PCI complications: coronary vasospasm: Difference between revisions
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==Overview== | ==Overview== | ||
[[Coronary vasospasm]] can be induced by [[percutaneous coronary intervention]] (PCI) secondary to [[endothelial]] denudation and [[nitric oxide]] loss. The main goal of the treatment is to reverse angioplasty-induced vasospasm. The initial treatment is [[intracoronary pharmacotherapy|intracoronary]] [[vasodilatation]] with [[calcium channel blockers]] and/or [[nitrates]], which should be given slowly when using [[PCI equipment: guiding catheter selection|guiding catheters]]. Therapies for [[vasospasm]] will usually take effect within seconds to one minute. | |||
==Classification== | |||
====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 artery|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== | |||
* [[Coronary vasospasm]] can be induced by [[PCI]] 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. | |||
==Differential Diagnosis== | |||
* The differential diagnosis of coronary spasm during [[PCI]] includes [[abrupt closure]] due to [[dissection]] or [[thrombus]] formation. | |||
==Epidemiology and Demographics== | |||
* [[Coronary vasospasm]] can occasionally be induced by [[PCI]]. | |||
* Rotablator cases are more prone to coronary vasospasm. The reported incidence of rotablator cases with [[coronary vasospasm]] ranges anywhere from 4 to 36%. | |||
==Risk factors== | |||
[[Smoking]] is a risk factor for [[coronary vasospasm]]. | |||
==Natural History, Complications and Prognosis== | |||
* [[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. | |||
==Diagnosis== | ==Diagnosis== | ||
* Physicians should suspect [[coronary vasospasm]] if [[ST segment elevation]] is detected in patients experiencing [[angina]], and if the [[ECG]] completely returns to baseline upon resolution of symptoms. | |||
* 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. | |||
* 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. | * 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 | * Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary [[vasodilator]]s. | ||
== | ==Treatment== | ||
* | ===Choices of Treatment=== | ||
====Intracoronary Vasodilator==== | |||
[[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 Vasodilators==== | |||
*[[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. | |||
===Step by Step Treatment Approach=== | |||
* [[Therapeutic]] treatment of PCI-induced [[vasospasm]] should be performed in this order (step-wise fashion): | * [[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]]. | :* 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]]. | ||
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:* [[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. | :* [[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. | ||
==Assessment of Response to Therapy== | |||
== | |||
Therapies for [[vasospasm]] will usually take effect within seconds to one minute. Anticipated outcomes include: | Therapies for [[vasospasm]] will usually take effect within seconds to one minute. Anticipated outcomes include: | ||
*Resolution of | *Resolution of the [[coronary vasospasm]] | ||
*Resolution of ECG changes ([[ST depression]] or elevation) | *Resolution of the [[ECG]] changes ([[ST depression]] or elevation) | ||
*Resolution of symptomatic [[angina]] and other symptoms, if present | *Resolution of symptomatic [[angina]] and other symptoms, if present | ||
== | ==References== | ||
{{reflist|2}} | |||
[[Category:Cardiology]] | |||
[[Category:Angiographic Definitions]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Up-To-Date cardiology]] | |||
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{{WikiDoc Sources}} | |||
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PCI complications: coronary vasospasm On the Web |
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Risk calculators and risk factors for PCI complications: coronary vasospasm |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Coronary vasospasm can be induced by percutaneous coronary intervention (PCI) secondary to endothelial denudation and nitric oxide loss. The main goal of the treatment is to reverse angioplasty-induced vasospasm. The initial treatment is intracoronary vasodilatation with calcium channel blockers and/or nitrates, which should be given slowly when using guiding catheters. Therapies for vasospasm will usually take effect within seconds to one minute.
Classification
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]
Pathophysiology
- Coronary vasospasm can be induced by PCI 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.
Differential Diagnosis
- The differential diagnosis of coronary spasm during PCI includes abrupt closure due to dissection or thrombus formation.
Epidemiology and Demographics
- Coronary vasospasm can occasionally be induced by PCI.
- Rotablator cases are more prone to coronary vasospasm. The reported incidence of rotablator cases with coronary vasospasm ranges anywhere from 4 to 36%.
Risk factors
Smoking is a risk factor for coronary vasospasm.
Natural History, Complications and Prognosis
- 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.
- 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.
Diagnosis
- Physicians should suspect coronary vasospasm if ST segment elevation is detected in patients experiencing angina, and if the ECG completely returns to baseline upon resolution of symptoms.
- 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.
Treatment
Choices of Treatment
Intracoronary Vasodilator
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.
- Intracoronary nitroglycerin 100-300 mcg. Generally well tolerated and have an additive effect.
- Intracoronary calcium channel blockers. 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 nitroprusside 100-300 mcg
Systemic Vasodilators
- 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 vessel spasm.
- Repeat prolonged (2-5 min) PTCA at low pressure (1-4 atmospheres). May mechanically "break" vasospasm.
- Stenting. 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.
Step by Step Treatment Approach
- Therapeutic treatment of PCI-induced vasospasm should be performed in this order (step-wise fashion):
- Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates, which should be given slowly when using 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 vessel spasm.
- Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres).
- Stenting should be a last ditch option, and used if above measures have failed, as it may lead to propagation of spasm to a new location. Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
Assessment of Response to Therapy
Therapies for vasospasm will usually take effect within seconds to one minute. Anticipated outcomes include:
- Resolution of the coronary vasospasm
- Resolution of the ECG changes (ST depression or elevation)
- Resolution of symptomatic angina and other symptoms, if present
References
- ↑ 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) - ↑ 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)