Treating Vasospastic Angina: Pharmacotherapy Should Be Guided by Patient-Specific Factors

Vasospastic angina was first identified as a form of angina pectoris by Myron Prinzmetal in 1959
Vasospastic angina was first identified as a form of angina pectoris by Myron Prinzmetal in 1959

Vasospastic angina was first identified as a form of angina pectoris by Myron Prinzmetal in 1959. Occurring primarily at rest and most often associated with ST-segment elevation, vasospastic angina is typically experienced initially in midlife and is “characterized by spontaneous episodes of angina due to reversible constriction of a focal segment or segments of the coronary artery.”1 Spasms may be focal, multifocal, or multivessel.

Patients with vasospastic angina—who experience frequent episodes of angina—have significant morbidity, leading to increased hospitalizations and decreased quality of life. Yet, clinical presentation of vasospastic angina is vague, reflecting lack of understanding of its pathophysiology or etiology. Genetic causes point to endothelium dysfunction, abnormal platelet activation, and upregulation of alpha-adrenergic receptor activity.

Generally, vasospastic angina is a diagnosis of exclusion. Many symptoms overlap with obstructive coronary artery disease, especially ST-segment elevation myocardial infarction. In fact, during exacerbations, patients primarily have ST-segment elevation on 12-lead electrocardiography (ECG). Clinical presentations may range from angina with minimal exertion to myocardial infarction due to vasospasm. Cold sweats, nausea, or vomiting—and rarely, syncope—may accompany chest pain, which is the presenting symptom, similar to that of stable exertional angina.

Those more likely to experience vasospastic angina are younger and female. In addition, vasospastic angina may occur in up to 60% of patients with obstructive coronary artery disease (CAD). Nicotine-containing products, hypomagnesemia, alcohol consumption, and illicit drug use are all risk factors for vasospastic angina. Coronary artery spasms may be exacerbated by agents that can induce vasoconstriction, such as the antimigraine triptans and the chemotherapeutic agents 5-fluorouracil and capecitabine as well as amphetamines, cocaine, marijuana, and ephedrine-based weight-loss products.

Noninvasive diagnostic methods include ECG, Holter monitoring, and exercise testing. These methods usually are concurrent with calcium channel blocker (CCB) or nitroglycerin treatment; alleviation of symptoms and ECG abnormalities may help guide clinical diagnosis.

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