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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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.
- Calcium channel blockers: Generally, well tolerated and can aid with hypertension control. A combination of dihyropyridine and non-dihydropyridine calcium channel blockers should be used in patients with refractory coronary vasospasm, particularly if it has resulted in ventricular arrhythmia. Multiple calcium channel blockers may be required in patients with refractory or multivessel spasm. A patient who has suffered VT/VF due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
- Diltiazem 240-360 mg PO qd
- Verapamil 240-480 mg PO qd
- Nifedipine XL 60-120 mg PO qd
- Nicardipine 40-160 mg PO qd
- Long-acting nitrates: Generally, well tolerated and can aid with hypertension control.
- Isosorbide mononitrate (Imdur) 60-240 mg PO qd
- Isosorbide dinitrate (Isordil) 20-40 mg PO tid
- Statins: May improve endothelial dysfunction and lower inflammation. A small, randomized control trial showed that fluvastatin 30 mg daily reduced rates of vasospasm. Statins also provide benefits of LDL lowering and plaque stabilization.
- Fluvastatin 30 mg PO qd
- Hormone replacement therapy: This remains controversial, particularly due to the risk of concern of increased cardiac events.
- Smoking cessation: Should be emphasized in all patients, as it contains non-cardiac benefits as well. It lowers future event rates of vasospasm and acute coronary syndromes.
- PTCA/stenting: While resolution occurs following PTCA/stenting in some cases, spasm can propagate to a new location, proximal or distal to the stented site.
- ICD placement: As described above for patients with VT/VF due to spontaneous coronary vasospasm without other provocation that may be treated.
- Surgical autonomic denervation/plexectomy: Can be useful in cases that are refractory to medical therapy or percutaneous intervention. It's reserved only for the most refractory cases.
Making a Selection
- 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.
Other Concerns
There are several additional factors that doctors should mindful of when considering coronary vasospasm treatments, complications, and outcomes.
- Coronary vasospasm can lead to life-threatening arrhythmias, depending on the vessel that is involved. Specifically, right coronary artery spasm can lead to sinus arrest or complete heart block, while left anterior descending artery spasm can lead to ventricular tachycardia or fibrillation. Multivessel spasm can also lead to ventricular arrhythmias.
- Patients who have coronary artery disease in addition to coronary vasospasm have an overall worse prognosis.
ESC Guidelines for Diagnostic Tests in Suspected Vasospastic Angina (DO NOT EDIT)[2]
| Class I |
| "1. ECG during angina if possible. (Level of Evidence: B)" |
| "2. Coronary arteriography in patients with characteristic episodic chest pain and ST-segment changes that resolve with nitrates and/or calcium channel blockers to determine the extent of underlying coronary disease. (Level of Evidence: B)" |
| Class IIa |
| "1. Intracoronary provocative testing to identify coronary spasm in patients with normal findings or nonobstructive lesions on coronary arteriography and the clinical picture of coronary spasm. (Level of Evidence: B)" |
| "2. Ambulatory ST Segment Monitoring to identify ST-deviation. (Level of Evidence: C)" |
ESC Guidelines for Pharmacological Therapy of Vasospastic Angina (DO NOT EDIT)[2]
| Class I |
| "1. Treatment with calcium channel blocker and if necessary nitrates in patients whose coronary arteriogram is normal or shows only non-obstructive lesions. (Level of Evidence: B)" |
References
- ↑ Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.
- ↑ 2.0 2.1 Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367.