PCI complications: coronary vasospasm

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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 of angioplasy- induced coronary vasospasm 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.

Pathophysiology

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.

Differential Diagnosis

• The differential diagnosis of coronary spasm during percutaneous coronary intervention includes abrupt closure due to dissection or thrombus formation.

Epidemiology and Demographics

• Occasionally, coronary vasospasm can be induced by angioplasty (PCI-induced).
• 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

Smoking is a risk factor for coronary vasospasm.

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.