Cerebral Collateral Flow Research Articles

Abstract TP127: Impact of Smoking on Collateral Blood Flow in Patients With Acute Ischemic Stroke With Large Cerebral Artery Embolic Occlusion

Introduction: Good collateral flow is associated with improved outcomes in acute embolic stroke. There is compelling data linking smoking to all types of stroke, with current smokers at a higher risk than former or never smokers. Smoking has, however, been shown to promote collaterals in coronary vascular bed in humans. It is unknown if there is a similar effect in cerebral collateral flow. We aimed to investigate if cigarette smoking was positively associated with collateral blood flow in a homogenous cohort of patients with acute large vessel occlusive embolic stroke. Methods: We identified all patients aged ≥18 with acute ischemic stroke showing embolic occlusion of ICA terminus/M1 MCA on admission CT angiography (CTA), between 2008 to 2018, through an institutional database. Patients with chronic occlusions and stenotic lesions were excluded. Individual CTAs were independently reviewed by two trained investigators to calculate collateral scores of the affected hemisphere using the modified Tan scale (0-4) as a reference. Details of cigarette smoking history were obtained from the electronic medical records. Patients were grouped into smokers (former and current smokers) and never smokers. Odds ratios (OR) and their 95% confidence intervals (CI) were estimated, and all tests were considered significant when P<0.05. Results: Of the 612 patients identified through the database, 429/612 patients (mean age 71±16 years, 45% [194/429] women) satisfied the inclusion criteria. 64.8% (278/429) had a positive history of smoking with an average of 47±12 pack-years. There was a significant association between good collateral scores (≥2) with smoking history (OR 1.74 CI 1.17-2.61, P=0.006). This trend remained significant even after comparing raw collateral scores (0-4) ( P=0.006, Spearman’s ρ=0.22). However, number of pack-years and collateral scores exhibited no statistically significant relationship (P=0.6). Conclusions: Our study shows that patients who have ever smoked have higher intracranial collateral vessel scores in the event of an acute embolic stroke. Increased impedance and reduced cerebral blood flow resulting from cigarette smoking may stimulate collateral recruitment in cerebral pial circulation, similar to the effect in coronary bed.

Predictors of poor cerebral collaterals and cerebrovascular reserve in patients with chronic total carotid occlusion

Background: This study aims to investigate the relationship between cerebrovascular reserve (CVR) capacity, as measured by single-photon emission computed tomography (SPECT) and collateral blood flow, according to a transcranial colour-coded duplex(TCCD), in patients with symptomatic total carotid occlusion (TCO). Additionally, the study aims to determine whether vascular risk factors have an effect on collateral blood flow, as well as on the CVR.Methods: Thirty-four patients with chronic TCO, diagnosed by carotid duplex scanning and confirmed by other vascular imaging modalities, who had ischaemic symptoms either as stroke or transient ischaemic attack, were subjected to clinical assessment, SPECT under dipyridamole stress, and grading of cerebral collateral blood flow using TCCD. Demographics and vascular risk factors were correlated with SPECT and TCCD findings.Results: CVR showed a significant positive correlation with the intensity of collaterals with P value <0.001 and a Spearman correlation coefficient of 0.686. Hypertension was the only predictor of poor collaterals (p value =0.049; OR =11.5 with 95% CI 1.01–131.16).Smoking was predictive of poor CVR as measured by qualitative SPECT (p value =0.02; OR =13.2 with 95% CI 1.4–120.6).Conclusion: Cerebral collaterals have an important role in the maintenance of CVR in patients with TCO. Preventive measures should be directed towards hypertension and smoking to preserve cerebral collateral patency and consequently improve CVR in patients with TCO.

Reversed ophthalmic artery flow following ischemic stroke: a possible predictor of outcomes following carotid artery stenting

ABSTRACTStroke is the leading cause of death worldwide and stenosis of the carotid artery accounts for more than half of all cases. Carotid duplex is an effective non-invasive ultrasound test which identifies stroke patients with moderate to severe carotid stenosis who are candidates for preventative intervention to reduce the risk of recurrence.In patients with moderate to severe carotid stenosis, reversed ophthalmic artery flow (ROAF) is often observed at the time of the carotid duplex scan. In this study, we investigated whether ROAF, denoting exhaustion of cerebral collateral flow in ischemic stroke patients affected mid-term functional outcomes following carotid artery stenting (CAS) procedures.In total, 144 consecutive patients with a first episode of ischemic stroke and subsequent CAS procedure conducted between January 2010 and November 2014 at Changhua Christian Hospital, Taiwan were included. Clinical data were obtained by medical record review. Disability was assessed at two time points by utilising the Barthel Index (BI) and modified Rankin Scale (mRS) before CAS and 12 months post-CAS.Among 85 patients presenting without ROAF, 48/85 (56.4%) had improved mRS scores following stenting. The condition remained unchanged (stationary) in 36/85 (43.5%) patients after stenting and one patient exhibited deteriorated condition 1/85(1.1%).In contrast, among the 59 patients presenting with ROAF, 24/59 (40.6%) had improved mRS score following stenting. The condition remained unchanged (stationary) in the remaining 35/59 (59.3%) patients after stenting, and no patient exhibited deteriorated condition 0/59 (0 %).This study provides evidence that CAS is a valid and effective treatment option regardless of whether patients exhibited ROAF or not. Patients without ROAF were significantly more likely to have improved mid-term functional outcomes compared to those with ROAF. In the group without ROAF admission, CRP may play a role in predicting subsequent functional outcomes, whereas admission Barthel Index was a predictor of outcome in the ROAF group.

Assessment of the Cerebral Hemodynamic Benefits of Carotid Artery Stenting for Patients with Preoperative Hemodynamic Impairment Using Cerebral Single Photon Emission Computed Tomography (SPECT) and Carbon Dioxide Inhalation.

BackgroundThe aim of this study was to evaluate the effects of carotid artery angioplasty and carotid artery stenting (CAS) on cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) in patients with preoperative cerebrovascular hemodynamic impairment.Material/MethodsSeventeen patients with unilateral severe internal carotid artery (ICA) stenosis and ipsilateral CVR impairment underwent CAS. CBF and CVR were measured by single photon emission computed tomography (SPECT) with inhalation of carbon dioxide (CO2) one week before and three months after CAS. Sixty-eight ROIs in the middle cerebral artery (MCA) territory were analyzed in 17 patients.ResultsBefore CAS, CVR was impaired in all ROIs. CBF was impaired in 16 ROIs (23.5%). The percentage of ROIs with impaired CBF was significantly increased in patients with ≥90% carotid artery stenosis (p=0.047) without collateral flow through the circle of Willis (p=0.005). CAS significantly increased CVR in ROIs with a normal preoperative CBF and impaired CVR, indicating mild hemodynamic impairment (0.9±6.7% vs. 4.9±8.6%) (p=0.014). CAS significantly increased CBF in ROIs with preoperative impaired CBF and impaired CVR, indicating severe hemodynamic impairment (79.1±7.5% vs. 86.7±10.0%) (p<0.001). Following CAS, ROIs with normal CBF and impaired CVR had a significantly increased percentage of improved CVR (p=0.047); ROIs with impaired CBF and impaired CVR had a significantly increased percentage of improved CBF (p=0.027).ConclusionsThe severity of preoperative hemodynamic impairment, which is related to the degree of carotid artery stenosis and cerebral collateral flow, may influence hemodynamic benefits by CAS.

Abstract 76: Long-term Regular Remote Ischemic Conditioning Promotes Arterial Collateral Opening and Reconstruction in Patients with Intracranial Atherosclerotic Stenosis

Background and purpose: A previous study (NCT01570231) showed that long-term remote ischemic preconditioning (RIPC) prevents cerebral ischemic events in patients with symptomatic intracranial atherosclerotic stenosis (SIAS). This study aims to further evaluate its beneficial impact on cerebral collateral flow and its underlying mechanisms. Methods: Patients with SIAS were randomized to RIPC group (n=30) or sham group (n=28, NCT01570231). RIPC was achieved by blocked bilateral arm arterial blood flow 5-min with double cuffs inflated to 200mmHg, followed by deflation for 5-min, and this was repeated 5 times automatically in every training cycle by the RIPC training device. Sham-RIPC was done in the same fashion with the exception of Inflating pressure at 60mmHg, which make the subjects feel a pressure but does not block the blood flow. RIPC and sham-RIPC were performed twice a day for 180 consecutive days. All subjects received standard background medical treatment. Status of cerebral collateral flow was evaluated with the regional leptomeningeal collateral (rLMC) score either by MRA and/or CTA. Plasma levels of VEGF were measured by ELISA, and circulating endothelial progenitor cells (EPCs) marked of CD45-CD133+CD34+VEGF-R2+ were quantified by flow cytometry from the mononuclear cells, which were isolated from venous blood samples at Day 0, Day 30 and 180. Results: 23(76.7%) patients in RIPC and 19(67.9%) in sham group completed MRA evaluation, and 7(23.5%) in RIPC and 9(32.1%) sham group finished CTA evaluation. The average rLMC score were 0.233±0.37, 1.133±0.24, and 2.066±0.31 in RIPC versus 0.214±0.35, 0.535±0.49 and 0.964±0.34 in sham group at Day0, 30 and 180(p 0 &gt;0.05, p 30 &lt;0.01, and p 180 &lt;0.01). Plasma VEGF levels were 33.03±7.41, 136.88±60.79, and 285.37±77.75 in RIPC group versus 34.31±8.41, 66.85±16.89, and 93.86±18.97 in sham group (p 0 &gt;0.05, p 30 &lt;0.01, and p 180 &lt;0.001). The ratios of EPCs were 0.018±0.012%, 0.086±0,015%, and 0.115±0.013% in RIPC group versus 0.019±0,011%, 0.045±0,012%, and 0.067±0,012% in sham group. Conclusions: Long-term regular RIPC appears to accelerate cerebral collateral open and vascular remodeling. It is associated with the elevated level of plasma VEGF and an increased ratio of circulating EPCs.

Impaired Collateral Flow Compensation During Chronic Cerebral Hypoperfusion in the Type 2 Diabetic Mice.

The presence of collaterals is associated with a reduced risk of stroke and transient ischemic attack in patients with steno-occlusive carotid artery disease. Although metabolic syndrome negatively impacts collateral status, it is unclear whether and to what extent type 2 diabetes mellitus affects cerebral collateral flow regulation during hypoperfusion. We examined the spatial and temporal changes of the leptomeningeal collateral flow and the flow dynamics of the penetrating arterioles in the distal middle cerebral artery and anterior cerebral artery branches over 2 weeks after unilateral common carotid artery occlusion (CCAO) using optical coherent tomography in db/+ and db/db mice. We also assessed the temporal adaptation of the circle of Willis after CCAO by measuring circle of Willis vessel diameters. After unilateral CCAO, db/db mice exhibited diminished leptomeningeal collateral flow compensation compared with db/+ mice, which coincided with a reduced dilation of distal anterior cerebral artery branches, leading to reduced flow not only in pial vessels but also in penetrating arterioles bordering the distal middle cerebral artery and anterior cerebral artery. However, no apparent cell death was detected in either strain of mice during the first week after CCAO. db/db mice also experienced a more severe early reduction in the vessel diameters of several ipsilateral main feeding arteries in the circle of Willis, in addition to a delayed post-CCAO adaptive response by 1 to 2 weeks, compared with db/+ mice. Type 2 diabetes mellitus is an additional risk factor for hemodynamic compromise during cerebral hypoperfusion, which may increase the severity and the risk of stroke or transient ischemic attack.

The Dual Role of Cerebral Autoregulation and Collateral Flow in the Circle of Willis After Major Vessel Occlusion.

Ischaemic stroke is a leading cause of death and disability. Autoregulation and collateral blood flow through the circle of Willis both play a role in preventing tissue infarction. To investigate the interaction of these mechanisms a one-dimensional steady-state model of the cerebral arterial network was created. Structural variants of the circle of Willis that present particular risk of stroke were recreated by using a network model coupled with: 1) a steady-state physiological model of cerebral autoregulation; and 2) one wherein the cerebral vascular bed was modeled as a passive resistance. Simulations were performed in various conditions of internal carotid and vertebral artery occlusion. Collateral flow alone is unable to ensure adequate blood flow ([Formula: see text] normal flow) to the cerebral arteries in several common variants during internal carotid artery occlusion. However, compared to a passive model, cerebral autoregulation is better able to exploit available collateral flow and maintain flows within [Formula: see text] of baseline. This is true for nearly all configurations. Hence, autoregulation is a crucial facilitator of collateral flow through the circle of Willis. Impairment of this response during ischemia will severely impact cerebral blood flows and tissue survival, and hence, autoregulation should be monitored in this situation.

Multi-site laser Doppler flowmetry for assessing collateral flow in experimental ischemic stroke: Validation of outcome prediction with acute MRI

High variability in infarct size is common in experimental stroke models and affects statistical power and validity of neuroprotection trials. The aim of this study was to explore cerebral collateral flow as a stratification factor for the prediction of ischemic outcome. Transient intraluminal occlusion of the middle cerebral artery was induced for 90 min in 18 Wistar rats. Cerebral collateral flow was assessed intra-procedurally using multi-site laser Doppler flowmetry monitoring in both the lateral middle cerebral artery territory and the borderzone territory between middle cerebral artery and anterior cerebral artery. Multi-modal magnetic resonance imaging was used to assess acute ischemic lesion (diffusion-weighted imaging, DWI), acute perfusion deficit (time-to-peak, TTP), and final ischemic lesion at 24 h. Infarct volumes and typology at 24 h (large hemispheric versus basal ganglia infarcts) were predicted by both intra-ischemic collateral perfusion and acute DWI lesion volume. Collateral flow assessed by multi-site laser Doppler flowmetry correlated with the corresponding acute perfusion deficit using TTP maps. Multi-site laser Doppler flowmetry monitoring was able to predict ischemic outcome and perfusion deficit in good agreement with acute MRI. Our results support the additional value of cerebral collateral flow monitoring for outcome prediction in experimental ischemic stroke, especially when acute MRI facilities are not available.

Clinical Significance of Fluid-Attenuated Inversion Recovery Vascular Hyperintensities in Borderzone Infarcts.

Fluid-attenuated inversion recovery vascular hyperintensities (FVHs) are seen in some cases with cerebral hemodynamic impairment and collateral flow. Because the worst outcomes of patients with borderzone infarcts were mainly correlated with impaired hemodynamics, the presence of FVH might provide another clue for predicting the prognosis of patients with borderzone infarcts. We reviewed 1377 consecutive patients with ischemic stroke. Cortical borderzone (CBZ) and internal borderzone infarcts were selected based on diffusion-weighted imaging. FVHs were defined as tubular- or serpentine-shaped hyperintensities in the subarachnoid space. We investigated the clinical significance of FVHs in borderzone-infarcted patients. Among 87 patients with borderzone infarcts, the presence of FVH was observed in 30 (34.5%). We identified 62 patients with CBZ infarcts and 25 patients with internal borderzone infarcts. In the cases with CBZ infarcts, the initial National Institutes of Health Stroke Scale scores and the portions of nonfavorable outcome at 3 months in the FVH(+) group were significantly higher than in the FVH(-) group (P<0.05 and P<0.001, respectively). Unlike the cases with CBZ infarcts, there were no significant differences of these clinical features between the FVH(+) group and the FVH(-) group in the patients with internal borderzone infarcts. The findings of FVH are associated with relatively severe clinical presentation and nonfavorable prognosis in patients with CBZ infarcts, but not in patients with internal borderzone infarcts. The presence of FVH may help to identify CBZ-infarcted patients who require close observation and hemodynamic control.

In vitro experiments of cerebral blood flow during aspiration thrombectomy: potential effects on cerebral perfusion pressure and collateral flow

BackgroundMechanical thrombectomy with stent retriever devices is associated with significantly better outcomes than thrombolysis alone in the treatment of acute ischemic stroke. Thrombus aspiration achieves high patency rates, but clinical...

Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.

Extent of collateralization predicting symptomatic cerebral vasospasm among pediatric patients: correlations among angiography, transcranial Doppler ultrasonography, and clinical findings.

Although the development and prevalence of cerebral vasospasm (CV) has been extensively investigated in adults, little data exist on the development of CV in children. The authors hypothesized that even though children have highly vasoreactive arteries, because of a robust cerebral collateral blood flow, they rarely develop symptomatic CV. The authors retrospectively reviewed their university hospital's neurointerventional database for children (that is, patients ≤ 18 years) who were examined or treated for aneurysmal or traumatic subarachnoid hemorrhage (SAH) during the period 1990-2013. Images from digital subtraction angiography (DSA) were analyzed for the extent of CV and collateralization of the cerebral circulation. Results from transcranial Doppler (TCD) ultrasonography were correlated with those from DSA. Cerebral vasospasm on TCD ultrasonography was defined according to criteria developed for adults. Clinical outcomes of CV were assessed with the pediatric modified Rankin Scale (mRS). Among 37 children (21 boys and 16 girls ranging in age from 8 months to 18 years) showing symptoms of an aneurysmal SAH (comprising 32 aneurysms and 5 traumatic pseudoaneurysms), 17 (46%) had CV confirmed by DSA; CV was mild in 21% of these children, moderate in 50%, and severe in 29%. Only 3 children exhibited symptomatic CV, all of whom had poor collateralization of cerebral vessels. Among the 14 asymptomatic children, 10 (71%) showed some degree of vessel collateralization. Among 16 children for whom TCD data were available that could be correlated with the DSA findings, 13 (81%) had CV according to TCD criteria. The sensitivity and specificity of TCD ultrasonography for diagnosing CV were 95% and 59%, respectively. The time to CV onset detected by TCD ultrasonography was 5 ± 3 days (range 2-10 days). Twenty-five (68%) of the children had good long-term outcomes (that is, had mRS scores of 0-2). Children have a relatively high incidence of angiographically detectable, moderate-to-severe CV. Children rarely develop symptomatic CV and have good long-term outcomes, perhaps due to robust cerebral collateral blood flow. Criteria developed for detecting CV with TCD ultrasonography in adults overestimate the prevalence of CV in children. Larger studies are needed to define TCD ultrasonography-based CV criteria for children.

The Impact of Absent A1 Segment on Ischemic Stroke Characteristics and Outcomes

A1 segment is the proximal portion of anterior cerebral artery. Absence of the A1 segment can compromise anterior cerebral collateral blood flow. Few studies have examined the association of an absent A1 segment and ischemic stroke outcome. We sought to determine the association between A1 absence and affected vessel territory, stroke volume, and outcomes among patients with acute ischemic stroke (AIS). A retrospective review of prospectively identified patients with AIS from July 2008 to March 2013 was performed. Patients without intracranial vascular imaging were excluded. We compared patients with absent A1 to patients with bilateral A1 segments in terms of demographics, stroke severity (as measured by National Institute of Health Stroke Scale [NIHSS]), vascular distribution, and in-hospital mortality using the chi-square test and logistic regression. Of the 1146 patients with AIS and intracranial vascular imaging, 5.9% patients (n = 68) had absent A1. Compared with other AIS patients, those with absent A1 were older (65 vs. 63 years old, respectively, P = .016). There was no difference between groups in terms of the vascular distribution or the side of the stroke. The median volume of the infracted tissue was similar across the groups even when it was stratified according to the Treatment of Acute Stroke Trial classification. Patients with an absent A1 had twice higher odds of in-hospital mortality (odds ratio, 2.4; 95% confidence interval, 1.1-5.2; P = .028); however, significance was lost after adjusting to age, NIHSS at baseline, and glucose on admission. Other outcome measures were similar across the groups. In our sample, patients with an absent A1 segment did not have a specific vascular distribution, larger infarct volume, or worse outcomes.

Nonenhanced ECG-gated time-resolved 4D Steady-state free precession (SSFP) MR angiography (MRA) for assessment of cerebral collateral flow: comparison with digital subtraction angiography (DSA)

To evaluate a nonenhanced time-resolved 4D SSFP MRA for dynamic visualization of intracranial collateral blood flow. 22 patients (59.0 ± 11.8 years) with steno-occlusive disease of brain-supplying arteries were included in this study. 4D SSFP MRA of the intracranial arteries was acquired with 15 temporal phases and a temporal resolution of 115 ms using 1.5 T MR. Cerebral DSA served as the reference standard and was available in all patients. Nonenhanced 4D SSFP MRA allowed for detailed dynamic visualization of blood flow in the circle of Willis and its branches in 21 of 22 (95.5%) patients. Collateral flow was excluded with both 4D SSFP MRA and DSA in 4 patients. In 17 patients, DSA detected anterior collateral flow (n = 8), posterior collateral flow via the right (n = 8) and left (n = 7) posterior communicating artery as well as patent EC-IC bypasses (n = 8). 29 of 31 collateral flow pathways were visualized by 4D SSFP MRA. As compared to DSA, 4D SSFP MRA showed a high sensitivity (92.3%), specificity (100%), positive predictive value (100%) and negative predictive value (95.2%) for visualization of intracranial collateral flow. 4D SSFP MRA is a promising non-invasive imaging technique for dynamic visualization of intracranial collateral flow.

Diagnosis and therapy for an extracranial carotid aneurysm

Objective To describe the diagnostic means and therapy employed in three cases of extracranial carotid aneurysms. Methods Retrospective analysis of three cases. Results For the diagnosis we obtained real-time pictures of each aneurysm by color Doppler ultrasonography before the angiography. Based on the result of cerebral collateral flow evaluation, ligation of both ends of the aneurysm was performed in one case, embolization of the artery in another, and resection of the aneurysm in the other; vascular reconstruction was not necessary. Although a carotid artery balloon occlusion test must be done before the operation, color Doppler ultrasonography and/or a transcranial color Doppler-guided Matas’ test were performed instead, because these patients needed immediate management. Conclusion The diagnostic procedures were very useful to decide what action to take in such urgent cases.

Diagnosing Cerebral Collateral Flow Patterns: Accuracy of Non-Invasive Testing

Objective: With routine use of non-invasive methods to assess the internal carotid artery, it becomes increasingly important to clarify the diagnostic accuracy of transcranial Doppler (TCD) ultrasound and magnetic resonance angiography (MRA) compared with intra-arterial digital subtraction angiography (iaDSA) for the detection of collateral flow via the major intracerebral collateral branches. Subjects and Methods: In a prospective study, we compared TCD via a temporal bone window and MRA (flow direction sensitive phase contrast and time of flight) examinations of the intracranial collateral flow with iaDSA in a cohort of 97 consecutive patients with recent transient or minor disabling cerebral ischaemia associated with an occlusion of the carotid artery (38 contralateral stenosis >70%). Results: iaDSA allowed the evaluation of collateral flow via the anterior and posterior circle of Willis in 97 and 67 patients, respectively, TCD in 76 of 97 and 66 of 67 patients, MRA in 95 of 97 and 66 of 67 patients. MRA and TCD collateral flow measurements via the anterior part of the circle of Willis yielded a sensitivity of 83 and 82%, a specificity of 77 and 79% and a similar accuracy of 80%. MRA and TCD collateral flow measurements via the posterior communicating artery yielded a sensitivity of 33 and 76%, a specificity of 88 and 47% and an accuracy of 47 and 68%. Conclusion: As compared with iaDSA, combined MRA and TCD has a moderate to good diagnostic value for the examination of intracranial collateral flow in patients with symptomatic carotid occlusion.

Dynamic cerebral autoregulation and collateral flow patterns in patients with severe carotid stenosis or occlusion.

The quality of collateral blood supply in carotid disease is pivotal for the resulting hemodynamic compromise. However, the interrelation between different patterns of collateral blood flow and actual impairment of cerebral autoregulation (CAR) has not been analyzed so far. Dynamic CAR was assessed noninvasively by the phase shift between respiratory-induced 0.1-Hz oscillations of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) in 101 patients with severe unilateral carotid stenosis (> or = 75%) or occlusion. CO(2)-vasomotor reactivity was assessed via inhalation of 7% CO(2). Spontaneously activated collaterals via primary (anterior/posterior communicating artery, type I, n = 65) and secondary (ophthalmic artery / leptomeningeal with or without primary pathways, group II, n = 24) pathways were assessed by transcranial Doppler/duplex sonography. Signs of functional stenosis in the anterior collateral pathways were subsumed under type III (n = 12). Best dynamic CAR (phase shift) on affected sides was observed for type I (n = 65), in which values did not differ significantly from contralateral sides. Reduced phase shift values were present in type II; poorest values were observed for type III. CO(2)-reactivity differed mainly between type I and the other types. A less distinct differentiation of autoregulatory impairment was found when dividing patients into groups of different degrees of stenosis. Symptomatic patients (previous TIA/stroke) were significantly less frequent in the group with type I collateral flow and had significantly lower phase shift and CO(2)-reactivity values. In conclusion, we found that dynamic CAR is substantially impaired if secondary collateral pathways are activated or if functional stenosis in the activated anterior collateral pathway is present. These hemodynamic constellations are also associated with a higher proportion of clinically symptomatic patients. Determination of dynamic CAR by transfer function analysis represents a convenient, sensitive method for detection of cerebral hemodynamic compromise in obstructive carotid disease.

Phenylephrine-induced hypertension does not improve outcome after closed head trauma in rats.

Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7+/-2 and 1.033+/-0.007 without phenylephrine and 8+/-2 and 1.035+/-0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335+/-92 mm3 without phenylephrine and 357+/-154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma.

Phenylephrine-Induced Hypertension Does Not Improve Outcome After Closed Head Trauma in Rats

Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7 +/- 2 and 1.033 +/- 0.007 without phenylephrine and 8 +/- 2 and 1.035 +/- 0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335 +/- 92 mm3 without phenylephrine and 357 +/- 154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. Implications: Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma. (Anesth Analg 1998;87:574-8)

Effects of Etomidate Administration on Cerebral Collateral Flow

Effects of Etomidate Administration on Cerebral Collateral Flow