Published online before print August 3, 2006, doi: 10.1161/01.STR.0000237208.77716.1c
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(Stroke. 2006;37:2210.)
© 2006 American Heart Association, Inc.
Letters to the Editor |
Hyperperfusion Syndrome After Intracranial Angioplasty and Stent Placement
Columbia Unversity, College of Physicians & Surgeons, Neurological Institute, New York, New York
Royal Perth Hospital, Perth, Australia
University of California at San Francisco, San Francisco, California
To the Editor:
Rezende et al1 incorrectly state that there is no prior report in the literature of hyperperfusion syndrome after stent revascularization of the intracranial vertebral artery. In fact, a nearly identical case was published with imaging proof of hyperperfusion based on cerebral blood flow (Figure) nearly 6 years ago in Neurosurgery.
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In July 2000, authors working at the University of California, San Francisco, were the first to publish a series examining the incidence of intracranial hemorrhage and cerebral hyperperfusion syndrome after cervical and cerebral stent placement.2 In our series of 140 patients at that time, the incidence of cerebral hyperperfusion was 5%, whereas the incidence of intracranial hemorrhage was 1.4%, but with 0% mortality. We also reported on patients with clinical or radiological manifestations of cerebral hyperperfusion syndrome without intracerebral hemorrhage, something the current authors did not attempt. Indeed, we observed the major contribution to the 5% incidence of cerebral hyperperfusion syndrome were these cases.
The incidence of intracranial hemorrhage after surgical carotid endarterectomy is &0.6%. In agreement with Rezende, this risk is increased by the presence of profound cerebral ischemia with impaired hemodynamic reserve.3 However, Rezende fails to indicate that other reports examining the incidence of cerebral hyperperfusion syndrome using perioperative transcranial Doppler studies have reported rates of up to 9%.4,5 Because the clinical findings in cerebral hyperperfusion syndrome may be subtle and ancillary investigations examining postprocedural cerebral blood flow, such as brain perfusion CT, nuclear medicine single-photon emission CT, xenon CT, and transcranial Doppler sonography, are not often performed, one may expect a significant reporting bias that can skew the published data.
Normal systemic blood pressure ("normotension") after a revascularization procedure is often excessive blood pressure (effective "hypertension") in the susceptible cerebral circulation. Already a low resistance system, the brain can sustain severe barotrauma because of the loss of cerebrovascular tone and reactivity. Our patient detailed in the Figure sustained a 100% increase in cerebral blood flow after stent revascularization meeting the specific definition of hyperperfusion. In general, pharmacologically induced hypotension is required in these cases while taking into account comorbidities which could be exacerbated by hypotension. In the future, imaging may better guide pharmacotherapy on an individualized patient basis.
Anticoagulation in the treatment of cerebral artery stenosis remains controversial, but one thing is clear: strong or multiple anticoagulants can cause cerebral hemorrhage. In both retrospective and prospective WASID studies, hemorrhagic complications substantially offset the benefit of anticoagulation for patients with posterior circulation stenosis.6,7 The WARSS trial found no benefit to warfarin over aspirin.8 Similarly, platelet inhibition must be used judiciously to balance the need to prevent stent thrombosis with the risk of hemorrhage. In carotid stent series using abciximab (a strong glycoprotein IIb/IIIa platelet inhibitor), there was a significant risk of cerebral hemorrhage.9,10 Although some authors advocate continued heparin infusion after neuroendovascular stent procedures, the coronary literature indicates little effect on the rate of stent thrombosis but a significant risk of hemorrhagic complications.11,12 Consequently, we use relatively smaller doses of heparin during revascularization procedures in which patients already take aspirin and clopidogrel, and we do not continue heparin after conclusion of the procedure.
With the advent of the Boston Scientific Wingspan system, and others like it, we are entering a time when routine stenting of cerebral arteries becomes possible. It is incumbent on the greater neuroscience community to maximize our knowledge based on the available case material in order to advance the field. We cannot afford to reinvent the wheel on a periodic basis. Our cardiological colleagues luxuriate in a relative abundance of treatable disease. To their credit, however, cardiology has masterfully engineered trial after trial to evaluate drugs, devices, and techniques. Neurosciences need to follow this example to advance our discipline at a commensurate rate.
Acknowledgments
Disclosures
None.
References
1. Rezende MT, Spelle L, Mounayer C, Piotin M, Abud DG, Moret J. Hyperperfusion syndrome after stenting for intracranial vertebral stenosis. Stroke. 2006; 37: e12–e14.
2. Meyers PM, Higashida RT, Phatouros CC, Malek AM, Lempert TE, Dowd CF, Halbach VV. Cerebral hyperperfusion syndrome after percutaneous transluminal stenting of the craniocervical arteries. Neurosurgery. 2000; 47: 335–343.[CrossRef][Medline] [Order article via Infotrieve]
3. Kaku Y, Yoshimura S, Kokuzawa J. Factors predictive of cerebral hyperperfusion after carotid angioplasty and stent placement. AJNR Am J Neuroradiol. 2004; 25: 1403–1408.
4. Gossetti B, Martinelli O, Guerricchio R, Irace L, Benedetti-Valentini F. Transcranial doppler in 178 patients before, during, and after carotid endarterectomy. 1997; 7: 213–216.
5. Dalman JE, Beenakkers IC, Moll FL, Leusink JA, Ackerstaff RG. Transcranial doppler monitoring during carotid endarterectomy helps to identify patients at risk of postoperative hyperperfusion. Eur J Vasc Endovasc Surg. 1999; 18: 222–227.[CrossRef][Medline] [Order article via Infotrieve]
6. Chimowitz MI, Kokkinos J, Strong J, Brown MB, Levine SR, Silliman S, Pessin MS, Weichel E, Sila CA, Furlan AJ. The warfarin-aspirin symptomatic intracranial disease study. Neurology. 1995; 45: 1488–1493.
7. Chimowitz MI, Lynn MJ, Howlett-Smith H, Stern BJ, Hertzberg VS, Frankel MR, Levine SR, Chaturvedi S, Kasner SE, Benesch CG, Sila CA, Jovin TG, Romano JG. Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis. N Engl J Med. 2005; 352: 1305–1316.
8. Mohr JP, Thompson JL, Lazar RM, Levin B, Sacco RL, Furie KL, Kistler JP, Albers GW, Pettigrew LC, Adams HP Jr, Jackson CM, Pullicino P. A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. 2001; 345: 1444–1451.
9. Qureshi AI, Saad M, Zaidat OO, Suarez JI, Alexander MJ, Fareed M, Suri K, Ali Z, Hopkins LN. Intracerebral hemorrhages associated with neurointerventional procedures using a combination of antithrombotic agents including abciximab. Stroke. 2002; 33: 1916–1919.
10. Qureshi AI, Suri MF, Ali Z, Kim SH, Lanzino G, Fessler RD, Ringer AJ, Guterman LR, Hopkins LN. Carotid angioplasty and stent placement: A prospective analysis of perioperative complications and impact of intravenously administered abciximab. Neurosurgery. 2002; 50: 466–473;discussion 473–465.
11. Ellis SG, Roubin GS, Wilentz J, Douglas JS Jr, King SB 3rd. Effect of 18- to 24-hour heparin administration for prevention of restenosis after uncomplicated coronary angioplasty. Am Heart J. 1989; 117: 777–782.[CrossRef][Medline] [Order article via Infotrieve]
12. Friedman HZ, Cragg DR, Glazier SM, Gangadharan V, Marsalese DL, Schreiber TL, O’Neill WW. Randomized prospective evaluation of prolonged versus abbreviated intravenous heparin therapy after coronary angioplasty. J Am Coll Cardiol. 1994; 24: 1214–1219.[Abstract]
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