Prinzmetal angina known as variant angina, and less commonly vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm.
It is a syndrome typically, unlike classical angina, triggered by exertion or exercise, commonly occurs in individuals at rest or even asleep.
Patients usually have repeated episodes of unexplained chest pain, light-headedness, excessive sweating, and/or reduced exercise tolerance that, unlike atherosclerosis-related angina pectoris, typically does not progress to myocardial infarction.
PA is caused by vasospasm, which is a narrowing of the coronary arteries due to contraction of the smooth muscle tissue in the vessel walls.
In classical angina it is due to the permanent occlusion of these vessels by atherosclerosis.
In classical angina attacks are triggered by exercise or other forms of exertion and relieved by rest and nitroglycerin.
PA commonly occurs in the absence of exercise or exertion.
It often awakens sufferers from their normal sleep.
Variant angina chest pain is concurrently associated with elevations in the ST segment on EKG.
Occurs more often in women than men, has a particularly high incidence in Japanese males as well as females.
Affects individuals who may smoke tobacco products but exhibit few other cardiovascular risk factors.
Rarely cases may exhibit symptom-free coronary artery spasm that is associated with cardiac muscle ischemia along with concurrent ischemic electrocardiographic changes.
The term vasospastic angina is sometimes used to include all of these atypical cases.
Variant angina may be a manifestation of a more generalized episodic smooth muscle-contractile disorder such as migraine, Raynaud’s phenomenon, or aspirin-induced asthma.
It is also the major complication of eosinophilic coronary periarteritis.
Patients with variant angina are generally younger and have fewer risk factors for coronary artery disease.
Cardiac examination of individuals with variant angina is usually normal in the absence of current symptoms.
With variant angina two-thirds of these individuals do have concurrent atherosclerosis of a major coronary artery, but this is often mild.
Persons with atherosclerosis-based occlusion(s) are predisposed to develop a variant angina form that has a poorer prognosis than most other forms of this disorder.
Diagnosis is suspected:
when an individual’s symptoms occur at rest or during sleep
an individual’s symptoms occur in clusters
an individual with a history of angina does not develop angina during treadmill stress testing.
an individual with a history of angina shows no evidence of other forms of cardiac disease
an individual without features of coronary artery atherosclerotic heart disease has a history of unexplained fainting.
ECG changes that are compatible with, but not indicative of variant angina include: elevations rather than depressions of the ST segment or an elevated ST segment plus a widening of the R wave to create a single, broad QRS complex peak termed the monophasic curve.
Some patients may show depressions, rather than elevations in the ST segments of their ECGs during angina pain, and may also show new U waves on ECGs during angina attacks.
A large percentage of patients are asymptomatic between episodes of coronary artery spasm.
Episodes may be far more frequent than expected, cause myocardial ischemia and be accompanied by potentially serious abnormalities in the rhythm.
Certain agents can trigger an attack: recreational agents, nicotine, alcoholic beverages, marijuana, cocaine, catecholamine-like stimulants, uterus-contracting drug, ergonovine, parasympathomimetic drugs, anti-migraine drugs and chemotherapeutic drugs.
Hyperventilation and stressful emotional or physical events causing increased in the blood levels of catecholamines may trigger variant angina.
The mechanisms that causes such intense vasospasm are hypothesized to be:
A response to reduced nitric oxide bioavailability caused by a defect in the endothelial nitric oxide synthetase enzyme which leads to endothelial function abnormalities.
Acetylcholine also stimulates endothelial cells to produce nitric oxide (NO), which then diffuses out of the endothelial cells, stimulating relaxation of the nearby smooth muscle cells.
In normal arterial walls relaxation induced by acetylcholine by nitric oxide production is of greater effect than contraction that is induced.
With an endothelium that is dysfunctional, stimulation with acetylcholine will fail to produce, adequate nitric oxide.
Thromboxane A2, serotonin, histamine, and endothelin are vasoconstrictor which activated platelets release and/or cause to be released.
Platelet activation results in the release of these mediators and coronary vasospasm.
Coronary spasm may be due to increased alpha-adrenergic receptor activity in epicardial coronary arteries or the excessive release of the catacholamines that activate these receptors.
Other factors associated with variant angina include: intrinsic hypercontractility of coronary artery smooth muscle; existence of significant atherosclerotic coronary artery disease; and reduced activity of the parasympathetic nervous system.
Documented in between 2% to 10% of angina patients.
ECG that suggests variant angina s
hows elevations in the ST segment or an elevated ST segment plus a widening of the R wave during symptoms that are triggered by a provocative agent.
However, the electrocardiogram may show depressions rather than elevations in ST segments.
All diagnosable cases clinical symptoms should be promptly relieved and ECC changes should be promptly reversed by rapidly acting sublingual or intravenous nitroglycerin.
The best method for diagnosing variant angina is to visualize coronary arteries before and after injection of a provocative agent such as ergonovine, methylergonovine or acetylcholine to precipitate an attack of vasospasm.
A positive test to these inducing agents is defined as ≥70-90% constriction of involved arteries.
Generally, such constrictions are fully reversed by rapidly acting nitroglycerin.
Patients may have undocumented episodes of symptom-free coronary artery spasm that are associated with poor blood flow to portions of the heart and subsequent serious heart arrhythmias.
Smoke cessation significantly reduces the incidence of variant angina attacks.
Avoid any triggers such as emotional distress, hyperventilation, unnecessary exposure to cold, and early morning exertion.
Avoidance of any of the recreational and therapeutic drugs associated with symptoms.
Beta blockers theoretically, may worsen vasospasm by inhibiting beta-2 adrenergic receptor vasodilation mediated by these receptors naturally occurring stimulator, epinephrine.
Aspirin should be used with caution and at low doses since at high doses it inhibits the production of the naturally occurring vasodilator, prostacyclin.
Patients undergoing acute attacks generally respond well to fast acting sublingual, intravenous, or spray nitroglycerin formulations.
The time of onset of symptom relief depends on which type of agent is used: intravenous administration is associated with relief almost immediately, while sublingual formulations act within 1-5 minutes, and spray formulations require, also about 1-5 minutes to act.
Maintenance sublingual nitroglycerin tablets can be taken 3-5 min before activity that causes angina.
For most patients, other drugs are used as maintenance therapy to avoid attacks of variant angina: Calcium channel blockers are regarded as first-line drugs to avoid angina attacks.
Long-acting nitroglycerins such as isosorbide dinitrate or intermittent use of short-acting nitroglycerin may be added to the calcium channel blocker regimen in individuals responding sub-optimally to the channel blockers.
Tolerance, meaning resistance, to the efficacy of continuously used long-acting nitroglycerin formulations is common.
To prevent tolerance nitroglycerin-free periods of between 12 and 14 hours between doses of long-acting nitroglycerin formulations is recommenced
In poorly controlled variant angina by a calcium blocker may benefit from addition of a long-acting nitroglycerin and/or a second calcium channel blocker of a different class than the blocker already in use.
About 20% of individuals fail to respond adequately to the two-drug calcium blocker plus long-acting nitroglycerin regimen.
If such patients have significant permanent occlusion of their coronary arteries, they may benefit by stenting their occluded arteries.
Coronary artery stenting is contraindicated in drug- refractory individuals who do not have significant organic occlusion of their coronary arteries.
Most individuals with variant angina have a favorable prognosis provided they are maintained on calcium channel blockers and/or long-acting nitrates.
Five year survival rates in this group are estimated as over 90%.