Literature DB >> 12624217

Monitoring of cerebral vasodilatory capacity with transcranial Doppler carbon dioxide inhalation in patients with severe carotid artery disease.

Randolph S Marshall1, Tanja Rundek, Douglas M Sproule, Brian-Fred M Fitzsimmons, Shauna Schwartz, Ronald M Lazar.   

Abstract

BACKGROUND AND
PURPOSE: Cerebral vasodilatory capacity (CVC) testing with transcranial Doppler has been shown to be useful in the assessment of stroke risk in patients with symptomatic and asymptomatic internal carotid artery (ICA) stenosis and occlusion, but whether hemodynamic status improves, deteriorates, or remains the same over time is uncertain.
METHODS: Thirty-five patients with >or=80% carotid artery stenosis or complete occlusion underwent CVC testing at baseline and 6 months later. CVC was assessed by measuring the increase in ipsilateral middle cerebral artery mean flow velocity in response to 5% inhaled CO2. Continuous tracings of left and right middle cerebral artery flow velocity, heart rate, respiratory rate, and Pco2 were recorded and then analyzed offline. One-way analysis of variance was used to compare baseline CVC in symptomatic and asymptomatic patients with control subjects. A paired t test was used to compare CVC before and after revascularization. Also, chi2 analysis was used to compare rates of cerebrovascular events in patients with low compared with normal CVC over the 6-month period and in 14 patients whose ICAs were revascularized.
RESULTS: Patients with high-grade stenosis or occlusion of the ICA who had ICA disease had an average CVC of 2.4+/-1.9%/mm Hg Pco2; control subjects averaged 4.2+/-1.1%/mm Hg Pco2. (P=0.01). In the revascularization group, CVC increased from an average of 1.4+/-1.7%/mm Hg Pco2 at baseline to an average of 2.8+/-1.0%/mm Hg Pco2 after revascularization, significantly different from the spontaneous change in the natural history group over 6 months (P=0.003). Over the 6-month follow-up period, in the natural history group and in the treatment group after revascularization, 4 ischemic events occurred, all in patients with abnormal CVCs; abnormal CVC was associated with ischemic events (Fisher's exact test, P=0.03).
CONCLUSIONS: In a timeframe pertinent to clinical decision making and clinical trial outcomes, cerebral hemodynamic status may not be constant. A higher ischemic risk may be present in patients with severe carotid artery disease whose CVC is poor at baseline, becomes poor over 6 months, or fails to normalize after revascularization.

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Year:  2003        PMID: 12624217     DOI: 10.1161/01.STR.0000062351.66804.1C

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  22 in total

Review 1.  Statins and cerebral hemodynamics.

Authors:  Sotirios Giannopoulos; Aristeidis H Katsanos; Georgios Tsivgoulis; Randolph S Marshall
Journal:  J Cereb Blood Flow Metab       Date:  2012-08-29       Impact factor: 6.200

Review 2.  Treatment of carotid artery disease: endarterectomy or angioplasty?

Authors:  Adrian Marchidann; Randolph S Marshall
Journal:  Curr Neurol Neurosci Rep       Date:  2011-02       Impact factor: 5.081

Review 3.  Pumps, aqueducts, and drought management: vascular physiology in vascular cognitive impairment.

Authors:  Randolph S Marshall; Ronald M Lazar
Journal:  Stroke       Date:  2010-12-09       Impact factor: 7.914

Review 4.  Pathophysiology and therapy of experimental stroke.

Authors:  Konstantin-Alexander Hossmann
Journal:  Cell Mol Neurobiol       Date:  2006-05-19       Impact factor: 5.046

Review 5.  Functional imaging of motor recovery after stroke: remaining challenges.

Authors:  John W Krakauer
Journal:  Curr Neurol Neurosci Rep       Date:  2004-01       Impact factor: 5.081

6.  Cyclooxygenase-derived vasoconstriction restrains hypoxia-mediated cerebral vasodilation in young adults with metabolic syndrome.

Authors:  John W Harrell; William G Schrage
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-11-08       Impact factor: 4.733

7.  Autoregulation in the vertebrobasilar system using transcranial Doppler and CO2 inhalation.

Authors:  Olga Noskin; Samuel Trocio; Roque Sia; Emmanuel Carrera; Randolph S Marshall
Journal:  Int J Stroke       Date:  2009-04       Impact factor: 5.266

8.  Are the local blood oxygen level-dependent (BOLD) signals caused by neural stimulation response dependent on global BOLD signals induced by hypercapnia in the functional MR imaging experiment? Experiments of long-duration hypercapnia and multilevel carbon dioxide concentration.

Authors:  Y J Liu; C J Juan; C Y Chen; C Y Wang; M L Wu; C P Lo; M C Chou; T Y Huang; H Chang; C H Chu; M H Li
Journal:  AJNR Am J Neuroradiol       Date:  2007 Jun-Jul       Impact factor: 3.825

9.  Cerebrovascular reactivity predicts stroke in high-grade carotid artery disease.

Authors:  Matthias Reinhard; Guido Schwarzer; Matthias Briel; Claudia Altamura; Paola Palazzo; Alice King; Natan M Bornstein; Nils Petersen; Edith Motschall; Andreas Hetzel; Randolph S Marshall; Catharina J M Klijn; Mauro Silvestrini; Hugh S Markus; Fabrizio Vernieri
Journal:  Neurology       Date:  2014-09-12       Impact factor: 9.910

10.  Ultrasonographic markers of vascular risk in patients with asymptomatic carotid stenosis.

Authors:  Mauro Silvestrini; Claudia Altamura; Raffaella Cerqua; Patrizio Pasqualetti; Giovanna Viticchi; Leandro Provinciali; Luca Paulon; Fabrizio Vernieri
Journal:  J Cereb Blood Flow Metab       Date:  2013-01-30       Impact factor: 6.200

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