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{{Infobox_Disease |
__NOTOC__
  Name          = {{PAGENAME}} |
  Image          = |
  Caption        = |
  DiseasesDB    = 13727 |
  ICD10          = |
  ICD9          = {{ICD9|413.1}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = 000159 |
  eMedicineSubj  = med |
  eMedicineTopic = 447 |
  MeshID        = D003329 |
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{{SI}}
{{SI}}
{{CMG}}
'''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]]'''


'''Associate Editors-in-Chief:'''  Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro M.D.; David M. Leder, 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.


{{Editor Join}}
{{SK}} Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina
 
, focal coronary artery vasospasm, dynamic coronary obstruction
'''Synonyms and related key words:''' Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina, Prinzmetal angina, Prinzmetal's angina, focal coronary artery vasospasm, dynamic coronary obstruction


==Overview==
==Overview==
Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of [[Lumen (anatomy)|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.  Also, the vasospasm can either be focal or multifocal (which compromises more than one vessel).
Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of [[Lumen (anatomy)|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).


==Subtypes of Vasospasm==
==Classification==
A subtype of epicardial coronary artery spasm is known as [[Prinzmetal's angina]]. In this subtype of epicardial coronary artery vasospasm, symptoms typically occur at rest, rather than on exertion (thus attacks usually occur at night). Two-thirds of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms. Prinzmetal's angina is typically associated with specific EKG changes (elevation rather than depression of the ST segment).
===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]].


'''(Cardiac) syndrome X''' is [[Angina pectoris|angina]] ([[chest pain]]) with signs associated with decreased blood flow to heart tissue but with normal [[coronary artery|coronary arteries]]. It is thought to involve the coronary microvasculature rather than the large epicardial arteries. It occurs more often in young women. Some studies have found increased risk of other vasospastic disorders in syndrome X patients, such as [[migraine]] and [[Raynaud's phenomenon]]. It is treated with [[calcium channel blocker]]s, such as [[nifedipine]], and usually carries a favorable prognosis.  This is a distinct diagnosis from [[Prinzmetal's angina]] which involves spasm of the main epicardial coronary arteries. Syndrome X involves spasm of the downstream microvasculature.  
====Multifocal coronary spasm====
Multifocal coronary spasm involves several localized segments of the same [[coronary artery]].


Coronary vasospasm can occur in either a single epicardial coronary artery or in multiple epicardial coronary arteryies. <ref name="pmid17620681">{{cite journal |author=Ahooja V, Thatai D |title=Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease |journal=J Invasive Cardiol |volume=19 |issue=7 |pages=E178–81 |year=2007 |month=July |pmid=17620681 |doi= |url=http://www.digitaljic.com/nxtbooks/hmp/jic0707/index.php?startpage=54}}</ref><ref name="pmid15118293">{{cite journal |author=Miwa K, Ishii K, Makita T, Okuda N |title=Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis |journal=Circ. J. |volume=68 |issue=5 |pages=483–7 |year=2004 |month=May |pmid=15118293 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/68.483?from=PubMed}}</ref> When it does occur in multiple vessels, the prognosis is worse as it may result in [[ventricular tachycardia]] or [[ventricular fibrillation]]. The patient with multivessel spasm may benefit from dual [[calcium channel blockade]].
====Multivessel coronary spasm====
Multivessel coronary spasm involves several coronary arteries.<ref name="pmid17620681">{{cite journal |author=Ahooja V, Thatai D |title=Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease |journal=J Invasive Cardiol |volume=19 |issue=7 |pages=E178–81 |year=2007 |month=July |pmid=17620681 |doi= |url=http://www.digitaljic.com/nxtbooks/hmp/jic0707/index.php?startpage=54}}</ref><ref name="pmid15118293">{{cite journal |author=Miwa K, Ishii K, Makita T, Okuda N |title=Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis |journal=Circ. J. |volume=68 |issue=5 |pages=483–7 |year=2004 |month=May |pmid=15118293 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/68.483?from=PubMed}}</ref>


==Pathophysiology==
===Classification by Clinical Syndrome===
The exact [[pathogenesis]] of coronary vasospasm is not well understood, but some causes and contributing factors are known.  Sometimes coronary vasospasm is induced by angioplasty ('''PCI-induced'''), which occurs secondary to [[endothelial]] denudation and [[nitric oxide]] loss.  Others are '''catheter-induced''', which is caused by a contact of a catheter without balloon deployment.  Catheter-induced coronary vasospasms are usually short-lived.  They are most prone to occur at the ostium of the [[right coronary artery]] (RCA), and the [[left main]] is less susceptible to ostial spasm. Additionally, the [[autonomic nervous system]] and [[endothelial]] dysfunction can lead to '''chronic intermittent vasospasm''', which usually occurs where a fixed, noncalcified [[stenosis]] is located.
Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.
====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]]. Click '''[[Prinzmetal's angina|here]]''' for more information about [[Prinzmetal's angina]].


==Epidemiology==
====Iatrogenic====
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.  Also, rotoblator cases are more prone to coronary vasospasm, with a 4-36% incidence.
* Coronary vasospasm can be secondary to [[PCI]].  Click '''[[PCI complications: coronary vasospasm|here]]''' for more information about [[PCI-induced coronary vasospasm]].


==Diagnosis==
==Pathophysiology==
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.
* The exact [[pathogenesis]] of coronary vasospasm is not well understood, but some causes and contributing factors are known.


* Coronary spasm can be explained by a hyperreactivity to vasoconstrictor stimuli that results from [[endothelium|endothelial dysfunction]] or primary hyperreactivity of [[smooth muscle cells]].  Vasoconstrictor stimuli include changes in the [[autonomic nervous system]], [[inflammation]], and [[calcium]] availability in the [[myocardium]].<ref name="pmid22007100">{{cite journal| author=Lanza GA, Careri G, Crea F| title=Mechanisms of coronary artery spasm. | journal=Circulation | year= 2011 | volume= 124 | issue= 16 | pages= 1774-82 | pmid=22007100 | doi=10.1161/CIRCULATIONAHA.111.037283 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22007100  }} </ref><ref name="pmid24345233">{{cite journal| author=Mahemuti A, Abudureheman K, Schiele F, Ecarnot F, Abudureyimu S, Tang B et al.| title=Association between inflammatory markers, hemostatic markers, and traditional risk factors on coronary artery spasm in patients with normal coronary angiography. | journal=J Interv Cardiol | year= 2014 | volume= 27 | issue= 1 | pages= 29-35 | pmid=24345233 | doi=10.1111/joic.12086 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24345233  }} </ref>  Dysfunction of the [[autonomic nervous system]] and [[endothelial]] dysfunction can lead to chronic intermittent vasospasm, which usually occurs where a fixed, non-calcified [[stenosis]] is located.


==Differential Diagnosis of Underlying Causes of Coronary Vasospasm==
* A significant group of patients with variant angina have underlying obstructive coronary artery disease.<ref name="pmid727129">Maseri A, Severi S, Nes MD, L'Abbate A, Chierchia S, Marzilli M et al. (1978) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=727129 "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: [http://pubmed.gov/727129 727129]</ref>


(In alphabetical order)
* 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===
* [[Acute pericarditis]]
* [[Acute pericarditis]]
* [[Angina pectoris]]
* [[Angina pectoris]]
Line 51: Line 49:
* [[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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* [[Unstable angina]]
* [[Unstable angina]]


==Treatment==
==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%.


The main goals of treating coronary vasospasm are to reverse the spontaneous, abrupt luminal diameter reduction, reverse PTCA-induced vasospasm, and to stabilize chronic intermittent vasospasm.
==Risk Factors==
*[[Autoimmune disease]]s
*[[Cocaine]] use
*Cold exposure
*[[Hyperventilation]]
*[[Insulin resistance]]
* Japanese descent
*[[Smoking]]


[[Calcium channel blockers]] and [[nitrates]] are the mainstay of chronic therapy for coronary vasospasm. [[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>
==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>


===Treatment of PCI-Induced Vasospasm===
==Treatment==
*'''Intracoronary vasodilators''' should be given slowly through guiding catheters with side holes to maximize the delivery into the artery with minimal dispersal through the catheter side holes.
*The main goals of treating coronary vasospasm are to:
**Intracoronary nitroglycerine 100-300 mcg.  Generally well tolerated.
:* Reverse the spontaneous abrupt luminal diameter reduction
**Intracoronary calcium channel blockers.  Small risk of transient heart block
:* Reverse PTCA-induced vasospasm
***Diltiazem 0.5-2.5 mg/min, up to 5-10mg
:* Stabilize chronic intermittent vasospasm.   
***Verapamil 100 mcg/min, up to 1.0-1.5 mg
*[[Calcium channel blockers]] and [[nitrates]] are the mainstay of chronic therapy for coronary vasospasm.
***Nicardipine 100-300 mcg
* [[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>
***Nifedipine 10 mg sublingual (SL)
**Intracoronary nitroprusside 100-300 mcg
*'''Systemic vasodilators'''
**Nifedipine 10mg sublingual
**Atropine 0.5mg 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- may minimize distal vessel spasm
**Repeat prolonged (2-5 min) PTCA at low pressure (1-4 atmospheres)
**Stenting.  This will improve focal spasm, but may also cause spasm in vessel adjacent to the hardware.  It should be avoided if possible.
 
===Treatments for chronic vasospasm===
*'''Calcium channel blockers'''.  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.  A patient who has suffered VT/VF due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
**Diltiazem 240-360mg PO qd
**Verapamil 240-480mg PO qd
**Nifedipine XL 60-120mg PO qd
**Nicardipine 40-160mg PO qd
*'''Long-acting nitrates'''
**Isosorbide mononitrate (Imdur) 60-240mg PO qd
**Isosorbide dinitrate (Isordil) 20-40mg PO tid
*'''Statins'''
**Fluvastatin 30mg 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.  It lowers future event rates of vasospasm and acute coronary syndromes.
*'''PTCA/stenting'''
*'''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''' is reserved only for the most refractory cases.
 
==One Sequence of Treatment Choices to Manage PCI-Induced Vasospasm==
Therapeutic treatment of PCI-induced vasospasm should be performed in this order:
*Intracoronary vasodilators (either nitroglycerin or calcium channel blockers may be given first
*Combined therapy of intracoronary nitroglycerine and calcium channel blockers
*Removal of hardware with guidewire in place
*Repeat PTCA
*Stenting if above measures have failed.  Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
 
==How To Know if Treatment of PCI-Induced Vasospam is Working==
Therapies for vasospasm will usually take effect within seconds to one minute.
*Repeat angiography
*Resolution of ECG changes (ST depression or elevation)
*Resolution of symptoms, if present
 
==Pathological Findings==


[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
====Contraindicated medications====


<gallery>
{{MedCondContrAbs|MedCond = Coronary artery vasospasm|Sumatriptan}}
Image:Coronary artery vasospasm 001.jpg|Coronary artery: Intramural Left Anterior Descending Artery: Micro, low mag, morphologically normal artery 72 years old female who developed anterior myocardial infarction after cholecystectomy
Image:Coronary artery vasospasm 002.jpg|Coronary artery: Intramural Left Anterior Descending Artery: Micro, med mag, trichrome, abnormal media with fibrous tissue, 72 years old female who developed anterior myocardial infarction after cholecystectomy, There is no sign of atherosclerosis, but left anterior descending artery is intramural.
</gallery>


==References==
==References==
{{reflist|2}}
{{reflist|2}}


==Further reading==
[[Category:Disease]]
* {{cite journal |author=Hibino H, Kurachi Y |title=A new insight into the pathogenesis of coronary vasospasm |journal=Circ. Res. |volume=98 |issue=5 |pages=579–81 |year=2006 |month=March |pmid=16543506 |doi=10.1161/01.RES.0000215571.12500.ab |url=http://circres.ahajournals.org/cgi/pmidlookup?view=long&pmid=16543506}}
[[Category:Ischemic heart diseases]]
[[Category:Cardiology]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]
[[Category:Up-To-Date]]
[[Category:Up-To-Date cardiology]]


{{Heart diseases}}
{{SIB}}
[[Category:Cardiology]]


{{WH}}
{{WH}}
{{WS}}
{{WS}}

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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