Hostname: page-component-8448b6f56d-gtxcr Total loading time: 0 Render date: 2024-04-24T18:31:13.268Z Has data issue: false hasContentIssue false
  • English
  • Français

Brain Stress Test for Assessing Risk for Hemodynamic Stroke

Published online by Cambridge University Press:  10 January 2023

Lashmi Venkatraghavan Open the ORCID record for Lashmi Venkatraghavan [Opens in a new window] ,
Casey Rosen ,
Larissa McKetton ,
Julien Poublanc ,
Olivia Sobczyk ,
James Duffin ,
Michael Tymianski ,
Joseph A. Fisher  and
David J. Mikulis
Lashmi Venkatraghavan*
Affiliation:
Department of Anaesthesia, University Health Network, Toronto, ON, Canada
Casey Rosen
Affiliation:
Division of Neuroradiology, Joint Department of Medical Imaging, University Health Network, Toronto, ON, Canada
Larissa McKetton
Affiliation:
Division of Neuroradiology, Joint Department of Medical Imaging, University Health Network, Toronto, ON, Canada
Julien Poublanc
Affiliation:
Division of Neuroradiology, Joint Department of Medical Imaging, University Health Network, Toronto, ON, Canada
Olivia Sobczyk
Affiliation:
Division of Neuroradiology, Joint Department of Medical Imaging, University Health Network, Toronto, ON, Canada
James Duffin
Affiliation:
Department of Physiology, The University of Toronto, Toronto, ON, Canada
Michael Tymianski
Affiliation:
Division of Neurosurgery, University Health Network, University of Toronto, Toronto, ON, Canada
Joseph A. Fisher
Affiliation:
Department of Anaesthesia, University Health Network, Toronto, ON, Canada
David J. Mikulis
Affiliation:
Division of Neuroradiology, Joint Department of Medical Imaging, University Health Network, Toronto, ON, Canada
*
Corresponding author: Dr. Lashmi Venkatraghavan, Associate Professor, Department of Anesthesia, University Health Network - Toronto Western Hospital, 399, Bathurst Street, MCL 2-405, Toronto, Ontario M5T 2S8, Canada. Email: Lashmi.Venkatraghavan@uhn.ca
Get access Rights & Permissions [Opens in a new window]

Abstract:

Background:

In patients with intracranial steno-occlusive disease (SOD), the risk of hemodynamic stroke depends on the poststenotic vasodilatory reserve. Cerebrovascular reactivity (CVR) is a test for vasodilatory reserve. We tested for vasodilatory reserve by using PETCO2 as the stressor, and Blood Oxygen Level Dependent (BOLD) MRI as a surrogate of blood flow. We correlate the CVR to the incidence of stroke after a 1-year follow-up in patients with symptomatic intracranial SOD.

Methods:

In this retrospective study, 100 consecutive patients with symptomatic intracranial SOD that had undergone CVR testing were identified. CVR was measured as % BOLD MR signal intensity/mmHg PETCO2. All patients with normal CVR were treated with optimal medical therapy; those with abnormal CVR were offered revascularization where feasible. We determined the incidence of stroke at 1 year.

Results:

83 patients were included in the study. CVR was normal in 14 patients and impaired in 69 patients ipsilateral to the lesion. Of these, 53 underwent surgical revascularization. CVR and symptoms improved in 86% of the latter. The overall incidence of stroke was 4.8 % (4/83). All strokes occurred in patients with impaired CVR (4/69; 2/53 in the surgical group, all in the nonrevascularized hemisphere), and none in patients with normal CVR (0/14).

Conclusion:

Our study confirms that CO2-BOLD MRI CVR can be used as a brain stress test for the assessment of cerebrovascular reserve. Impaired CVR is associated with a higher incidence of stroke and normal CVR despite significant stenosis is associated with a low risk for stroke.

Résumé :

RÉSUMÉ :

Étude de la vasoréactivité cérébrale dans l’évaluation du risque d’accident vasculaire cérébral hémodynamique.

Contexte :

Dans les cas de maladie sténo-occlusive (MSO) intracrânienne, le risque d’accident vasculaire cérébral (AVC) hémodynamique dépend de la réserve de vasodilatation en aval de la sténose. La réactivité vasculaire cérébrale (RVC) est une mesure de la réserve de vasodilatation. Celle-ci a été effectuée, dans l’étude, à l’aide de la pression partielle du CO2 (pCO2) en fin d’expiration utilisée comme agent stressant, et de l’IRM avec signal BOLD (Blood Oxygen Level Dependent) comme substitut du débit sanguin. Une corrélation a établie entre la RVC et l’incidence d’AVC au bout de un an de suivi chez les patients atteints d’une MSO intracrânienne symptomatique.

Méthode :

Il s’agit d’une étude rétrospective à laquelle ont participé 100 patients consécutifs qui présentaient une MSO intracrânienne symptomatique et qui ont été soumis à une mesure de la RVC, exprimée sous forme de pourcentage de l’intensité du signal BOLD en IRM/la pCO2 en fin d’expiration, en mmHg. Tous les patients qui avaient une RVC normale ont été soumis au traitement médical optimal, tandis que ceux chez qui la RVC était anormale se sont vu offrir la revascularisation lorsque le traitement s’y prêtait. L’incidence des AVC a été déterminée au bout de un an.

Résultats :

Ont été retenus 83 patients dans l’étude. La RVC était normale chez 14 sujets et altérée chez 69 porteurs d’une lésion homolatérale. De ces derniers, 53 ont subi une revascularisation chirurgicale et, chez 86 % d’entre eux, on a observé une amélioration de la RVC ainsi qu’une diminution des symptômes. L’incidence globale des AVC s’est élevée à 4,8 % (4/83), et tous les accidents vasculaires sont survenus chez les patients ayant une RVC altérée (4/69; 2/53 dans le groupe de traitement chirurgical, tous du côté de l’hémisphère non revascularisé); aucun ne s’est produit chez les patients ayant une RVC normale (0/14).

Conclusion :

D’après les résultats de l’étude, la mesure de la RVC par IRM à l’aide du signal BOLD et de la pCO2 peut servir d’étude de la vasoréactivité cérébrale pour l’évaluation de la réserve vasculaire cérébrale. Une RVC altérée est associée à une incidence plus élevée d’AVC, et une RVC normale, malgré une sténose importante, est associée à un faible risque d’AVC.

Keywords

Cerebrovascular reserveMRIBrain stress testStrokeCO2Hypercapnia
Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 51 , Issue 1 , January 2024 , pp. 57 - 63
Copyright
© The Author(s), 2023. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Klijn, CJ, Kappelle, LJ. Hemodynamic stroke: clinical features, prognosis, and management. Lancet Neurol. 2010;9:1008–17.CrossRefGoogle ScholarPubMed
Tzeng, YC, Ainslie, PN. Blood pressure regulation ix: cerebral autoregulation under blood pressure challenges. Eur J Appl Physiol. 2014;114:545–59.CrossRefGoogle ScholarPubMed
Liebeskind, DS. Collateral circulation. Stroke. 2003;34:2279–84.CrossRefGoogle ScholarPubMed
Strother, MK, Anderson, MD, Singer, RJ, et al. Cerebrovascular collaterals correlate with disease severity in adult North American patients with Moyamoya disease. AJNR Am J Neuroradiol. 2014;35:1318–24.CrossRefGoogle ScholarPubMed
Liebeskind, DS, Cotsonis, GA, Saver, JL, et al. Collaterals dramatically alter stroke risk in intracranial atherosclerosis. Ann Neurol. 2011;69:963–74.CrossRefGoogle ScholarPubMed
Vernieri, F, Pasqualetti, P, Matteis, M, et al. Effect of collateral blood flow and cerebral vasomotor reactivity on the outcome of carotid artery occlusion. Stroke. 2001;32:1552–8.CrossRefGoogle ScholarPubMed
Liebeskind, DS, Cotsonis, GA, Saver, JL, et al. Collateral circulation in symptomatic intracranial atherosclerosis. J Cereb Blood Flow Metab. 2011;31:1293–301.CrossRefGoogle ScholarPubMed
Sahoo, SS, Suri, A, Bansal, S, Devarajan, SL, Sharma, BS. Outcome of revascularization in moyamoya disease: evaluation of a new angiographic scoring system. Asian J Neurosurg. 2015;10:252–9.Google ScholarPubMed
Lau, AY, Wong, EH, Wong, A, Mok, VC, Leung, TW, Wong, KS. Significance of good collateral compensation in symptomatic intracranial atherosclerosis. Cerebrovasc Dis. 2012;33:517–24.CrossRefGoogle ScholarPubMed
Willie, CK, Macleod, DB, Shaw, AD, et al. Regional brain blood flow in man during acute changes in arterial blood gases. J Physiol. 2012;590:3261–75.CrossRefGoogle ScholarPubMed
Rudzinski, W, Swiat, M, Tomaszewski, M, Krejza, J. Cerebral hemodynamics and investigations of cerebral blood flow regulation. Nucl Med Rev Cent East Eur. 2007;10:29–42.Google ScholarPubMed
Spano, VR, Mandell, DM, Poublanc, J, et al. CO2 blood oxygen level-dependent MR mapping of cerebrovascular reserve in a clinical population: safety, tolerability, and technical feasibility. Radiology. 2013;266:592–8.CrossRefGoogle Scholar
Mandell, DM, Han, JS, Poublanc, J, et al. Quantitative measurement of cerebrovascular reactivity by blood oxygen level-dependent MR imaging in patients with intracranial stenosis: preoperative cerebrovascular reactivity predicts the effect of extracranial-intracranial bypass surgery. Am J Neuroradiol. 2011;32:721–7.CrossRefGoogle ScholarPubMed
Sobczyk, O, Battisti-Charbonney, A, Poublanc, J, et al. Assessing cerebrovascular reactivity abnormality by comparison to a reference atlas. J Cereb Blood Flow Metab. 2015;35:213–20.CrossRefGoogle ScholarPubMed
Mandell, DM, Han, JS, Poublanc, J, et al. Mapping cerebrovascular reactivity using blood oxygen level-dependent MRI in patients with arterial steno-occlusive disease: comparison with arterial spin labelling MRI. Stroke. 2008;39:2021–8.CrossRefGoogle Scholar
Slessarev, M, Han, J, Mardimae, A, et al. Prospective targeting and control of end-tidal CO2 and O2 concentrations. J Physiol. 2007;581:1207–19.CrossRefGoogle ScholarPubMed
Kretschmann, H, Weinrich, W. Cranial Neuroimaging and Clinical Neuroanatomy. 2nd ed., revised and expand edn. Stuttgart: Georg Thieme Verlag; 2004. pp. 375 Google Scholar
Kernan, WN, Ovbiagele, B, Black, HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:2160–236.CrossRefGoogle ScholarPubMed
Kim, JS, Bang, OY. Medical treatment of intracranial atherosclerosis: an update. J Stroke. 2017;19:261–70.CrossRefGoogle ScholarPubMed
Gupta, A, Chazen, JL, Hartman, M, et al. Cerebrovascular reserve and stroke risk in patients with carotid stenosis or occlusion: a systematic review and meta-analysis. Stroke. 2012;43:2884–91.CrossRefGoogle ScholarPubMed
Reinhard, M, Schwarzer, G, Briel, M, et al. Cerebrovascular reactivity predicts stroke in high-grade carotid artery disease. Neurology. 2014;83:1424–31.CrossRefGoogle ScholarPubMed
Derdeyn, CP, Chimowitz, MI, Lynn, MJ, et al. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): the final results of a randomised trial. Lancet. 2014;383:333–41.CrossRefGoogle ScholarPubMed
Fierstra, J, Poublanc, J, Han, JS, Silver, F, Tymianski, M, Crawley, AP. Steal physiology is spatially associated with cortical thinning. J Neurol Neurosurg Psychiatry. 2010;81:290–3.CrossRefGoogle ScholarPubMed
Fierstra, J, van Niftrik, C, Warnock, G, et al. Staging hemodynamic failure with blood oxygen-level-dependent functional magnetic resonance imaging cerebrovascular reactivity. Stroke. 2018;49:621–9.CrossRefGoogle ScholarPubMed