Dr. Alberto Cremonesi,
Carotid angioplasty and stenting (CAS) for the treatment of severe carotid obstructive disease is becoming more widely performed, and is now widely accepted as a less invasive technique that provides an attractive alternative for many patients, particularly those with significant co-morbidities. Complication rates range from 0.9% to 9.3% following the experience of different centres (1-10). It is of fundamental importance that physicians be able to recognise and manage the various possible complications of carotid angioplasty and stenting.
The potential procedural and peri-procedural complications that may be related to carotid angioplasty and stenting may be categorised as minor or major complications:
A - Minor complications
B - Major complications
A- Minor Complicatons 1/ Carotid artery spasm Spasm of the distal internal carotid artery (ICA) following distal deployment of a filter is a complication that usually resolves spontaneously after the filter-wire has been removed from the vessel. In our experience, a gentle approach as well as the use of soft-tipped filter-wires minimises the occurence of distal carotid artery spasm. A flow-limiting spasm could be a potential hazard in the presence of occlusion of the contralateral ICA or in cases of incomplete circle of Willis. Intra-arterial administration of 100 to 400 micrograms of nitroglycerin through the guiding sheath generally leads to a rapid resolution of the spasm.
2/ Transient bradycardia and hypotension Transient sinus bradycardia or asystole are relatively common physiological responses to balloon dilatation of carotid bifurcation lesions, particularly during post-dilatation stenting (5). This phenomenon is less commonly observed with treatment of re-stenotic lesions following carotid endarterectomy (CEA) because the receptors may have been denervated by the surgical dissection. These hemodynamic instabilities are effectively avoided by pretreatment with 0.5 to 1 mg of intravenous atropine. Large doses of atropine should be avoided in elderly patients, as they can result in confusion and make accurate neurological assessment more difficult. Careful hemodynamic monitoring of all patients during the procedure and in the first hours following carotid artery stenting (CAS) is crucial for early recognition and management of the situation.
Note that in this clinical setting, there are other potential sources of hypotension which must be excluded:
Hypotension should be promptly corrected in the following situations:
Generally, hypotension responds well to intravenous hydration and/or small dose of intravenous vasopressors.
3/ Severe, sustained hypotension Persistent hypotension has been reported to occur following 4 to11% of carotid stenting procedures and was not usually associated with any adverse clinical events in the hospital or during the 30-day follow-up period (5). Adverse events related to this phenomenon did, however, occur in two small series (11,12). The degree of hypotension appears to be more pronounced in patients with heavily calcified lesions. Independent predictors of sustained hypotension following CAS (6,8) are:
The mechanism of sustained hypotension following CAS may be explained on the basis of the carotid sinus reflex arc (13). Balloon dilatation and the radial force of the self-expanding stent result in increased radial pressure within the carotid sinus, leading to inappropriate activation of baroreceptors and subsequent development of sustained hypotension. Careful hemodynamic monitoring in the 24 hours following CAS is crucial for proper management of patients with this complication. Generally, this phenomenon responds well to intravenous hydration and prolonged administration of small doses of intravenous vasopressors.
4/ Distal embolisation (minor: TIAs; MAJOR: STROKES) Symptomatic distal embolisation is the most frequent and important complication of CAS (1,2). It is caused by the release of material (thrombotic, necrotic, or atherosclerotic) from the site of the lesion during the intervention (7,8,14). Extensive use of embolic protection devices has been demonstrated to reduce the incidence of this complication (6,10) Risk factors for periprocedural distal embolizstion during CAS are the following:
It is essential to monitor a patient's neurological status after each step of the procedure. If a significant change in neurological status appears and does not resolve within a short lapse of time, general care should be instituted with emphasis on maintaining normal blood pressure, expanding intravenous volume, stabilising the patient's heart rate, maintaining a viable airway, and administering oxygen as necessary. If the patient becomes uncooperative and agitated, particularly if he or she has a compromised airway, the assistance of an anesthesiologist should be sought. Intracranial angiography is performed in anteroposterior and lateral projections. If possible, angiography of the contralateral carotid artery and at least one vertebral artery should be performed. Angiograms must be examined carefully to determine the site and extent of intracranial vessel embolism. The most likely sites of intracranial embolism are the distal ICA and the middle cerebral artery with its branches. Large vessel occlusion is usually easy to detect, but embolism in the smaller branches requires careful scrutiny. Acute occlusion of small branches may be detected only by comparing post- and pre-procedural angiograms. The availability of a good pre-procedural intracranial angiogram is, therefore, essential in all patients undergoing carotid stenting. Given that "time is brain", once a distal embolisation of a large vessel has been recognised, attempts should be made to recanalise the occluded branch as soon as possible (with balloon angioplasty, mechanical devices for thrombus removal, thrombolytic agents, IIb/IIIa inhibitors). If there is a neurological deficit and small branch occlusion, the patient can be hydrated, given heparin and his or her blood pressure raised. It is important to remember that changes of neurological status can also be related to intracerebral bleeding or hyperperfusion syndrome. If there are signs of a localised, expanding phenomenon on angiography indicating intracerebral hemorrhage, anticoagulation should be reversed and computed tomography scanning of the brain performed.
1/ Intracranial hemorrhage Cerebral hemorrhage is a life-threatening and usually fatal complication (15,17). In the authors’ experience, it occurs in approximately 0.3% of endovascular carotid procedures. Sudden loss of consciousness preceded by severe headaches in the absence of intracranial vessel occlusion should alert the operator to this life-threatening event. If a cerebral hemorrhage is suspected, the procedure should be terminated. Anticoagulation should be reversed with protamine and emergency computed tomography performed. In the literature, cerebral hemorrhage has been associated with a combination of excessive anticoagulation, poorly controlled hypertension, aggressive attempts at intracranial neurovascular rescue, presence of a vulnerable berry aneurysm, or CAS in the presence of a recent (less than 3 weeks previously) ischemic stroke.
2/ Hyperperfusion syndrome The reported incidence of cerebral hyperperfusion syndrome following CEA ranges from 0.3% to 2.7% (18,20). Clinical manifestations of this complication are varied and include:
The syndrome typically occurs in patients with severe carotid stenosis and poor collateral circulation, particularly in those with complete occlusion of the contralateral ICA or patients with an underdeveloped circle of Willis. The mechanism is related to long-standing hypoperfusion that results in impaired autoregulation of the microcirculation (18). Following revascularisation, the increased perfusion pressure overwhelms the ability of the dilated arterioles to constrict, resulting in the development of the clinical syndrome. In the authors' experience, hyperperfusion syndrome occurs in approximately 0.5% of cases. Several factors may contribute to its development during CAS: severe carotid artery stenosis with contralateral ICA occlusion, recanalisation of a completely occluded carotid artery, concomitant bilateral carotid stenting during the same procedure (9). Unlike the surgical hyperperfusion syndrome, in which symptoms usually develop within a few days following CEA, the endovascular hyperperfusion syndrome develops during the stenting procedure itself or in the immediate post-procedural aftermath (15,17). This is likely related to heparin administration and the use of antiplatelet agents, particularly intravenous glycoprotein IIB/IIIA antagonists. Given the lack of evidence for a beneficial effect of glycoprotein IIB/IIIA antagonists during CAS, we do not routinely administer these agents during carotid interventions. Current management of the hyperperfusion syndrome consists of identification of patients predisposed to this complication, careful monitoring, and meticulous blood pressure control, since this last factor appears to be the most important one contributing to adverse outcome (18). It is, therefore, important to control blood pressure levels during the periprocedural period using intravenous antihypertensive agents if necessary.
3/ Carotid artery dissection Carotid artery dissection is a rare but important complication of CAS. Factors which may predispose to this complication include: (a) Severe "bends" or "kinks" in the ICA (b) Aggressive hardware (guide wires, balloon catheters, stents) within the ICA (c) Postdilatation of the distal stent edge within the ICA (d) Aggressive manipulation of the guiding sheath tip, which is usually located in the common carotid artery Stenting of lesions that are adjacent to severe distal kinks or bends can be a technical challenge and predispose to the development of vascular dissections. Spasms, pseudo-spasms, and distally displaced kinks should be recognised, and stenting of these side effects must be avoided. Generally, dissections are treated by additional stenting prior to removal of the guiding catheter/sheath. When there is suspicion of a carotid dissection, it is essential mandatory to maintain the guide wire position until the final angiographic assessment has been completed and the presence or absence of dissections has been ascertained.
4/ Carotid artery perforation Carotid artery perforation during CAS is an extremely rare event. In the authors' experience of over 1,150 stented carotid arteries, a single case was observed. This perforation occurred following aggressive balloon dilatation of the middle part of the stent using a 6.0-mm diameter balloon in order to optimise the final result in a post-radiation carotid stenosis (9). We now appreciate that residual luminal narrowing of less than 25%, parietal irregularities, and residual ulcerations external to the stent are of no prognostic significance in terms of immediate or late results.
5/ Acute stent thrombosis Acute stent thrombosis is a remarkably rare event after CAS. The use of appropriate doses of adjunctive double antiplatelet therapy (1, 2) has lowered the rates of stent thrombosis and periprocedural embolic events. Beside the antiplatelet regimen, stenting techniques can play a positive role in preventing acute stent thrombosis. The stenting strategies that minimise the risk of acute stent thrombosis include:
Late in-stent thrombosis is possible, but it is actually very difficult to determine its real frequency because only symptomatic late occlusion is clinically detectable. As a general rule, based mostly on common sense, we treat patients referred for non-atherosclerotic lesions or with sub-optimal results with double antiplatelet agents (aspirin + ticlopidine/clopidogrel) indefinitely.
6/ Contrast agent encephalopathy Contrast encephalopathy is very rare (< 0.1%), and is defined as a transient neurological syndrome mostly related to a prolonged procedure in which a large volume of contrast medium is used. The patient can develop profound neurological deficits related to the involved hemisphere, with marked contrast enhancement "staining" in the basal ganglion and the cortex, but no radiographic brain abnormalities on computed tomography. Usually no angiographic vascular abnormalities are detected by intracranial angiography. Given that contrast medium does not pass through the blood-brain barrier, this phenomenon may be caused by fine particulate embolisation and/or excessive local contrast injection (21,22). Patients typically recover completely within 24 hours without a permanent neurological deficit. From a clinical stand point, the interventionist must differentiate this phenomenon from a massive cerebral infarction or hyperperfusion syndrome.
Complications at the site of the vascular access Puncture site complications can be minimised with :
It should be taken into account that early ambulation and discharge can counteract the activated carotid sinus reflex and the occasionally observed post-procedural hypotension (23). If a manual technique of sheath removal is used, the sheath should be removed by experienced personnel under additional local anesthesia 2 to 4 hours after the procedure has been completed when the activated coagulation time has shortened to 150 seconds or less. Patients are usually kept on bed rest for 4 to 6 hours following removal of the sheath.
It is of fundamental importance that physicians can recognise and manage the various possible complications of carotid angioplasty and stenting.
1. Yadav JS, Roubin GS, Iyer S, Vitek J, King P, Jordan WD, et al. Elective stenting of the extracranial carotid arteries. Circulation 1997;95(2):376-81. 2. Roubin GS, New G, Iyer SS, Vitek JJ, Al-Mubarak N, Liu MW, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery stenosis: a 5-year prospective analysis. Circulation 2001;103(4):532-7.
3. Morey SS. AHA updates guidelines for carotid endarterectomy. Am Fam Physician 1998;58(8):1898, 1903-4. 4. Wholey MH, Al-Mubarek N. Updated review of the global carotid artery stent registry. Catheter Cardiovasc Interv 2003;60(2):259-66. 5. Al-Mubarak N, Liu MW, Dean LS. Incidences and outcomes of prolonged hypotension following carotid artery stenting. J Am Coll Cardiology 1999;33:65. 6. Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351(15):1493-501. 7. Mas JL, Chatellier G, Beyssen B, Branchereau A, Moulin T, Becquemin JP, et al. Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis. N Engl J Med. 2006;355(16):1660-71. 8. Ringleb PA, Allenberg J, Bruckmann H, Eckstein HH, Fraedrich G, Hartmann M, et al. 30 day results from the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial. Lancet 2006;368(9543):1239-47. 9. Cremonesi A, Setacci C, Manetti R, de Donato G, Setacci F, Balestra G, et al. Carotid angioplasty and stenting: lesion related treatment strategies. EuroIntervention. 2005;1(3):289-95. 10. Cremonesi A, Gieowarsingh S, Spagnolo B, Manetti R, Liso A, Furgieri A, et al. Safety, Efficacy and Long-term Durability of Endovascular Therapy for Carotid Artery Disease: The tailored Carotid Artery Stenting Experience of a single high-volume center (tailored-CASE Registry). EuroIntervention. 2009;5:589-598. 11. Mendelsohn FO, Weissman NJ, Lederman RJ, Crowley JJ, Gray JL, Phillips HR, et al. Acute hemodynamic changes during carotid artery stenting. Am J Cardiol 1998;82(9):1077-81. 12. Dangas G, Laird JR, Jr., Satler LF, Mehran R, Mintz GS, Larrain G, et al. Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes. Radiology. 2000;215(3):677-83. 13. Berne RM, Levy MN. The peripheral circulation and its control. In: Mosby, editor. Cardiovascular physiology. New York: Berne RM, Levy, MN; 1992. p. 184-188. 14. Ohki T, Marin ML, Lyon RT, Berdejo GL, Soundararajan K, Ohki M, et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg 1998;27(3):463-71. 15. McCabe DJ, Brown MM, Clifton A. Fatal cerebral reperfusion hemorrhage after carotid stenting. Stroke 1999;30(11):2483-6. 16. Chamorro A, Vila N, Obach V, Macho J, Blasco J. A case of cerebral hemorrhage early after carotid stenting. Stroke 2000;31(3):792-793. 17. Al-Mubarak N, Roubin GS, Vitek JJ, Iyer SS, New G, Leon MB. Subarachnoidal hemorrhage following carotid stenting with the distal-balloon protection. Catheter Cardiovasc Interv 2001;54(4):521-3. 18. Naylor AR, Ruckley CV. The post-carotid endarterectomy hyperperfusion syndrome. Eur J Vasc Endovasc Surg 1995;9(4):365-7. 19. Sundt TM, Jr., Sharbrough FW, Piepgras DG, Kearns TP, Messick JM, Jr., O'Fallon WM. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy: with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc 1981;56(9):533-43. 20. Breen JC, Caplan LR, DeWitt LD, Belkin M, Mackey WC, O'Donnell TP. Brain edema after carotid surgery. Neurology 1996;46(1):175-81. 21. Torvik A, Walday P. Neurotoxicity of water-soluble contrast media. Acta Radiol Suppl 1995;399:221-9. 22. Caille JM, Allard M. Neurotoxicity of hydrosoluble iodine contrast media. Invest Radiol 1988;23 Suppl 1:S210-2. 23. Al-Mubarak N, Roubin GS, Vitek JJ, New G, Iyer SS. Procedural safety and short-term outcome of ambulatory carotid stenting. Stroke 2001;32(10):2305-9.
Fausto Castriota1, Alberto Cremonesi1, Luigi Tavazzi2
GVM Hospitals of Care and Research 1 Interventional Cardio-Angiology Unit, 2 Research Unit - Villa Maria Cecilia Hospital – Cotignola (RA) – Italy
Corresponding author: Fausto Castriota, MD Co-Director, Interventional Cardio-Angiology Unit Department of Medical and Surgical Cardiology Villa Maria Cecilia Hospital Via Corriera 1, 48010 Cotignola (RA) - Italy Tel. +39 0545 37202 Fax +39 0545 37208 Email: firstname.lastname@example.org
Our mission: To reduce the burden of cardiovascular disease
© 2018 European Society of Cardiology. All rights reserved