Coronary vasospasm: Difference between revisions

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{{SI}}
'''For patient information, click [[Coronary vasospasm (patient information)|here]]'''
'''For patient information, click [[Coronary vasospasm (patient information)|here]]'''<br>
'''For information about Prinzmetal's angina, click [[Prinzmetal's angina|here]]'''<br>
'''For information about PCI-induced coronary vasospasm, click [[PCI complications: coronary vasospasm|here]]'''


{{CMG}}; '''Associate Editor(s)-in-Chief:'''  [[Lakshmi Gopalakrishnan]], M.B.B.S.; Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro M.D.
{{CMG}}; '''Associate Editor(s)-in-Chief:'''  [[Lakshmi Gopalakrishnan]], M.B.B.S.; Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro M.D.


{{SK}} Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina, prinzmetal angina, prinzmetal's angina, focal coronary artery vasospasm, dynamic coronary obstruction
{{SK}} Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina
, focal coronary artery vasospasm, dynamic coronary obstruction


==Overview==
==Overview==
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Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.
Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.
====Spontaneous====
====Spontaneous====
* A subtype of epicardial coronary artery spasm is known as [[prinzmetal's angina]].  Prinzmetal's angina is characterized by the sudden onset of chest pain at rest with [[ST elevation]] on [[ECG]]
* A subtype of epicardial coronary artery spasm is known as [[Prinzmetal's angina]].  Prinzmetal's angina is characterized by the sudden onset of chest pain at rest with [[ST elevation]] on [[ECG]]. Click '''[[Prinzmetal's angina|here]]''' for more information about [[Prinzmetal's angina]].
 
====Iatrogenic====
====Iatrogenic====
* Coronary vasospasm can be secondary to [[PCI]].
* Coronary vasospasm can be secondary to [[PCI]].  Click '''[[PCI complications: coronary vasospasm|here]]''' for more information about [[PCI-induced coronary vasospasm]].


==Pathophysiology==
==Pathophysiology==
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* [[Cocaine toxicity]]
* [[Cocaine toxicity]]
* [[Coronary dissection]] can mimic and can cause spasm
* [[Coronary dissection]] can mimic and can cause spasm
* [[Drugs]]- [[Naratriptan]], [[Sumatriptan]]
* [[Esophageal motility disorders]]
* [[Esophageal motility disorders]]
* [[Esophageal spasm]]
* [[Esophageal spasm]]
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*[[Hyperventilation]]
*[[Hyperventilation]]
*[[Insulin resistance]]
*[[Insulin resistance]]
*Japanese descent
* Japanese descent
*[[Smoking]]
*[[Smoking]]


==Coronary Vasospasm in Japanese Patients==
==Coronary Vasospasm in Japanese Patients==
A discrepancy in the prevalence of coronary artery spasm exists across different ethnicities; in particular, the Japanese population has been reported to have a greater prevalence of this condition compared to Caucasians.<ref name="pmid15172469">{{cite journal| author=Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M et al.| title=Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women. | journal=Eur Heart J | year= 2004 | volume= 25 | issue= 11 | pages= 970-7 | pmid=15172469 | doi=10.1016/j.ehj.2004.02.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15172469  }} </ref>  In fact, according to a study involving 2251 patients, coronary artery spasm has been estimated to account for approximately 41% of Japanese patients with [[angina pectoris]] who underwent [[angiography]].<ref>Yasue H, Sasayama S, Kikuchi K, Okumura K, Matsubara T, Miwa K, et al. The study on the role of coronary spasm in ischemic heart disease. In: Annual report of the research on cardiovascular diseases. Osaka: National Cardiovascular Center; 2000. p. 96–7 (in Japanese).</ref>  In addition, coronary spasm in Japanese is characterized by a diffuse hyperreactivity as manifested by a segmental pattern of spasm as well as by a multivessel involvement compared to focal involvement in other populations.<ref name="pmid10334407">{{cite journal| author=Beltrame JF, Sasayama S, Maseri A| title=Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients. | journal=J Am Coll Cardiol | year= 1999 | volume= 33 | issue= 6 | pages= 1442-52 | pmid=10334407 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10334407  }} </ref>  Moreover, following the administration of [[acetylcholine]] early after [[myocardial infarction]] for provocation of spasm, there has been three fold higher incidence of coronary spasm and a higher incidence of multivessel spasm among Japanese compared to Caucasians.<ref name="pmid10715255">{{cite journal| author=Pristipino C, Beltrame JF, Finocchiaro ML, Hattori R, Fujita M, Mongiardo R et al.| title=Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction. | journal=Circulation | year= 2000 | volume= 101 | issue= 10 | pages= 1102-8 | pmid=10715255 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10715255  }} </ref>  These findings highlight that the vasomotor reactivity of [[coronary artery]] is not homogeneous across the different populations and is most likely related to genetic and environmental factors.  Since [[endothelium|endothelial]] dysfunction and enhanced vasoconstriction are part of the multifactorial pathophysiology of coronary spasm, it has been suggested that gene polymorphism of [[NO synthase]], [[angiotensin converting enzyme]], angiotensin receptor type 1 as well as other enzymes and susceptibility genes can explain the predisposition of the Japanese population to coronary spasm.<ref name="pmid15172469">{{cite journal| author=Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M et al.| title=Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women. | journal=Eur Heart J | year= 2004 | volume= 25 | issue= 11 | pages= 970-7 | pmid=15172469 | doi=10.1016/j.ehj.2004.02.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15172469  }} </ref>
A discrepancy in the prevalence of coronary artery spasm exists across different ethnicities; in particular, the Japanese population has been reported to have a greater prevalence of this condition compared to Caucasians.<ref name="pmid15172469">{{cite journal| author=Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M et al.| title=Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women. | journal=Eur Heart J | year= 2004 | volume= 25 | issue= 11 | pages= 970-7 | pmid=15172469 | doi=10.1016/j.ehj.2004.02.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15172469  }} </ref>  In fact, according to a study involving 2251 patients, coronary artery spasm has been estimated to account for approximately 41% of Japanese patients with [[angina pectoris]] who underwent [[angiography]].<ref>Yasue H, Sasayama S, Kikuchi K, Okumura K, Matsubara T, Miwa K, et al. The study on the role of coronary spasm in ischemic heart disease. In: Annual report of the research on cardiovascular diseases. Osaka: National Cardiovascular Center; 2000. p. 96–7 (in Japanese).</ref>  In addition, coronary spasm in Japanese is characterized by a diffuse hyperreactivity as manifested by a segmental pattern of spasm as well as by a multivessel involvement compared to focal involvement in other populations.<ref name="pmid10334407">{{cite journal| author=Beltrame JF, Sasayama S, Maseri A| title=Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients. | journal=J Am Coll Cardiol | year= 1999 | volume= 33 | issue= 6 | pages= 1442-52 | pmid=10334407 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10334407  }} </ref>  Moreover, following the administration of [[acetylcholine]] early after [[myocardial infarction]] for provocation of spasm, there has been three fold higher incidence of coronary spasm and a higher incidence of multivessel spasm among Japanese compared to Caucasians.<ref name="pmid10715255">{{cite journal| author=Pristipino C, Beltrame JF, Finocchiaro ML, Hattori R, Fujita M, Mongiardo R et al.| title=Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction. | journal=Circulation | year= 2000 | volume= 101 | issue= 10 | pages= 1102-8 | pmid=10715255 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10715255  }} </ref>  These findings highlight that the vasomotor reactivity of [[coronary artery]] is not homogeneous across the different populations and is most likely related to genetic and environmental factors.  Since [[endothelium|endothelial]] dysfunction and enhanced vasoconstriction are part of the multifactorial pathophysiology of coronary spasm, it has been suggested that gene polymorphism of [[NO synthase]], [[angiotensin converting enzyme]], angiotensin receptor type 1 as well as other enzymes and susceptibility genes can explain the predisposition of the Japanese population to coronary spasm.<ref name="pmid15172469">{{cite journal| author=Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M et al.| title=Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women. | journal=Eur Heart J | year= 2004 | volume= 25 | issue= 11 | pages= 970-7 | pmid=15172469 | doi=10.1016/j.ehj.2004.02.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15172469  }} </ref>
==Natural History, Complications and Prognosis==
* The prognosis of vasospastic angina depends on the extent of underlying [[coronary artery disease| coronary artery disease (CAD)]].
* When it does occur in multiple vessels, the prognosis is worse as it may result in [[ventricular tachycardia]] or [[ventricular fibrillation]].
==Diagnosis==
* Physicians should suspect vasospasm if [[ST segment elevation]] is detected in patients experiencing [[angina]], and if the [[ECG]] completely returns to baseline upon resolution of symptoms.
* Once detected, aggressive management of coronary vasospasm is necessary, as vasospasm can provoke fatal [[arrhythmias]] or [[myocardial infarction]].
* The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven to be reversible.
* Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators.
* The differential diagnosis of coronary spasm during [[percutaneous coronary intervention]] includes:
:*[[Abrupt closure]] due to [[dissection]] or thrombus formation
:* [[ST elevation]] classically observed on [[ECG]] during an episode of [[vasospasm]].
:* Intracoronary [[acetylcholine]] or [[ergonovine]] provocation test used to diagnose [[vasospasm]]. 


==Treatment==
==Treatment==
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* [[Atropine]] has also been used to treat the condition.<ref name="pmid17228071">{{cite journal |author=Turkoglu S, Arpag U, Timurkaynak T |title=Spontaneous coronary vasospasm in the catheterisation laboratory: prompt resolution after atropine injection |journal=Heart |volume=93 |issue=2 |pages=215 |year=2007 |month=February |pmid=17228071 |doi=10.1136/hrt.2006.093187 |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=17228071}}</ref>
* [[Atropine]] has also been used to treat the condition.<ref name="pmid17228071">{{cite journal |author=Turkoglu S, Arpag U, Timurkaynak T |title=Spontaneous coronary vasospasm in the catheterisation laboratory: prompt resolution after atropine injection |journal=Heart |volume=93 |issue=2 |pages=215 |year=2007 |month=February |pmid=17228071 |doi=10.1136/hrt.2006.093187 |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=17228071}}</ref>


===Treatment of PCI-Induced Vasospasm===
====Contraindicated medications====
*[[Intracoronary pharmacotherapy|Intracoronary]] [[vasodilator]]s should be given slowly through [[PCI equipment: guiding catheter selection|guiding catheters]] with side holes to maximize the delivery into the [[artery]] with minimal dispersal through the catheter side holes.
**[[Intracoronary pharmacotherapy|Intracoronary]] [[nitroglycerin]] 100-300 mcg. Generally well tolerated and have an additive effect.
**[[Intracoronary pharmacotherapy|Intracoronary]] [[calcium channel blocker]]s. Generally well tolerated, have an additive effect, and have a small risk of transient [[heart block]].
***[[Diltiazem]] 0.5-2.5 mg/min, up to 5-10 mg
***[[Verapamil]] 100 mcg/min, up to 1.0-1.5 mg
***[[Nicardipine]] 100-300 mcg
***[[Nifedipine]] 10 mg [[sublingual]] (SL)
**[[Intracoronary pharmacotherapy|Intracoronary]] [[nitroprusside]] 100-300 mcg
*[[Systemic]] [[vasodilator]]s
**[[Nifedipine]] 10 mg [[sublingual]]
**[[Atropine]] 0.5 mg IV. Particularly useful in the setting of [[hypotension]] or [[bradycardia]].
*Device related treatments
**Removal of interventional hardware with [[guide wire]] in place to minimize mechanical provocation. This strategy may minimize [[distal]] [[vasospasm|vessel spasm]].
**Repeat prolonged (2-5 min) [[PTCA]] at low pressure (1-4 atmospheres). May mechanically "break" [[vasospasm]].
**[[Stent]]ing. May improve focal spasm, but may simply propagate the site of spasm to a location [[proximal]] or [[distal]] to the [[stent]] within the [[vessel]], so it should be avoided if possible.
 
===Treatments for Chronic Vasospasm===
*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 [[Ventricular tachycardia|VT]]/[[Ventricular fibrillation|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 [[Ventricular tachycardia|VT]]/[[Ventricular fibrillation|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==
===PCI-Induced Vasospasm===
* [[Therapeutic]] treatment of PCI-induced [[vasospasm]] should be performed in this order (step-wise fashion):
:* Initial step is [[intracoronary pharmacotherapy|intracoronary]] [[vasodilatation]] with [[intracoronary pharmacotherapy|IC]] [[calcium channel blockers]] and/or [[nitrates]], which should be given slowly when using [[PCI equipment: guiding catheter selection|guiding catheters]] with side holes to avoid dispersal of the drug through the holes instead of into the [[coronary artery]].
:* If one agent is unsuccessful, combined [[therapy]] should be implemented as these medications have an additive effect. Be mindful for [[heart block]] with [[CCB]] [[therapy]].
:* [[IV]] [[atropine]] can be useful if there is associated [[hypotension]] of [[bradycardia]].
:* Should medical [[therapy]] fail, remove all hardware and leave the [[guide wire]] in place to maintain position. This may minimize [[distal]] [[vasospasm|vessel spasm]].
:* Repeat prolonged [[PTCA]] for 2-5 minutes at low pressures (1-4 atmospheres).
:* [[Stent]]ing should be a last ditch option, and used if above measures have failed, as it may lead to propagation of [[vasospasm|spasm]] to a new location. Refractory [[vasospasm]] may be indicative of [[dissection]], which is also an indication for [[stent]]ing.
 
===Chronic Vasospasm===
* 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.
 
==How To Know if Treatment of PCI-Induced Vasospam is Working==
Therapies for [[vasospasm]] will usually take effect within seconds to one minute.  Anticipated outcomes include:
*Resolution of acute or chronic coronary vasospasm
*Resolution of ECG changes ([[ST depression]] or elevation)
*Resolution of symptomatic [[angina]] and other symptoms, if present
*Repeat [[angiography]]
 
==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 [[VT|ventricular tachycardia]] or [[VF|fibrillation]].  Multivessel spasm can also lead to ventricular arrhythmias.
* The [[right coronary artery]] ostium is prone to catheter-induced spasm, giving the appearance of an ostial lesion on angiography.  Pre-treatment with 200 mcg of IC [[nitroglycerin]] should be administered prior to intervention of this area.
* 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)<ref name="pmid16735367">{{cite journal| author=Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F et al.| title=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. | journal=Eur Heart J | year= 2006 | volume= 27 | issue= 11 | pages= 1341-81 | pmid=16735367 | doi=10.1093/eurheartj/ehl001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16735367  }} </ref>==
 
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[European society of cardiology#Classes of Recommendations|Class I]]
 
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' [[Chronic stable angina electrocardiography|ECG]] during [[Chronic stable angina definition|angina]] if possible. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' Coronary arteriography in patients with characteristic episodic [[chest pain]] and ST-segment changes that resolve with [[Chronic stable angina treatment nitrates|nitrates]] and/or [[Chronic stable angina treatment calcium channel blockers|calcium channel blockers]] to determine the extent of underlying [[CAD|coronary disease]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|}
 
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LemonChiffon"|[[European society of cardiology#Classes of Recommendations|Class IIa]]
 
|-
| bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''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. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|-
| bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''2.''' [[Chronic stable angina ambulatory ST segment monitoring|Ambulatory ST Segment Monitoring]] to identify ST-deviation. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
|}
 
==ESC Guidelines for Pharmacological Therapy of Vasospastic Angina (DO NOT EDIT)<ref name="pmid16735367">{{cite journal| author=Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F et al.| title=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. | journal=Eur Heart J | year= 2006 | volume= 27 | issue= 11 | pages= 1341-81 | pmid=16735367 | doi=10.1093/eurheartj/ehl001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16735367  }} </ref>==
 
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[European society of cardiology#Classes of Recommendations|Class I]]


|-
{{MedCondContrAbs|MedCond = Coronary artery vasospasm|Sumatriptan}}
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' Treatment with [[Chronic stable angina treatment calcium channel blockers|calcium channel blocker]] and if necessary [[Chronic stable angina treatment nitrates|nitrates]] in patients whose coronary arteriogram is normal or shows only non-obstructive lesions. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|}


==References==
==References==

Latest revision as of 19:26, 13 December 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Lakshmi Gopalakrishnan, M.B.B.S.; Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro M.D.

Synonyms and keywords: Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina , focal coronary artery vasospasm, dynamic coronary obstruction

Overview

Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of luminal diameter of an epicardial coronary artery due to inappropriate constriction of coronary smooth muscle that can generate distal ischemia. This may occur spontaneously or in the context of angioplasty, particularly if denudation of the endothelium or dissection occurs. In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel).

Classification

Classification by Location

Coronary artery spasm can be classified according to the location of vasoconstriction:

Focal coronary spasm

Focal coronary spasm is limited to a localized segment of the coronary artery.

Multifocal coronary spasm

Multifocal coronary spasm involves several localized segments of the same coronary artery.

Multivessel coronary spasm

Multivessel coronary spasm involves several coronary arteries.[1][2]

Classification by Clinical Syndrome

Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.

Spontaneous

Iatrogenic

Pathophysiology

  • The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.
  • A significant group of patients with variant angina have underlying obstructive coronary artery disease.[5]
  • Occasionally, coronary vasospasm can be induced by angioplasty (PCI-induced), which occurs secondary to endothelial denudation and nitric oxide loss. Some cases are catheter-induced which is caused by a contact of a catheter without balloon deployment. Catheter-induced coronary vasospasm is usually short-lived. Catheter-induced coronary vasospasm is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm.

Causes

Causes in Alphabetical Order

Epidemiology and Demographics

  • Young patients with fewer cardiovascular risk factors (with the exception of smoking) are at a higher risk for coronary vasospasm, as are noncalcified lesions and eccentric plaques.
  • Rotoblator cases are more prone to coronary vasospasm. The reported incidence of rotoblater cases with coronary vasospasm ranges anywhere from 4 to 36%.

Risk Factors

Coronary Vasospasm in Japanese Patients

A discrepancy in the prevalence of coronary artery spasm exists across different ethnicities; in particular, the Japanese population has been reported to have a greater prevalence of this condition compared to Caucasians.[6] In fact, according to a study involving 2251 patients, coronary artery spasm has been estimated to account for approximately 41% of Japanese patients with angina pectoris who underwent angiography.[7] In addition, coronary spasm in Japanese is characterized by a diffuse hyperreactivity as manifested by a segmental pattern of spasm as well as by a multivessel involvement compared to focal involvement in other populations.[8] Moreover, following the administration of acetylcholine early after myocardial infarction for provocation of spasm, there has been three fold higher incidence of coronary spasm and a higher incidence of multivessel spasm among Japanese compared to Caucasians.[9] These findings highlight that the vasomotor reactivity of coronary artery is not homogeneous across the different populations and is most likely related to genetic and environmental factors. Since endothelial dysfunction and enhanced vasoconstriction are part of the multifactorial pathophysiology of coronary spasm, it has been suggested that gene polymorphism of NO synthase, angiotensin converting enzyme, angiotensin receptor type 1 as well as other enzymes and susceptibility genes can explain the predisposition of the Japanese population to coronary spasm.[6]

Treatment

  • The main goals of treating coronary vasospasm are to:
  • Reverse the spontaneous abrupt luminal diameter reduction
  • Reverse PTCA-induced vasospasm
  • Stabilize chronic intermittent vasospasm.

Contraindicated medications

Coronary artery vasospasm is considered an absolute contraindication to the use of the following medications:

References

  1. ↑ Ahooja V, Thatai D (2007). "Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease". J Invasive Cardiol. 19 (7): E178–81. PMID 17620681. Unknown parameter |month= ignored (help)
  2. ↑ Miwa K, Ishii K, Makita T, Okuda N (2004). "Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis". Circ. J. 68 (5): 483–7. PMID 15118293. Unknown parameter |month= ignored (help)
  3. ↑ Lanza GA, Careri G, Crea F (2011). "Mechanisms of coronary artery spasm". Circulation. 124 (16): 1774–82. doi:10.1161/CIRCULATIONAHA.111.037283. PMID 22007100.
  4. ↑ Mahemuti A, Abudureheman K, Schiele F, Ecarnot F, Abudureyimu S, Tang B; et al. (2014). "Association between inflammatory markers, hemostatic markers, and traditional risk factors on coronary artery spasm in patients with normal coronary angiography". J Interv Cardiol. 27 (1): 29–35. doi:10.1111/joic.12086. PMID 24345233.
  5. ↑ Maseri A, Severi S, Nes MD, L'Abbate A, Chierchia S, Marzilli M et al. (1978) "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 42 (6):1019-35. PMID: 727129
  6. ↑ 6.0 6.1 Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M; et al. (2004). "Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women". Eur Heart J. 25 (11): 970–7. doi:10.1016/j.ehj.2004.02.020. PMID 15172469.
  7. ↑ Yasue H, Sasayama S, Kikuchi K, Okumura K, Matsubara T, Miwa K, et al. The study on the role of coronary spasm in ischemic heart disease. In: Annual report of the research on cardiovascular diseases. Osaka: National Cardiovascular Center; 2000. p. 96–7 (in Japanese).
  8. ↑ Beltrame JF, Sasayama S, Maseri A (1999). "Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients". J Am Coll Cardiol. 33 (6): 1442–52. PMID 10334407.
  9. ↑ Pristipino C, Beltrame JF, Finocchiaro ML, Hattori R, Fujita M, Mongiardo R; et al. (2000). "Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction". Circulation. 101 (10): 1102–8. PMID 10715255.
  10. ↑ Turkoglu S, Arpag U, Timurkaynak T (2007). "Spontaneous coronary vasospasm in the catheterisation laboratory: prompt resolution after atropine injection". Heart. 93 (2): 215. doi:10.1136/hrt.2006.093187. PMID 17228071. Unknown parameter |month= ignored (help)


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