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Prinzmetal's angina, also known as variant angina or angina inversa, is chest pain at rest that occurs in periodic cycles. It is unrelated to exertion although can occur with exertion.
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.
Attacks can be precipitated by an emotional stress, hyperventilation, exercise, or exposure to cold. A circadian variation in the episodes of angina is most often present, with most attacks occurring in the early morning.
It is characterized by transient ST-segment elevation that spontaneously resolves or resolves with nitroglycerin use without progression to MI. The majority of patients have normal exercise tolerance, and stress testing may be negative.
Because the anginal discomfort usually occurs at rest without a precipitating cause, it may simulate UA/NSTEMI secondary to coronary atherosclerosis.
Mechanism
The precise mechanisms have not been established, but a systemic alteration in nitric oxide production or an imbalance between endothelium-derived relaxing and contracting factors may be causative.
Enhanced phospholipase C (PLC) activity has also been documented.
An inflammatory etiology is supported by the finding of elevated levels of serum hs-CRP in these patients.
Histological findings in patients undergoing coronary atherectomy suggest that repetitive coronary vasospasm may provoke vascular injury and lead to the formation of neointimal hyperplasia at the initial site of spasm, leading to rapid progression of coronary stenosis in some patients.
Diagnosis
The key to the diagnosis of variant angina is the documentation of ST-segment elevation in a patient during transient chest discomfort and that resolves with the relief of chest discomfort.
Continuous 12-lead ECG monitoring can be performed for this purpose in-hospital or as an outpatient.
Typically, NTG is extremely effective in relieving the spasm.
In variant angina, the spasm can be superimposed on severe or non-severe coronary stenosis or supervene in an angiographically normal coronary artery segment. Hence, coronary angiography is usually part of the workup of these patients and can help guide the treatment.
Provocative tests can be used to precipitate coronary artery spasm when the diagnosis is suspected but not objectively documented.
Although the spasm is usually promptly relieved with NTG administered intracoronarily or intravenously, it may at times be refractory to therapy with NTG and can lead to MI and even death. For these reasons, provocative tests are now rarely used.
Treatment
Coronary spasm is usually very responsive to NTG, longacting nitrates, and calcium channel blockers, which are considered first-line therapies.
Calcium antagonists have proved extremely effective in preventing the coronary artery spasm of variant angina and they should ordinarily be prescribed in maximally tolerated doses on a long-term basis. Because nitrates and calcium channel blockers act through different mechanisms, they may have additive vasodilatory effect.
Beta-blockers have theoretical adverse potential, and their clinical effect is controversial.
Nicorandil, a vasodilator that influences coronary arterial tone by acting through potassium channel activation, appears to be effective for the treatment of vasospastic angina.
Aspirin, helpful in unstable angina, may theoretically increase the severity of ischemic episodes in patients with variant angina because it inhibits biosynthesis of the naturally occurring coronary vasodilator prostacyclin.
Revascularization may be helpful in patients with variant angina and discrete, proximal fixed obstructive lesions.
Patients who have experienced ischemia-associated ventricular fibrillation who continue to manifest ischemia despite maximal medical treatment should receive an implantable cardioverter-defibrillator.
2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes (DO NOT EDIT) [1]
Medical Regimen and Use of Medications at Discharge
"1.CCBs alone or in combination with long-acting nitrates are useful to treat and reduce the frequency of vasospastic angina.(Level of Evidence: B)"
"2.Treatment with HMG-CoA reductase inhibitor, cessation of tobacco use, and additional atherosclerosis risk factor modification and are useful in patients with vasospastic angina. (Level of Evidence: B)"
"3.Coronary angiography (invasive or noninvasive) is recommended in patients with episodic chest pain accompanied by transient ST-elevation to rule out severe obstructive CAD. (Level of Evidence: C)"
"1. Provocative testing during invasive coronary angiography†† may be considered in patients with suspected vasospastic angina when clinical criteria and noninvasive testing fail to establish the diagnosis (Level of Evidence: B)"
2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non -ST-Elevation Myocardial Infarction (DO NOT EDIT)[2][3]
"2. Provocative testing may be considered in patients with no significant angiographic CAD and no documentation of transient ST segment elevation when clinically relevant symptoms possibly explained by coronary artery spasm are present. (Level of Evidence: C)"
References
↑ Ezra A. Amsterdam, MD, FACC; Nanette K. Wenger, MD et al.2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. JACC. September 2014 (ahead of print)
↑ 3.03.1Anderson JL, Adams CD, Antman EM; et al. (2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". JACC. 50 (7): e1–e157. PMID17692738. Text "doi:10.1016/j.jacc.2007.02.013 " ignored (help); Unknown parameter |month= ignored (help)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)