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Coronary Artery Vasospasm Treatment & Management

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Eric H Yang, MD  more...
Updated: Nov 21, 2015

Initial Measures

Patients with vasospastic angina presenting with active symptoms of ischemia often require admission. Initial evaluation should include 12-lead electrocardiography (ECG), continuous telemetry monitoring, and serial cardiac enzyme and troponin measurements. Further evaluation should include assessment for coexisting or contributory atherosclerotic coronary artery disease (CAD). This may involve stress testing with myocardial perfusion imaging or even coronary angiography (see Workup).

Because atherosclerosis is common in patients with vasospastic angina, medical and lifestyle interventions for preventing or treating atherosclerosis should be implemented when appropriate.


Pharmacologic Therapy

Initial medical treatment should include sublingual, topical, or intravenous (IV) nitrate therapy. Nitroglycerin administered by any route (intracoronary, IV, topical, or sublingual) effectively treats episodes of angina and myocardial ischemia within minutes, and long-acting nitrate preparations reduce the frequency of recurrent events.

Until atherosclerotic coronary disease (a much more frequent cause of chest pain) is excluded, standard therapies, including antiplatelet or antithrombotic agents, statins, and beta blockers, may be administered. Statin therapy appears to improve clinical outcomes in patients with coronary spasm–induced acute myocardial infarction with nonobstructive coronary arteries.[41]

Once the diagnosis of coronary artery vasospasm is made, calcium channel blockade and long-acting nitrates may be used for long-term prophylaxis.

The calcium channel blockers nifedipine, amlodipine, verapamil, and diltiazem effectively prevent coronary vasospasm and variant angina, and they should be administered in preference to beta blockers. Amlodipine may be preferable because of its long half-life.[42]

Bet -blockers are beneficial in most patients with atherosclerotic coronary stenoses and exertional angina pectoris and are sometimes helpful in combination with the above drugs to achieve control of symptoms in these patients. However, nonselective beta blockers may be detrimental in some patients because blockade of the beta receptors, which mediate vasodilation, allows unopposed alpha receptor–mediated coronary vasoconstriction to occur and may worsen vasospastic angina in selected cases.

Other agents have been tried with variable success, including endothelin antagonists such as bosentan.[43] Early experience with cilostazol has been positive but limited;[44] additional research is needed to validate its clinical use.

Spontaneous remission may occur, and some patients may be able to wean or reduce their drug therapy after an initial 3-month symptom-free period.


Percutaneous and Surgical Revascularization

Up to one fifth of patients may continue to have vasospasm despite medical therapy. Mechanical revascularization has been used successfully in patients with medically resistant vasospasm. Scattered reports of coronary stenting suggest that a percutaneous strategy may be feasible in such patients.[45] The results for surgical revascularization have been variable, but overall, bypass surgery appears to provide clinical benefit to less than 50% of patients.[24] The efficacy of surgical treatment is greater in patients who also have significant obstructive atherosclerotic lesions. In patients without baseline obstruction, however, the risk of early graft closure is elevated.

For patients who continue to have significant symptoms or signs of coronary vasospasm despite maximally tolerated medical therapy, in whom the culprit segment can be identified, coronary stenting may be considered on a case-by-case basis. However, bypass grafting of arteries without baseline obstruction should be reserved for patients with life-threatening ischemia that is refractory to maximal medical therapy. In these patients, adding complete plexectomy to the procedure may provide additional benefit.[46]

Contributor Information and Disclosures

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 College of Cardiology, American Heart Association, American Society of Echocardiography, Texas Medical Association, American Academy of Sleep Medicine, American Stroke Association, American Society of Nuclear Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

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

Disclosure: Nothing to disclose.


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

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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 .
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