PCI complications: coronary vasospasm: Difference between revisions
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==Overview== | ==Overview== | ||
==Diagnosis== | ==Differential Diagnosis== | ||
* The differential diagnosis of coronary spasm during [[percutaneous coronary intervention]] includes [[abrupt closure]] due to [[dissection]] or thrombus formation. | |||
==Diagnosis== | ==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. | * 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 vasodilators. | * Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators. | ||
==Treatment== | ==Treatment== |
Revision as of 20:04, 2 May 2014
Percutaneous coronary intervention Microchapters |
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PCI complications: coronary vasospasm On the Web |
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Directions to Hospitals Treating Percutaneous coronary intervention |
Risk calculators and risk factors for PCI complications: coronary vasospasm |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Differential Diagnosis
- The differential diagnosis of coronary spasm during percutaneous coronary intervention includes abrupt closure due to dissection or thrombus formation.
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.
- 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
- 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.
- 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.
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 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.