Hyperperfusion Syndrome following Carotid Artery Stenting: The Largest Single-Operator Series to Date

被引:0
作者
Brantley, Hutton P. [1 ]
Kiessling, Jennifer L. [1 ]
Milteer, Hugh B., Jr. [2 ]
Mendelsohn, Farrell O. [3 ]
机构
[1] Baptist Hlth Syst Inc, Birmingham, AL USA
[2] Univ Alabama, Sch Med, Birmingham, AL USA
[3] Cardiol PC, Birmingham, AL USA
关键词
INTRACEREBRAL HEMORRHAGE; CEREBRAL HYPERPERFUSION; INTRACRANIAL HEMORRHAGE; ENDARTERECTOMY; ANGIOPLASTY; RISK;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Cerebral hyperperfusion syndrome.(HPS) results from autoregulatory failure of cerebral blood flow following carotid endarterectomy (CEA) or carotid artery stenting (CAS) and encompasses a range of neurological findings including headache, seizure, intracranial hemorrhage (ICH), altered mental status and focal neurological changes. This report is the largest single-operator series evaluating the incidence and predictors of HPS following CAS. Methods. A retrospective review was conducted on 482 consecutive patients who underwent CAS between August 1999 and December 2007 at Baptist Medical Center - Princeton, Birmingham, Alabama. All interventions were performed by a single operator (FM). The mean patient age was 70.4 +/- 10.3 years and 36% were symptomatic. All patients were high-risk for CEA. After cerebral protection catheters were routinely available, they were used in all but 6 cases (98.1%) where the anatomy precluded delivery. Brain computed tomography (CT) was performed immediately for any neurological change or significant headache following CAS. After neurological consultation and imaging, HPS was diagnosed if: 1) a neurological change occurred (not simply a headache); 2) CT revealed ipsilateral sulcal effacement/cerebral edema; and 3) stroke or transient ischemic attack (TIA) was excluded. Results. Seven patients (1.45%) developed. HPS following CAS. All patients achieved complete neurological recovery 6-24 hours following the procedure. Patients who developed HPS were significantly more likely to have had recent transient ischemic attack (TIA) symptoms than patients without HPS (p = 0.04). Unlike previous reports, there were no significant differences in procedural details, lesion characteristics and post-procedure blood pressure between the HPS and non-HPS patients, although the number of cases was small. Overall, the HPS cohort had a higher prevalence of comorbidites, though these differences did not reach statistical significance. Hypertension was present in all 7 HPS patients. Other complications in the series were death (0.83%), stroke (1.87%) and TIA (1.45%). Conclusions. The incidence of HPS is low (1.45%) following CAS, but it is an important complication to distinguish from stroke and TIA. Patients with a recent TIA may be predisposed to HI'S. This report may underestimate the incidence of HPS, since patients with an isolated headache did not meet our diagnostic criteria and routine post-procedure brain CT imaging was not performed. The clinical predictors of HI'S and its optimum management remain to be determined.
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页码:27 / 30
页数:4
相关论文
共 15 条
[1]   Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting - Risk factors, prevention, and treatment [J].
Abou-Chebl, A ;
Yadav, JS ;
Reginelli, JP ;
Bajzer, C ;
Bhatt, D ;
Krieger, DW .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2004, 43 (09) :1596-1601
[2]   Intensive treatment of hypertension decreases the risk of hyperperfusion and intracerebral hemorrhage following carotid artery stenting [J].
Abou-Chebl, Alex ;
Reginelli, Joel ;
Bajzer, Chris T. ;
Yadav, Jay S. .
CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, 2007, 69 (05) :690-696
[3]   ACCF/SCAI/SVMB/SIR/ASITN 2007 clinical expert consensus document on carotid stenting - A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents (ACCF/SCAI/SVMB/SIR/ASITN Clinical Expert Consensus Document Committee on Carotid Stenting) [J].
Bates, Eric R. ;
Babb, Joseph D. ;
Casey, Donald E., Jr. ;
Cates, Christopher U. ;
Duckwiler, Gary R. ;
Feldman, Ted E. ;
Gray, William A. ;
Ouriel, Kenneth ;
Peterson, Eric D. ;
Rosenfield, Kenneth ;
Rundback, John H. ;
Safian, Robert D. ;
Sloan, Michael A. ;
White, Christopher J. ;
Harrington, Robert A. ;
Abrams, Jonathan ;
Anderson, Jefrey L. ;
Eisenberg, Mark J. ;
Grines, Cindy L. ;
Hlatky, Mark A. ;
Lichtenberg, Robert C. ;
Lindner, Jonathan R. ;
Pohost, Gerald M. ;
Schofield, Richard S. ;
Shubrooks, Samuel J., Jr. ;
Stein, James H. ;
Tracy, Cynthia M. ;
Vogel, Robert A. ;
Wesley, Deborah J. .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2007, 49 (01) :126-170
[4]   Hyperperfusion syndrome: Toward a stricter definition [J].
Coutts, SB ;
Hill, MD ;
Hu, WY ;
Sutherland, GR .
NEUROSURGERY, 2003, 53 (05) :1053-1058
[5]  
Kaku Y, 2004, AM J NEURORADIOL, V25, P1403
[6]   THE ROLE OF NEUROEFFECTOR MECHANISMS IN CEREBRAL HYPERPERFUSION SYNDROMES [J].
MACFARLANE, R ;
MOSKOWITZ, MA ;
SAKAS, DE ;
TASDEMIROGLU, E ;
WEI, EP ;
KONTOS, HA .
JOURNAL OF NEUROSURGERY, 1991, 75 (06) :845-855
[7]   Cerebral hyperperfusion syndrome after percutaneous transluminal stenting of the craniocervical arteries [J].
Meyers, PM ;
Higashida, RT ;
Phatouros, CC ;
Malek, AM ;
Lempert, TE ;
Dowd, CF ;
Halbach, VV .
NEUROSURGERY, 2000, 47 (02) :335-343
[8]  
Morrish W, 2000, AM J NEURORADIOL, V21, P1911
[9]   Intracerebral hemorrhage after carotid endarterectomy: Incidence, contribution to neurologic morbidity, and predictive factors [J].
Ouriel, K ;
Shortell, CK ;
Illig, KA ;
Greenberg, RK ;
Green, RM .
JOURNAL OF VASCULAR SURGERY, 1999, 29 (01) :82-87
[10]  
PEIPGRAS DG, 1988, J NEUROSURG, V68, P532