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The vascular steal phenomenon is an incomplete contributor to negative cerebrovascular reactivity in patients with symptomatic intracranial stenosis.

ABSTRACT: 'Vascular steal' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n=40) underwent a multimodal 3.0T MRI protocol including structural (T1-weighted and T2-weighted fluid-attenuated inversion recovery) and hemodynamic (BOLD and CBF-weighted arterial spin labeling) functional MRI during room air and hypercarbic gas administration. CBF changes in regions demonstrating negative BOLD reactivity were recorded, as well as clinical correlates including symptomatic hemisphere by infarct and lateralizing symptoms. Fifteen out of forty participants exhibited negative BOLD reactivity. Of these, a positive relationship was found between BOLD and CBF reactivity in unaffected (stenosis degree<50%) cortex. In negative BOLD cerebrovascular reactivity regions, three patients exhibited significant (P<0.01) reductions in CBF consistent with vascular steal; six exhibited increases in CBF; and the remaining exhibited no statistical change in CBF. Secondary findings were that negative BOLD reactivity correlated with symptomatic hemisphere by lateralizing clinical symptoms and prior infarcts(s). These data support the conclusion that negative hypercarbia-induced BOLD responses, frequently assigned to vascular steal, are heterogeneous in origin with possible contributions from autoregulation and/or metabolism.

SUBMITTER: Arteaga DF

PROVIDER: S-EPMC4158662 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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The vascular steal phenomenon is an incomplete contributor to negative cerebrovascular reactivity in patients with symptomatic intracranial stenosis.

Arteaga Daniel F DF Strother Megan K MK Faraco Carlos C CC Jordan Lori C LC Ladner Travis R TR Dethrage Lindsey M LM Singer Robert J RJ Mocco J J Clemmons Paul F PF Ayad Michael J MJ Donahue Manus J MJ

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 20140611 9

'Vascular steal' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n=40) underwent a multimodal 3.0T MRI protocol including structural (T1-weighted and T2-weighted fluid-attenua ...[more]

PMID: 24917040

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Project description:In patients with carotid artery stenosis (CAS), the risk of stroke, its severity, and response to revascularization are strongly related to the availability of collateral blood flow. Unfortunately, there is poor agreement between observers in assessing collateral flow using flow-based imaging. We used changes in blood-oxygen-level-dependent (BOLD) MRI as a surrogate of changes in regional cerebral blood flow in response to a hypercapnic stimulus [i.e., cerebrovascular reactivity (CVR)] as indicating flow reserve ipsilateral to CAS. We hypothesized that some patients with hemodynamically significant CAS develop functional collateral flow as indicated by normalization of ipsilateral CVR. We identified 55 patients in our CVR database with various degrees of CAS assessed by angiography and classed them as <50% stenosis, 50-69% stenosis, 70-90% stenosis, >90% stenosis, and full occlusion. CVR was measured as the change in BOLD signal in response to changes in end-tidal partial pressure of CO2 (Δ BOLD/Δ PETCO2) and normalized voxel-wise relative to the mean and standard deviation of the CVR in the corresponding voxels of an atlas of 46 healthy controls (CVR z scores). CVR and z scores were then averaged over gray matter (GM) and white matter (WM) on each side of the middle cerebral artery (MCA) territory. As hypothesized, CVR varied for each severity of CAS. Ipsilateral MCA territory CVR was less than normal in each class, including that with <50% stenosis (Student t-test, two-tailed; p = 0.0014 for GM and p = 0.030 for WM), with a trend of decreasing average CVR with increasing stenosis. Remarkably, the considerable individual variability in MCA CVR included some patients with normal CVR in each class - including that with complete occlusion. We conclude that, in general, CAS depresses downstream vascular reserve, but the extent of collateralization is highly variable and not predictable from the degree of stenosis, including both <50% stenosis and complete occlusion. CVR may be the more reliable marker for recruitable collateral blood flow than degree of CAS.

Project description:AimsWe performed a meta-analysis to indirectly compare the treatment effectiveness of balloon angioplasty and stenting for patients with intracranial arterial stenosis.MethodsLiterature searches were performed in well-known databases to identify eligible studies published before January 04, 2021. The incidence of restenosis, transient ischemic attack (TIA), stroke, death, and dissection after balloon angioplasty or stenting were pooled. An indirect comparison of balloon angioplasty vs. stenting was performed, and the ratios of incidence (RIs) with 95% confidence intervals (CIs) were calculated using the random-effects model.Results120 studies that recruited 10,107 patients with intracranial arterial stenosis were included. The pooled incidence of restenosis after balloon angioplasty and stenting were 13% (95%CI: 8-17%) and 11% (95%CI: 9-13%), respectively, with no significant difference between them (RI: 1.18; 95%CI: 0.78-1.80; P = 0.435). Moreover, the pooled incidence of TIA after balloon angioplasty and stenting was 3% (95%CI: 0-6%) and 4% (95%CI: 3%-5%), and no significant difference was observed (RI: 0.75; 95%CI: 0.01-58.53; P = 0.897). The pooled incidence of stroke after balloon angioplasty and stenting was 7% (95%CI: 5-9%) and 8% (95%CI: 7-9%), respectively, and the difference between groups was found to be statistically insignificant (RI: 0.88; 95%CI: 0.64-1.20; P = 0.413). Additionally, the pooled incidence of death after balloon angioplasty and stenting was 2% (95%CI: 1-4%) and 2% (95%CI: 1-2%), with no significant difference between groups (RI: 1.00; 95%CI: 0.44-2.27; P = 1.000). Finally, the pooled incidence of dissection after balloon angioplasty and stenting was 13% (95%CI: 5-22%) and 3% (95%CI: 2-5%), respectively, and balloon angioplasty was associated with a higher risk of dissection than that with stenting for patients with intracranial arterial stenosis (RI: 4.33; 95%CI: 1.81-10.35; P = 0.001).ConclusionThis study found that the treatment effectiveness of balloon angioplasty and stenting were similar for patients with symptomatic intracranial arterial stenosis.

Project description:OBJECTIVES:The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. DESIGN:Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. SETTING:University laboratory. SUBJECTS:Male Sprague-Dawley rats. INTERVENTIONS:At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (? intracranial pressure/? mean arterial pressure) and induced cerebrovascular reactivity (? cerebral blood flow/? mean arterial pressure). MEASUREMENTS AND MAIN RESULTS:At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). CONCLUSIONS:Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.

Project description:Background Comprehensive hemodynamic impairment mapping using blood oxygenation-level dependent (BOLD) cerebrovascular reactivity (CVR) can be used to identify hemodynamically relevant symptomatic unilateral carotid artery disease. Methods and Results This prospective cohort study was conducted between February 2015 and July 2020 at the Clinical Neuroscience Center of the University Hospital Zurich, Zurich, Switzerland. One hundred two patients with newly diagnosed symptomatic unilateral internal carotid artery (ICA) occlusion or with 70% to 99% ICA stenosis were included. An age-matched healthy cohort of 12 subjects underwent an identical BOLD functional magnetic resonance imaging examination. Using BOLD functional magnetic resonance imaging with a standardized CO2 stimulus, CVR impairment was evaluated. Moreover, embolic versus hemodynamic ischemic patterns were evaluated on diffusion-weighted imaging. Sixty-seven patients had unilateral ICA occlusion and 35 patients unilateral 70% to 99% ICA stenosis. Patients with ICA occlusion exhibited lower whole-brain and ipsilateral hemisphere mean BOLD-CVR values as compared with healthy subjects (0.12±0.08 versus 0.19±0.04, P=0.004 and 0.09±0.09 versus 0.18±0.04, P<0.001) and ICA stenosis cohort (0.12±0.08 versus 0.16±0.05, P=0.01 and 0.09±0.09 versus 0.15±0.05, P=0.01); however, only 40 (58%) patients of the cohort showed significant BOLD-CVR impairment. Conversely, there was no difference in mean BOLD-CVR values between healthy patients and patients with ICA stenosis, although 5 (14%) patients with ICA stenosis showed a significant BOLD-CVR impairment. No significant BOLD-CVR difference was discernible between patients with hemodynamic ischemic infarcts versus those with embolic infarct distribution (0.11±0.08 versus 0.13±0.06, P=0.12). Conclusions Comprehensive BOLD-CVR mapping allows for identification of hemodynamically relevant symptomatic unilateral carotid artery stenosis or occlusion.

Project description:OBJECTIVE:Cerebrovascular reactivity (CR) is a mechanism that maintains stable blood flow supply to the brain. Pressure reactivity index (PRx), the correlation coefficient between slow waves of invasive arterial blood pressure (ABP) and intracranial pressure (ICP) has been validated for CR assessment. However, in clinical ward, not every subarachnoid hemorrhage (SAH) patient has invasive ABP monitoring. Pulse transit time (PTT), the propagation time of a pulse wave travelling from the heart to peripheral arteries, has been suggested as a surrogate measure of ABP. In this study, we proposed to use PTT instead of invasive ABP to monitor CR. APPROACH:Forty-five SAH patients with simultaneous recordings of invasive ABP, ICP, oxygen saturation level (SpO2) and electrocardiograph (ECG) were included. PTT was calculated as the time from the ECG R-wave peak to the onset of SpO2. PTT based pressure reactivity index (tPRx) was calculated as the correlation coefficient between slow waves of PTT and ICP. Wavelet tPRx (wtRx) was calculated as the cosine of wavelet phase shift between PTT and ICP. Meanwhile, PRx and wPRx were also calculated using invasive ABP and ICP as input. MAIN RESULTS:The result showed a negative relationship between PTT and ABP (r??=??-0.58, p???<??0.001). tPRx negatively correlated with PRx (r??=??-0.51, p???=??0.003). Wavelet method correlated well with correlation method demonstrated through positive relationship between wPRx and PRx (r??=??0.82, p???<??0.001) as well as wtPRx and tPRx (r??=??0.84, p???<??0.001). SIGNIFICANCE:PTT demonstrates great potential as a useful tool for CR assessment when invasive ABP is unavailable. Key points • Pulse transit time (PTT), defined as the propagation time of a pulse wave travelling from the heart to the peripheral arteries, has been proposed as a surrogate measure of ABP. The relationship between PTT and ABP in SAH patients remains unknown. • Cerebrovascular reactivity (CR) assessment through PTT has advantages over invasive ABP, as it avoids bleeding and infection risk, and can be used outside of the ICU. • We introduced a new method to assess CR using PTT and ICP through correlation based method and wavelet based method. • We found that beat-to-beat PTT was negatively related with invasive ABP in SAH patients. A significant linear relationship exists between PTT-based CR parameter and a well validated method, PRx. PTT demonstrates great potential as a useful tool for CR assessment when invasive ABP is unavailable in SAH patients.

Dataset Information

The vascular steal phenomenon is an incomplete contributor to negative cerebrovascular reactivity in patients with symptomatic intracranial stenosis.

Publications

The vascular steal phenomenon is an incomplete contributor to negative cerebrovascular reactivity in patients with symptomatic intracranial stenosis.

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