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Percutaneous carotid stenting with a distal-protection device is now considered an alternative to standard carotid endarterectomy. Although distal-protection filter devices have been reported to reduce the risk of embolism and stroke, their use is associated with such iatrogenic complications as vasospasm, dissection, and guidewire entrapment. Herein, we report a case of symptomatic carotid vasospasm caused by a distal-protection filter device during right internal carotid artery intervention in a woman who had underlying coronary artery disease. We also discuss the management of iatrogenic carotid spasm.
At a time of rapid advancement in endovascular interventions, carotid artery stenting in association with the use of a distal-protection device (DPD) has been shown1 to be safe and efficacious in the treatment of atherosclerotic extracranial carotid artery disease; indeed, it is becoming an alternative to standard carotid endarterectomy. The use of a DPD during carotid intervention is effective in decreasing the stroke rate by preventing atheroembolism.2,3 However, DPD use can cause some iatrogenic sequelae, like local vasospasm, dissection, and guidewire entrapment.4 We herein report a case of marked symptomatic spasm of the right internal carotid artery in association with the use of a filter during protected stenting of that vessel.
In January 2009, a 57-year-old hypertensive woman presented at our outpatient department after sustaining, in March 2008, a single transient ischemic neurologic attack with left hemiparesis. She had a history of coronary artery disease, having undergone coronary artery bypass surgery in December 1999 for double-vessel disease. She had been asymptomatic for her cardiac disease from 1999 to 2008. Clinical examination revealed a right carotid bruit; the rest of the systemic examination was normal. Carotid Doppler sonography showed 80% stenosis of the right internal carotid artery (ICA) at its origin. Coronary angiography revealed a dominant normal right coronary artery, total occlusion of the mid-segment of the left anterior descending coronary artery (LAD) and the proximal segment of the left circumflex coronary artery, and patent grafts (left internal mammary artery to LAD and right radial artery to obtuse marginal branch). Left ventricular angiography showed a left ventricular ejection fraction of 0.60 and no regional wall-motion abnormality. Aside from 80% angiographic stenosis of the right ICA at its origin (Fig. 1), the rest of the extracranial cerebral arteries (such as the left ICA and the bilateral vertebral arteries) were normal upon angiography.
After giving informed consent, the patient was transferred for percutaneous carotid intervention. The right common carotid artery was cannulated with a 7F carotid sheath via the transfemoral approach. A temporary pacing wire was placed in the right ventricle for backup pacing, which at our institute is a routine substitute for prophylactic intravenous atropine during carotid intervention. A 7-mm ANGIOGUARD™ XP Emboli Capture Guidewire System (Cordis, a Johnson & Johnson company; Miami Lakes, Fla) was positioned in the right ICA beyond the lesion. Slow flow was observed in the ICA at the site of the filter, after the filter's deployment (Fig. 2). An 8 × 30-mm Cordis Precise® Nitinol Stent (Cordis) was deployed across the lesion without pre-dilation. After stent deployment, the patient had sudden hypotension and bradycardia. She also had left hemiparesis with a motor power of 1/5, as evaluated in accordance with the method described by Martin and colleagues.5 We administered intravenous atropine and started the dopamine infusion. Without delay, we post-dilated the stent with a 6 × 20-mm balloon (Cordis). Although there was good flow across the stent, the flow across the ANGIOGUARD XP device decreased markedly (Fig. 3), compared with flow shown in the initial angiogram (Figs. 1 and and2).2). There was no improvement in the patient's clinical condition. The filter device was promptly retrieved. After its retrieval, there was improvement in ICA flow (Fig. 4), followed by further improvement after the intra-arterial administration of nitroglycerin (Fig. 5). Upon macroscopic examination, the filter basket showed no evidence of emboli or other material that might have clogged it. The patient's motor power on her left side improved to 3/5 at the end of the procedure. She was transferred to the coronary care unit on temporary pacing support and an infusion of dopamine. Ninety minutes after the intervention, the patient's left-side motor power had normalized to 5/5. A computed tomographic scan of the brain performed after the stabilization did not reveal any fresh infarction. Dopamine infusion was stopped after 24 hours. On post-procedural day 3, she was discharged from the hospital in satisfactory condition, with no residual neurologic deficit. At the 30-day follow-up, she was asymptomatic.
In recent years, various protective devices have been developed in an effort to prevent stroke during percutaneous carotid intervention. The most common are guidewire-mounted distal filter devices.6 There is emerging consensus in regard to the routine use of these protective devices during intervention for carotid artery atherosclerosis.6 However, the use of a DPD is not always safe, for it can be associated with such adverse effects as vasospasm, intimal dissection, and entrapment of the guidewire and filter device.4 Our patient experienced intense and progressive vasospasm of the ICA at the site of the DPD. The sudden onset of left hemiparesis after stent deployment can be explained either by a decrease in cerebral blood flow secondary to local vasospasm or by cerebral microembolism despite the DPD, which is known to occur with these filter devices.6 Transcranial Doppler study can detect microembolization during various sequential steps of protected carotid intervention.7 However, the usefulness of transcranial Doppler imaging in evaluating the clinical outcome of carotid revascularization is still not clear.6 In our patient, the presence of local carotid vasospasm, the rapid improvement of neurologic deficit after treatment of the spasm, and the lack of evidence of cerebral infarction upon computed tomographic scanning of the head all favor carotid vasospasm, instead of cerebral microembolism, as the cause of neurologic deficit. The treatment of intense vasospasm includes the intra-arterial administration of nitroglycerin and, if necessary, the retrieval of the filter device.8 Although intra-arterial nitroglycerine is the preferred drug for relief of vasospasm, drugs like calcium-channel blockers and papaverine are also effective in such a situation.9,10 The prophylactic use of nitroglycerin is not recommended, in view of its hypotensive effect. In our patient, we promptly retrieved the device after completion of the procedure and also administered intra-arterial nitroglycerin for local vasospasm. The proposed mechanisms of local spasm when caused by a DPD are the outward radial force of the device's basket—causing endothelial irritation and injury—and the axial friction of the guidewire-mounted basket as it moves during angioplasty, stenting, and deployment or retrieval of the DPD.11 Intra-arterial nitroglycerin administration to relieve vasospasm can worsen hypotension during the procedure, which might result in cerebral hypoperfusion and adverse cardiac events in the presence of critical coronary artery disease.12
In our patient, we confirmed, before carotid intervention, the patency of coronary bypass grafts, the severity of native coronary artery disease, and the adequacy of the left ventricular ejection fraction, in order to avoid periprocedural adverse cardiac events. We would also like to observe that the use of a fixed-basket, 1st-generation filter device like the FilterWire EZ™ Embolic Protection System (Boston Scientific Corporation; Natick, Mass) is associated with a higher incidence of carotid vasospasm than is use of a newer, 2nd-generation mobile-basket filter device like the RX ACCUNET Embolic Protection System (Abbott Vascular, a division of Abbott Laboratories; Abbott Park, Ill) or the SpiderFX™ Embolic Protection Device (ev3® Endovascular, Inc./Peripheral Vascular; Plymouth, Minn).8 The ANGIOGUARD XP that was used in our patient is also a fixed-basket filter device, which might be associated with increased vasospasm.
In conclusion, although filter devices are useful for the prevention of cerebral embolism during carotid intervention, their use can be associated with iatrogenic sequelae, including symptomatic vasospasm. Carotid vasospasm is self-limiting in most cases; but an intense, symptomatic vasospasm needs prompt management to avoid neurovascular complications.
Address for reprints: Rajesh Vijayvergiya, MD, DM, Department of Cardiology, Postgraduate Institute of Medical Education & Research, 160012 Chandigarh, India