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| | #Redirect [[PCI complications: coronary vasospasm]] |
| {{WikiDoc Cardiology Network Infobox}}
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| {{CMG}}<br>
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| '''Associate Editors-in-Chief:''' Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro; David M. Leder, M.D.
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| {{Editor Help}}
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| ==Background==
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| 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.
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| The exact [[pathogenesis]] of coronary vasospasm is not well understood, but some causes and contributing factors are known. Some coronary vasospasms are PTCA-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.
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| 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 vaspspasm, with a 4-36% incidence.
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| ==Diagnosis==
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| The 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.
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| ==Treatment Choices==
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| ===Treatments during PCI===
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| *'''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.
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| **Intracoronary nitroglycerine 100-300 mcg. Generally well tolerated.
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| **Intracoronary calcium channel blockers. Small risk of transient heart block
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| ***Diltiazem 0.5-2.5 mg/min, up to 5-10mg
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| ***Verapamil 100 mcg/min, up to 1.0-1.5 mg
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| *'''Systemic vasodilators'''
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| **Nifedipine 10mg sublingual
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| **Atropine 0.5mg IV. Particularly useful in the setting of hypotension or bradycardia.
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| *'''Angioplastic treatments'''
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| **Removal of interventional hardware with guide wire in place to minimize mechanical provocation- may minimize distal vessel spasm
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| **Repeat prolonged PTCA at low pressure (1-4 atmospheres)
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| **Stenting. This will improve focal spasm, but may also cause spasm in vessel adjacent to the hardware.
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| ===Treatments for chronic vasospasm===
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| *'''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.
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| **Diltiazem 240-360mg PO qd
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| **Verapamil 240-480mg PO qd
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| **Nifedipine XL 60-120mg PO qd
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| **Nicardipine 40-160mg PO qd
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| *'''Long-acting nitrates'''
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| **Isosorbide mononitrate (Imdur) 60-240mg PO qd
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| **Isosorbide dinitrate (Isordil) 20-40mg PO tid
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| *'''Hormone replacement therapy.''' This remains controversial, particularly due to the risk of concern of increased cardiac events.
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| *'''Smoking cessation''' should be emphasized in all patients. It lowers future event rates of vasospasm and acute coronary syndromes.
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| *'''PTCA/stenting'''
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| *'''ICD placement''' as described above for patients with VT/VF due to spontaneous coronary vasospasm without other provocation that may be treated.
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| *'''Surgical autonomic denervation''' is reserved only for the most refractory cases.
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| ==Selecting a therapy in the setting of PCI-induced vasospasm==
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| Therapeutic treatment of PCI-induced vasospasm should be performed in this order:
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| *Intracoronary vasodilators (either nitroglycerin or calcium channel blockers may be given first
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| *Combined therapy of intracoronary nitroglycerine and calcium channel blockers
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| *Removal of hardware with guidewire in place
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| *Repeat PTCA
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| *Stenting if above measures have failed. Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
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| ===Assessment of treatment efficacy with PCI-induced vasospasm===
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| Therapies for vasospasm will usually take effect within seconds to one minute.
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| *Repeat angiography
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| *Resolution of ECG changes (ST depression or elevation)
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| *Resolution of symptoms, if present
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| {{SIB}}
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| [[Category:Cardiology]]
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