Carotid Artery Stenting Risk Reduction

Knowing the risk factors for periprocedural complications can dramatically improve our CAS planning and outcomes.

By Robert S. Dieter, MD, and John R. Laird, Jr, MD
 

To view the tables related to this article, please refer to the print version of our September issue, page 69.

The ultimate goal of carotid artery stenting (CAS) is to reduce the risk of stroke and its attendant morbidity and mortality. To achieve these results, the operator will need to have a clear understanding of the patient and lesion characteristics associated with an increased risk of stroke after the procedure.

THE LEARNING CURVE
As we move closer to the possible FDA approval of CAS, plans are underway to establish training programs around the country that will provide the appropriate training for individuals interested in performing this procedure. There will be controversy regarding the number of procedures needed before one can be considered proficient enough to operate independently. Also, there is heightened interest in the role the learning curve plays in the incidence of complications during CAS. Periprocedural 30-day risk of neurologic complications and death rates appear to be inversely related to the operator volume. There is a general trend in the reduction of complications as the procedural volume increases, with a 19% to 100% relative reduction in neurologic (including TIA) events and 30-day mortality.1,2

When undertaking CAS, it is essential that the operator obtain the appropriate training and work with an individual already experienced with the procedure for a specified number of cases.3 It is likely that as training programs are established, a network of “proctors” will be generated to assist with this process. Early in the learning curve, appropriate patient selection will be especially key for operators who are developing their technique and hoping to maintain an acceptably low complication rate.

PATIENT CHARACTERISTICS THAT INCREASE THE RISKS OF CAS

Analysis of the outcomes of patients undergoing CAS has revealed specific patient characteristics that increase the risk associated with the procedure. Appropriate patient selection based on knowledge of these risk factors will be necessary to maintain complication rates within the accepted guidelines (Table 1).

Age
Although some trials have shown that age is not a predictor of poor outcomes after CAS at 48 hours and 30 days, most trials have demonstrated a correlation between age and periprocedural 30-day events.4-7 Patients older than 80 years seem to be at particularly high risk (16%-25%) for neurologic complications after stenting.5,6

Hypertension
Patients with uncontrolled hypertension are at an increased risk for periprocedural complications. Although not necessarily evident at 48 hours, the odds ratio for a periprocedural event at 30 days is as high as 3.45 in this population.4-6

Gender
Unlike CEA trials, there appears to be little difference in periprocedural neurologic events or death at 30 days between men and women undergoing CAS.5,6,8,9 However, numerous trials in the cardiology literature suggest that female patients are at an increased risk for catheterization-related complications; particularly, access complications will likely be more frequent.

Symptomatic Status
Data from large prospective studies are inconsistent but suggest an increase in the risk of CAS based on the symptomatic status of the patient.4-6 The symptomatic carotid lesion is more likely to contain thrombus and, thus, is theoretically more likely to be associated with distal embolic complications.4 This possibility has led some operators to treat the symptomatic patient with
4 to 6 weeks of warfarin prior to the stenting procedure.

Renal Insufficiency
Data from a large prospective series of patients undergoing CAS at the Washington Hospital Center have demonstrated that baseline renal insufficiency is an important risk factor for complications after CAS. For those patients with normal baseline renal function, the 30-day neurologic event rate was 5.4%. For patients with severe renal insufficiency (creatinine clearance <50 mL/min), the neurologic event rate was 16.9%. The exact mechanism for this very high event rate is unclear, but it is consistent with numerous other interventional trials and with studies evaluating the rate of complications after CEA.

Unforgiving Hemodynamic Comorbidities
Patients with significant contralateral or intracranial arterial disease, severe coronary artery disease, valvular heart disease (aortic stenosis), or preload-dependent states (eg, pulmonary hypertension and severe diastolic dysfunction/restrictive physiology) may not tolerate the hemodynamic instability during CAS. Measures to prevent or ameliorate these hemodynamic perturbations will be critical to the safe completion of the CAS procedure for these challenging patients.

ANATOMIC AND LESION CHARACTERISTICS THAT INCREASE THE RISKS OF CAS
General Anatomic Considerations
The normal aging process, coupled with pathologic changes in the large arteries caused by atherosclerosis and other comorbid conditions (eg, hypertension) can cause elongation, dilation, and posterior displacement of the aortic arch. These anatomic changes often lead to severe angulation of the brachiocephalic artery and the common carotid arteries (Figure 1). Engagement of these arteries with a catheter can therefore become problematic.10

Proximal Common Carotid and Brachiocephalic Stenosis
Approximately 1.8% of patients with internal carotid artery stenosis have an associated arch vessel stenosis.11 It may be necessary to predilate ostial lesions to gain access to the lesion in the internal carotid artery. Stenting of the ostial lesion with a balloon-expandable stent is best performed as the final procedure, after successful treatment of the internal carotid artery lesion.

Distal Common Carotid Artery Stenosis
The presence of disease in the distal common carotid artery or external carotid artery may require modification of the procedure that is employed to place the sheath or guiding catheter into the common carotid artery. The usual practice of advancing the 0.038-inch guidewire or diagnostic catheter into the external carotid artery should be avoided in this setting (Figure 2).

Angiographic High-Risk Lesion Features
Lesion severity and length. There is a direct relationship between lesion severity and periprocedural risk, with lesions >90% representing the highest risk.6 Furthermore, multivariate analysis confirms long
(>10 mm) or multiple lesions as increased risk from CAS (Table 2).4,6

Calcification. An analysis of intravascular ultrasound studies performed during CAS procedures at the Washington Hospital Center (Washington, DC) identified lesion calcification (arc of calcium) as an independent predictor of increased neurologic events after stenting, as well as a greater likelihood of prolonged hypotension after the procedure. Lesion calcification should alert the interventionalist that higher-pressure balloon predilation might be required.

Ultrasound High-Risk Lesion Features
Studies have demonstrated that patients with echolucent (hypoechoic) plaques are more symptomatic than those with more echogenic (hyperechoic) plaques.12-14 Heterogeneous plaques have also been correlated with neurologic symptoms.15 Histopathologic examination of echolucent and heterogeneous plaques reveals intraplaque hemorrhage and atheroma, whereas echogenic plaques are composed of more biologically stable fibrous tissue (Figure 3).16

EMBOLIZATION PROTECTION DEVICES
Distal embolization occurs throughout the CAS procedure. By using transcranial Doppler insonation of the ipsilateral middle cerebral artery, it is possible to quantify the degree of particulate embolization by counting the microembolic signals. Approximately 20% of the microembolic signals occur during sheath placement and wire manipulation, another 20% during lesion predilation, 45% during stent deployment, and approximately 15% during postdilation.17 To preserve neurologic and neuropsychologic functioning after CAS, reduction in the number of emboli is necessary. This reduction can be achieved through appropriate patient and lesion selection and use of distal embolization protection devices. Only a minority of lesions are unsuitable for distal embolization protection devices due to anatomic considerations.

Current areas of device development focus upon limiting the embolization during predilation, stent deployment, and postdilation. Various designs have been used to prevent distal embolization. These can be broadly classified as distal balloon occlusion catheters, proximal balloon occlusion catheters, shunting, and filters.

HEMODYNAMIC CONSIDERATIONS
The carotid sinus is located at the common carotid artery bifurcation. Stimulation of the carotid sinus baroreceptors, located in the outer muscle layer, result in an increase in vagal tone and decrease in sympathetic discharge, causing bradycardia and hypotension, respectively.18 Because hemodynamic alterations have been associated with increased periprocedural risk and a greater likelihood of neurologic events, the interventionalist must be continuously aware of patient hemodynamic variables and be able to rapidly correct any aberration.18

Bradycardia is seen consistently during predilation, stent deployment, and postdilation; there is, however, a trend toward greater hypotension during the stent delivery and postdilation.18 Bradycardia (heart rate <60 beats per minute) occurs in 13% to 38% of patients and hypotension (systolic pressure <90 mm Hg) occurs in 5% to 26% of patients undergoing CAS.18,19 Predictably, bradycardia and hypotension are more common with internal carotid artery lesions (up to 45.8%) than common carotid artery lesions (13.5%).20

Predictors of postprocedural hypotension include intraprocedural hypotension and previous history of myocardial infarction.21 Aside from the increased structural rigidity and potential for stent deformation, balloon-expandable stents are associated with 2.5 times the rate of postprocedural hypotension and should be used in only select cases.20,22

Periprocedural hypertension (systolic >160 mm Hg) is seen in 38.8% of patients.23 Multivariate analysis demonstrates that a history of ipsilateral CEA, intraprocedural hypertension, and preprocedural diastolic blood pressure as independent predictors of postprocedural hypertension.23 Periprocedural hypertension should be treated with adequate patient sedation, intravenous nitroglycerin, and, if necessary, nitroprusside.

CEREBRAL REPERFUSION HEMORRHAGE
High-grade cervical carotid artery stenosis can lead to cerebral hypoperfusion, despite maximal arterial vasodilation. Once the carotid artery stenosis is relieved, the maximally dilated cerebral vessels are presented with significantly increased blood flow. Until the intracranial resistance vessels can adapt, vasoconstrict, and resume autoregulation, there is the potential for loss of vascular integrity, protein leak, edema, and ultimately vessel rupture (Figure 4).24,25 The risk of cerebral reperfusion hemorrhage underscores the importance of tight blood pressure control.25

CONCLUSIONS
Perhaps the most important component of periprocedural risk reduction with CAS is understanding which patients and lesions can be safely approached with this technology. To achieve results that are competitive with CEA for both high- and low-risk patients with carotid artery disease, there will need to be strict attention paid to patient and lesion selection. The importance of the learning curve should not be underestimated. During the learning stage of CAS, the operator should restrict his caseload to low-risk lesions in low-risk patients. As experience develops, more complex lesions can be safely approached. Only through meticulous attention to detail, careful patient selection, and rigorous periprocedural patient care will the risks of CAS be minimized. 

Robert S. Dieter, MD, is a cardiovascular medicine interventional fellow at the University of Wisconsin, in Madison, Wisconsin. He may be reached at (202) 877-5975; rsd@medicine.wisc.edu.

John R. Laird, MD, is Director of Peripheral Vascular Interventions at the Cardiovascular Research Institute, and is Assistant Clinical Professor of Medicine at Georgetown University Medical Center, Washington, DC. He also is the Co-Director of the Center of Vascular Care at the Washington Hospital Center, Washington, DC. Dr. Laird may be reached at (202) 877-5975; John.R.Laird@medstar.net.

1. Ahmadi R, Willfort A, Lang W, et al. Carotid artery stenting: effect of learning curve and intermediate-term morphological outcome. J Endovasc Ther. 2001;8:539-546.
2. Roubin GS, New G, Iyer SS, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery disease: a 5-year prospective analysis. Circulation. 2001;103:532-537.
3. Naylor AR, Bolia A, Abbott RJ, et al. Randomized study of carotid angioplasty and stenting versus carotid endarterectomy: a stopped trial. J Vasc Surg. 1998;28:326-334.
4. Qureshi AI, Luft AR, Janardhan V, et al. Identification of patients at risk for periprocedural neurological deficits associated with carotid angioplasty and stenting. Stroke. 2000;31:376-382.
5. Roubin GS, New G, Iyer SS, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery stenosis: a five year prospective analysis. Circulation. 2001;103:532-537.
6. Mathur A, Roubin GS, Iyer SS, et al. Predictors of stroke complicating carotid artery stenting. Circulation. 1998;97:1239-1245.
7. Stankovic G, Liistro F, Moshiri S, et al. Carotid artery stenting in the first 100 consecutive patients: results and follow up. Heart. 2002;88:381-386.
8. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995; 273:1421–1428.
9. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaboration. N Engl J Med. 1991;325:445-453.
10. Myla S. Carotid access techniques: an algorithm approach. Carotid Intervent. 2001;3:2-12.
11. Arko FR, Buckley CJ, Lee SD, et al. Combined carotid endarterectomy with transluminal angioplasty and primary stenting of the supra-aortic vessels. J Cardiovasc Surg. 2000;41:737-742.
12. Golledge J, Cuming R, Ellis M, et al. Carotid plaque characteristics and presenting symptom. Br J Surg. 1997;84:1697-1701.
13. Tegos TJ, Mavrophoros D, Sabetai MM, et al. Types of neurovascular symptoms and carotid plaque ultrasonic textural characteristics. J Ultrasound Med. 2001;20:113-121.
14. El-Barghouti N, Nicolaides AN, Tegos T, et al. The relative effect of carotid plaque heterogeneity and echogenicity on ipsilateral cerebral infarction and symptoms of cerebrovascular disease. Internat Angiol. 1996;15:300-306.
15. AbuRahma AF, Covelli MA, Robinson PA, et al. The role of carotid duplex ultrasound in evaluating plaque morphology: potential use in selecting patients for carotid stenting. J Endovasc Surg. 1999;6:59-65.
16. Ohki T, Marin ML, Lyon RT, et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg. 1998;27:463-471.
17. Al-Mubarak N, Roubin G, Vitek JJ, et al. Effect of the distal-balloon protection system on microembolization during carotid artery stenting. Circulation. 2001;104:1999-2002.
18. Mendelsohn FO, Weissman NJ, Lederman RJ, et al. Acute hemodynamic changes during carotid artery stenting. Am J Cardiol. 1998;82:1077-1081.
19. Al-Mubarak N, Roubin GS, Vitek JJ, et al. Procedural safety and short-term outcome of ambulatory carotid stenting. Stroke. 2001;32:2305-2309.
20. D’Audiffret A, Desgranges P, Kobeiter H, et al. Technical aspects and current results of carotid stenting. J Vasc Surg. 2001;33:1001-1007.
21. Dangas G, Laird JR Jr, Satler LF, et al. Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes. Radiology. 2000;215:677-683.
22. Dangas G, Laird JR Jr, Mehran R, et al. Carotid artery stenting in patients with high-risk anatomy for carotid endarterectomy. J Endovasc Ther. 2001;8:39-43.
23. Qureshi AI, Luft AR, Sharma M, et al. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke. 1999;30:2086-2093.
24. Wholey MH, Wholey MH, Tan WA, et al. Management of neurological complications of carotid artery stenting. J Endovasc Ther. 2001;8:341-353.
25. McCabe DHJ, Brown MM, Clifton A. Fatal cerebral reperfusion hemorrhage after carotid stenting. Stroke. 1999;30:2483-2486.


Figure 1. Difficult arch with the origin of the brachiocephalic artery and left common carotid artery arising from the ascending portion of the thoracic aorta.


Figure 2. Severe tortuosity of the proximal Internal carotid artery.


Figure 3. Thrombus containing lesion (arrow) in the proximal internal carotid artery.


Figure 4. Cerebral hyperperfusion hemorrhage after CAS.

 

Contact Info

For advertising rates and opportunities, contact:
Craig McChesney
484-581-1816
cmcchesney@bmctoday.com

Stephen Hoerst
484-581-1817
shoerst@bmctoday.com

Charles Philip
484-581-1873
cphillip@bmctoday.com

About Endovascular Today

Endovascular Today is a publication dedicated to bringing you comprehensive coverage of all the latest technology, techniques, and developments in the endovascular field. Our Editorial Advisory Board is composed of the top endovascular specialists, including interventional cardiologists, interventional radiologists, vascular surgeons, neurologists, and vascular medicine practitioners, and our publication is read by an audience of more than 22,000 members of the endovascular community.