentation and various options in management of variant angina. Eur J Cardiothorac Surg. May 2006;29(5):748-59. [Medline].

  24. Yasue H, Takizawa A, Nagao M, Nishida S, Horie M, Kubota J, et al. Long-term prognosis for patients with variant angina and influential factors. Circulation. Jul 1988;78(1):1-9. [Medline].

  25. Onaka H, Hirota Y, Shimada S, Suzuki S, Kono T, Suzuki J, et al. Prognostic significance of the pattern of multivessel spasm in patients with variant angina. Jpn Circ J. Jul 1999;63(7):509-13. [Medline].

  26. Ong P, Athanasiadis A, Borgulya G, Voehringer M, Sechtem U. 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. Jan 11 2011;57(2):147-52. [Medline].

  27. Figueras J, Cortadellas J, Gil CP, Domingo E, Soler JS. Comparison of clinical and angiographic features and longterm follow-up events between patients with variant angina and patients with ST elevation myocardial infarction. Int J Cardiol. Aug 10 2006;111(2):256-62. [Medline].

  28. Previtali M, Klersy C, Salerno JA, Chimienti M, Panciroli C, Marangoni E, et al. Ventricular tachyarrhythmias in Prinzmetal's variant angina: clinical significance and relation to the degree and time course of S-T segment elevation. Am J Cardiol. Jul 1983;52(1):19-25. [Medline].

  29. Rosamond W. Are migraine and coronary heart disease associated? An epidemiologic review. Headache. May 2004;44 Suppl 1:S5-12. [Medline].

  30. Hendriks ML, Allaart CP, Bronzwaer JG, Res JJ, de Cock CC. Recurrent ventricular fibrillation caused by coronary artery spasm leading to implantable cardioverter defibrillator implantation. Europace. Dec 2008;10(12):1456-7. [Medline].

  31. Hirano Y, Uehara H, Nakamura H, Ikuta S, Nakano M, Akiyama S, et al. Diagnosis of vasospastic angina: comparison of hyperventilation and cold-pressor stress echocardiography, hyperventilation and cold-pressor stress coronary angiography, and coronary angiography with intracoronary injection of acetylcholine. Int J Cardiol. Apr 4 2007;116(3):331-7. [Medline].

  32. Miwa K, Kambara H, Kawai C, Murakami T. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks. Jpn Circ J. Dec 1983;47(12):1415-22. [Medline].

  33. Miwa K, Murakami T, Kambara H, Kawai C. U wave inversion during attacks of variant angina. Br Heart J. Oct 1983;50(4):378-82. [Medline]. [Full Text].

  34. Sueda S, Kohno H, Fukuda H, Ochi N, Kawada H, Hayashi Y, et al. Clinical impact of selective spasm provocation tests: comparisons between acetylcholine and ergonovine in 1508 examinations. Coron Artery Dis. Dec 2004;15(8):491-7. [Medline].

  35. Taylor SH. Usefulness of amlodipine for angina pectoris. Am J Cardiol. Jan 27 1994;73(3):28A-33A. [Medline].

  36. Krishnan U, Win W, Fisher M. First report of the successful use of bosentan in refractory vasospastic angina. Cardiology. 2010;116(1):26-8. [Medline].

  37. Khitri A, Jayasuriya S, Habibzadeh MR, Movahed MR. Coronary stenting in patients with medically resistant vasospasm. Rev Cardiovasc Med. Fall 2010;11(4):264-70. [Medline].

  38. Bertrand ME, Lablanche JM, Rousseau MF, Warembourg HH Jr, Stankowtak C, Soots G. Surgical treatment of variant angina: use of plexectomy with aortocoronary bypass. Circulation. May 1980;61(5):877-82. [Medline].

 
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This electrocardiogram (ECG) is from a patient who underwent urgent cardiac catheterization, which revealed diffuse severe coronary spasm (most marked in the left circumflex system) without any fixed obstructive lesions. Severe left ventricular wall motion abnormalities were present, involving the anterior and inferior segments. A question of so-called takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) is also raised (see Bybee et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Int Med 2004:141:858-65). The latter is most often reported in postmenopausal, middle-aged to elderly women in the context of acute emotional stress and may cause ST elevations acutely with subsequent T wave inversions. A cocaine-induced cardiomyopathy (possibly related to coronary vasospasm) is a consideration but was excluded here. Myocarditis may also be associated with this type of ECG and the cardiomyopathic findings shown here. No fixed obstructive epicardial coronary lesions were detected by coronary arteriography. The findings in this ECG include low-amplitude QRS complexes in the limb leads (with an indeterminate QRS axis), loss of normal precordial R wave progression (leads V1-V3), and prominent anterior/lateral T wave inversions. Image courtesy of http://ecg.bidmc.harvard.edu .
 
 
 
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