Prinzmetal's angina
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Chronic stable angina Microchapters | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
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Diagnosis | ||
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Alternative Therapies for Refractory Angina | ||
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Guidelines for Asymptomatic Patients | ||
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Prinzmetal's angina On the Web | ||
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Prinzmetal's angina, also known as variant angina or angina inversa, is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in periodic cycles. Prinzmetal's angina is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than fixed narrowings of the coronary arteries due to atherosclerosis (buildup of fatty plaque and hardening of the arteries).
History and Eponym
It was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).[1]
Signs and Symptoms
While the symptoms of chronic stable angina occur with exertion, the symptoms of Prinzmetal's angina typically occur at rest. The symptoms may occur reproducibly at certain times of the day or night. In the classic description, the symptoms often come on at night.
Electrocardiographic Changes
Prinzmetal's angina is associated with transmural injury and ST segment elevation rather than ST segment depression.
Diagnosis
- Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome" patient, and are generally evaluated with serial testing of cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may in some cases be abnormal or positive, as coronary spasm can lead to myocardial necrosis in severe cases.
- Two-thirds of patients have concurrent atherosclerosis of a major coronary artery. This is often mild or not in proportion to the degree of symptoms.
- The gold standard test is coronary angiography including the administration of provocative agents via the intracoronary route. It should be noted that two-thirds of patients with Prinzmetal's angina have concurrent atherosclerosis of a major coronary artery, but the extent of the atherosclerosis is generally mild, and the symptoms are out of proportion to the extent of disease. Depending on the local protocol, provocative testing may utilize either ergonovine, methylergonovine or acetylcholine. Exaggerated spasm is diagnostic of Prinzmetal's angina. Care should be taken to have nitrates and calcium channel agents readily available to reverse the spasm.
EKG findings during spasm include ST segment elevation rather than ST depression.
Treatment
Prinzmetal angina typically responds to nitrates and calcium channel blockers. Patients with multivessel spasm, refractory spasm, spasm that results in sudden death may benefit from dual calcium channel blocker therapy.
- Treatment of chronic vasospasm should be performed in this order (step-wise fashion): medical therapy, percutaneous intervention, and then, surgery.
Medical Therapy
- Risk factor modification (smoking cessation, lipid control) is recommended for all patients.
- Begin pharmacologic therapy with oral calcium channel blockers (diltiazem, verapamil, nifedipine) and/or nitrates. If monotherapy is ineffective, begin combination therapy which is generally well tolerated (10% of patients may require 2 calcium channel blockers). If refractory or multi-vessel spasm is present, multiple CCBs are likely necessary, as these patients are at high risk for ventricular arrhythmias. Alpha blockers may also be useful if there is incomplete response to CCB and nitrates.
- Due to their ability to improve endothelial function, statins should be considered for vasospasm.
- Certain medications should be avoided: nonselective beta blockers, aspirin, and sumatriptan can exacerbate vasospasm. Hormone replacement therapy (estrogen-progestin) have been associated with an increase in cardiac events (HERS-II and WHI trials) and should also be avoided.
Percutaneous Intervention (PCI)
- If vasospasm has a clearly definable area that is associated with coronary artery disease and refractory to medical therapy, stenting may be an effective strategy. However, stenting may simply propagate the spasm to a proximal or distal location in the vessel.
- Following any PCI, adjunctive medical therapy must be continued.
- Resolution of symptoms, ECG changes, and angiographic vasospasm is usually apparent within one minute post-procedure.
- Refractory spasm occurring during PCI is likely secondary to dissection, which requires stenting unless the artery is small and the patient is clinically stable.
- The role of revascularization in the setting of multivessel vasospasm is uncertain.
Surgery
- In the rare circumstance that a patient is refractory to pharmacologic and percutaneous therapy, surgical denervation and plexectomy have been effective.
References
- ↑ Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.