Synonym: variant angina, Prinzmetal's angina
First described by Prinzmetal et al in 1959, coronary artery vasospasm may be associated with acute myocardial infarction, serious ventricular arrhythmias and sudden death. Most patients also have underlying coronary artery disease but some have normal arteries.
- The prevalence of coronary artery spasm is variable in different countries and lower in Western populations than in Japan. The prevalence is higher in people aged 40-70 years and tends to decrease after the age of 70 years.
- Smoking and high-sensitivity C-reactive protein (hs-CRP) are significant risk factors.
Episodes of coronary artery spasm (particularly in the morning when spontaneous coronary artery spasm is most likely to occur) can be precipitated by:
- Physical or mental stress.
- Magnesium deficiency.
- Alcohol consumption.
- The Valsalva manoeuvre.
- Pharmacological agents such as cocaine.
- Sympathomimetic agents - eg, adrenaline (epinephrine), noradrenaline (norepinephrine).
- Parasympathomimetic agents - eg, methacholine, pilocarpine.
- Ergot alkaloids - eg, ergotamine.
- These are variable, from brief unnoticed episodes to severe prolonged angina.
- This variant of angina occurs at rest, usually lasting for between 5 and 30 minutes. Most episodes occur between midnight and early morning.
- Any episode, include brief and otherwise unnoticed episodes, can result in myocardial ischaemia, life-threatening arrhythmias and sudden death.
- A few patients have a general abnormality of vasomotor tone. They may also present with symptoms of migraine headache and Raynaud's phenomenon.
- Finding other evidence of diffuse atherosclerotic disease does not differentiate patients with variant angina from those with unstable angina. Physical examination does not reliably differentiate between variant angina and occlusive coronary artery disease.
See also separate Chest Pain and Cardiac-type Chest Pain Presenting in Primary Care articles.
- Distinguishing Prinzmetal's angina from an acute coronary syndrome is very difficult and so patients usually require hospital assessment and admission.
- Many patients with coronary artery spasm also have obstructive coronary artery disease.
- FBC, renal function, electrolytes, fasting blood glucose and lipid levels.
- Cardiac enzymes and troponins to assess for acute coronary syndrome.
- ECG: transient ST-segment elevation corresponding to the distribution of the affected coronary artery during attacks is characteristic.
- Ambulatory ECG monitoring may be required because episodes of coronary artery vasospasm are often brief and ECG findings are often normal between attacks.
- Coronary angiography is the gold standard for the diagnosis of variant angina. Several provocative tests for coronary spasm are used, including ergonovine, acetylcholine, neuropeptide Y and dopamine.
- If coronary revascularisation is not being considered or invasive coronary angiography is not clinically appropriate or acceptable to the person, offer non-invasive functional imaging. Options for non-invasive functional testing include:
- Myocardial perfusion scintigraphy (MPS) using single photon emission computed tomography (SPECT).
- Stress echocardiography.
- First-pass contrast-enhanced magnetic resonance (MR) perfusion.
- MR imaging for stress-induced wall motion abnormalities.
There is no specific cure. Managing lifestyle factors is important in prevention. Smoking, alcohol, and high levels of anxiety have a significant role in coronary spasm.
Specific measures include:
- Patients with angina at rest should be admitted to a hospital for observation, evaluation and initial management.
- Co-existing coronary artery disease is common and so management includes assessment and modification of all cardiovascular risk factors.
- Nitrates and calcium-channel blockers are the mainstay of medical therapy:
- Glyceryl trinitrate effectively treats episodes of angina and myocardial ischaemia and long-acting nitrate preparations reduce the frequency of recurrent events.
- Calcium-channel blockers are very effective in preventing coronary vasospasm and variant angina.
- Beta-blockers, especially those with non-selective adrenoceptor blocking effects, may aggravate coronary artery spasm and therefore should be avoided.
- Implantable cardioverter defibrillator devices have been used in patients who survive ventricular tachycardia or fibrillation due to coronary artery spasm. This treatment is controversial for primary prevention but should be considered for high-risk patients.
- Coronary artery stenting may be required for refractory spasm.
- Coronary revascularisation may be required for associated fixed stenosis due to coronary artery disease.
- Myocardial infarction:
- One review found that 6% of patients presenting with acute myocardial infarction did not have obstructed coronary arteries.
- The incidence and prognosis of myocardial infarction in patients with variant angina appear to be associated with the extent and severity of any underlying atherosclerotic coronary stenoses.
- Syncope and presyncope may be associated with variant angina and are usually due to any associated significant arrhythmias.
- There is an association with various arrhythmias, including sinus bradycardia, sinus arrest with or without junctional escape beats, complete atrioventricular block, paroxysmal atrial fibrillation, ventricular premature complex, ventricular tachycardia, ventricular fibrillation and asystole.
- The risk of sudden death is increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not in those with fixed coronary stenosis.
- The overall prognosis is good if the patients take calcium-channel blockers and avoid smoking.
- Multivessel spasms have a greater risk of fatal arrhythmias.
Further reading and references
; Coronary artery spasm: review and update. Int J Med Sci. 2014 Aug 2811(11):1161-71. doi: 10.7150/ijms.9623. eCollection 2014.
; Mechanisms of coronary artery spasm. Circulation. 2011 Oct 18124(16):1774-82. doi: 10.1161/CIRCULATIONAHA.111.037283.
; Coronary artery spasm--clinical features, diagnosis, pathogenesis, and treatment. J Cardiol. 2008 Feb51(1):2-17. Epub 2008 Feb 1.
; NICE Clinical Guideline (March 2010, updated Nov 2016)
; Provocative testing for coronary reactivity and spasm. J Am Coll Cardiol. 2014 Jan 2163(2):103-9. doi: 10.1016/j.jacc.2013.10.038. Epub 2013 Nov 6.
; Coronary artery spasm and ventricular arrhythmias. Postgrad Med J. 2012 Aug88(1042):465-71. doi: 10.1136/postgradmedj-2011-130494. Epub 2012 Mar 21.
; Coronary vasospasm: a case report and review of the literature. Can J Cardiol. 2005 Sep21(11):953-7.
; Systematic review of patients presenting with suspected myocardial infarction and nonobstructive coronary arteries. Circulation. 2015 Mar 10131(10):861-70. doi: 10.1161/CIRCULATIONAHA.114.011201. Epub 2015 Jan 13.
; Variant angina and coronary artery spasm: the clinical spectrum, pathophysiology, and management. J Nihon Med Sch. 201178(1):4-12.
I have had prinzmetal's angina for over 7 years. Information about prinzmetal's says that pain occurs at night while in bed. Well not in my case. I get angina pain in the day time as well at night....Guest
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