Unstable angina / non ST elevation myocardial infarction prinzmetal's angina


 * Associate Editor-In-Chief: Smita Kohli, M.D.

Synonyms and related keywords: Prinzmetal's angina, variant angina, angina inversa

Overview of Prinzmetal's Angina in UA / NSTEMI

 * 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 NTG 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 prevail.


 * 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 nonsevere 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.
 * Nitrates and calcium channel blockers should be withdrawn well before provocative testing. These tests are more often used during coronary angiography.
 * Acetylcholine and methacholine are now predominantly used for pharmacological provocative tests.
 * 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.
 * Alpha-receptor blockers have been reported to be of benefit.
 * 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.

==ACC / AHA Guidelines (DO NOT EDIT) == {{cquote|

Class I
1. Diagnostic investigation is indicated in patients with a clinical picture suggestive of coronary spasm, with investigation for the presence of transient myocardial ischemia and ST-segment elevation during chest pain. (Level of Evidence: A)

2.Coronary angiography is recommended in patients with episodic chest pain accompanied by transient ST segment elevation. (Level of Evidence: B)

3. Treatment with nitrates and calcium channel blockers is recommended in patients with variant angina whose coronary angiogram shows no or non obstructive coronary artery lesions. Risk factor modification is recommended, with patients with atherosclerotic lesions considered to be at higher risk. (Level of Evidence: B)

Class IIb
1.Percutaneous coronary intervention may be considered in patients with chest pain and transient ST segment elevation and a significant coronary artery stenosis. (Level of Evidence: B)

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)

Class III
1. Provocative testing is not recommended in patients with variant angina and high-grade obstructive stenosis on coronary angiography. (Level of Evidence: B)}}