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Coronary Artery Vasospasm Medication

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

Medication Summary

Nitrates and calcium channel blockers are the mainstays of medical therapy for vasospastic angina. Other agents have been tried with variable success, including endothelin antagonists such as bosentan.


Nitrates, Angina

Class Summary

Nitrates produce a direct, endothelium-independent vasodilatation of the large coronary arteries. In addition, they reduce preload by dilating venous capacitance vessels, which results in decreased myocardial oxygen consumption. Nitrates act as an exogenous source of nitric oxide, which causes vascular smooth muscle relaxation and may have a modest effect on platelet aggregation and thrombosis.

Nitroglycerin (Nitrolingual, Nitrostat, Minitran, Nitro-Bid, Nitro-Dur)


Nitroglycerin causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate (GMP). The result is a decrease in blood pressure. Dosage forms include sublingual, transdermal, and intravenous (IV) preparations. The distinction between short-acting preparations for treatment of acute attacks and long-acting preparations for prevention of recurrent episodes is important.

Isosorbide dinitrate (Isordil, Dilatrate SR)


Isosorbide dinitrate relaxes vascular smooth muscle by stimulating intracellular cyclic GMP. It decreases preload and afterload, causing decreased myocardial oxygen demand. Isosorbide dinitrate is used for the treatment and prevention (sustained-release preparations) of variant angina. The onset of action is approximately 3.5 minutes, and the antianginal effect lasts about 2 hours.

Isosorbide mononitrate (ISMO, Imdur, Monoket)


Isosorbide mononitrate is used for the prevention of variant angina. The onset of action of oral isosorbide mononitrate is not sufficiently quick to permit its use as an acute antianginal agent. The half-life is approximately 5 hours.


Calcium Channel Blockers

Class Summary

Calcium antagonists relax coronary smooth muscle and produce coronary vasodilation, which in turn improves myocardial oxygen delivery. Dihydropyridines (eg, amlodipine and felodipine) exhibit greater vascular selectivity than nondihydropyridines (eg, verapamil and diltiazem), which also inhibit impulse conduction within the sinoatrial and atrioventricular nodes.

Nifedipine (Nifediac CC, Adalat CC, Procardia, Procardia XL)


Nifedipine is the prototypical dihydropyridine, indicated for treatment of acute attacks and prevention of recurrent attacks. Sublingual administration is generally safe, despite theoretical concerns.

Amlodipine (Norvasc)


Amlodipine is generally regarded as a dihydropyridine, though experimental evidence suggests that it may also bind to nondihydropyridine binding sites. It has a substantially longer half-life than nifedipine and is administered daily. It is appropriate for prophylaxis of variant angina.

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)


Verapamil is a nondihydropyridine that is appropriate for prophylaxis of variant angina. It is recommended for rate control in atrial fibrillation or flutter. During depolarization, verapamil inhibits the entry of calcium ions into slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.

Diltiazem (Cardizem, Cardizem CD, Cartia XT, Dilacor XR, Tiazac)


Diltiazem is a nondihydropyridine that is appropriate for prophylaxis of variant angina. During depolarization, it inhibits the entry of calcium ions into slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.

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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