Improvement of Collateral Circulation after Arterial Thrombosis with Indomethacin Therapy

1980 ◽  
Vol 44 (02) ◽  
pp. 069-071 ◽  
Author(s):  
Cecelia Helenski ◽  
Robert G Schaub ◽  
Royce Roberts
Keyword(s):  
Blood Flow ◽  
Platelet Activation ◽  
Arterial Thrombosis ◽  
Collateral Circulation ◽  
Thromboxane A2 ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Vasoactive Substance ◽  
Aortic Thrombosis ◽  
Platelet Counts

SummaryWe compared development of feline hindlimb collateral circulation and coagulation changes 3 hours following aortic thrombosis in five non-treated and five indomethacin treated (20 mg/kg) cats. Coagulation changes were monitored with the one stage prothrombin time (OSPT), partial thromboplastin time (PTT), protamine sulfate dilution test for fibrin monomer (PSD), and platelet counts. Collateral circulation was assessed with aortograms. Significant changes in coagulation parameters with the exception of platelet counts were not observed in either group. Platelet counts of non-treated cats were reduced to 63 ± 5% of control while platelet counts of treated cats were 96 ± 3% of control. Aortograms of non-treated cats indicated poor hindlimb perfusion around the thrombus, while aortograms of indomethacin treated animals indicated significant blood flow to the hindlimbs through collateral channels. These results support a role for the platelet in post thrombosis vasospasms and suggest that anti-platelet therapy could have positive effects in reducing the extent of ischemic damage which follows arterial thrombosis.Several studies, using cat and dog models, have demonstrated a significant reduction of collateral blood flow can occur following formation of an occlusive arterial thrombus (1–5). The collateral flow which developed after thrombosis was significantly less than when occlusion was accomplished with mechanical methods such as ligation (1, 3, 4). This suggested the presence of a thrombus produced effects on blood vessels more complex than simple mechanical obstruction. Imhoff originally suggested that the inhibition of collateral flow which followed thrombosis was related to the release or formation of a vasoactive substance which would induce constriction of collateral source or re-entry vessels (1). Butler, in later studies, suggested that it was serotonin which was responsible for the post thrombosis inhibition of collateral blood flow (2). The involvement of serotonin would seem logical, since the majority of blood serotonin is found in the platelet (6), is released upon platelet activation (7-9), and is a potent vasoconstrictor (10). A mechanism for serotonin involvement has proposed that the platelets in the flowing blood come into contact with the thrombus, are activated and release serotonin (2–4). Consideration of the biochemistry of platelet activation makes it apparent that serotonin is neither the only nor the most powerful vasoactive substance released by the platelet. Thromboxane A2 (TxA) is a critical substance in the activation, release, and aggregation of platelets (11, 12, 13). Thromboxane A2 is a particularly powerful vasoconstrictor which would be a more likely candidate to produce the type of long lasting vasospasm necessary to reduce collateral flow in the post thrombosis state (11, 12, 13). The relationship between thromboxane A2 and serotonin is suggested by recent studies which demonstrate that serotonin can initiate thromboxane A2 release from canine and feline platelets (14). Therefore, serotonin could be an intermediate mechanism in the process of collateral inhibition.If this hypothesis is correct, then inhibition of TxA synthesis should prove as beneficial in improving collateral flow after thrombosis as serotonin antagonists. To test this hypothesis we examined the effect of indomethacin treatment on development of collateral circulation following aortic thrombosis. Indomethacin is a non-steroidal, anti-inflammatory drug which inhibits cyclooxygenase, the major enzyme in the PG and TxA synthetic pathway (15–19).

scholarly journals Depression of Collateral Blood Flow Following Arterial Thrombosis

1977 ◽  
Author(s):  
R.G. Schaub ◽  
K.M. Meyers
Keyword(s):  
Blood Flow ◽  
Arterial Thrombosis ◽  
Collateral Circulation ◽  
Therapeutic Interventions ◽  
Collateral Blood Flow ◽  
Flow Measurements ◽  
Clinical Consequences ◽  
Blood Flow Measurements ◽  
Collateral Vessels ◽  
Iliac Bifurcation

Permanent ligation of the feline aorta at the iliac bifurcation is followed by rapid opening of pre-existing collateral blood vessels. However, if ligation is combined with formation of a clot these protective collateral vessels do not function. This study was undertaken to determine if drugs which alter serotonin (5-HT) function can improve collateral blood flow after arterial thrombosis. Permanent ligations were placed at the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. Control cats (8) were acutely ligated. In all other cats a clot was produced in the aorta by injection of 0.1 ml of thromboplastin. Clotted cats were untreated (8); had blood 5-HT depleted using a single dose of reserpine (0.1 mg/kg i.m.) followed by para-chlorophenylalanine (p-CPA) (100 mg/kg orally) every 3 days (9); or were treated prior to surgery with a 5-HT antagonist cinanserin HCl (4 mg/kg i.v.) (8). Collateral circulation was determined by blood flow measurements and aortograms 3 days after occlusion of the aorta. The hindlimb blood flow of untreated clotted animals was 20% of the acutely ligated control animals 3 days following aortic occlusion. However, hindlimb blood flow was 90% of control in reserpine and p-CPA treated cats and 60% of control in cinanserin HCl treated cats. Blood flow measurements correlated with aortograms. These results suggest: (1) The clinical consequences of arterial thrombosis cannot be entirely attributed to mechanical occlusion of an artery, but may be due to depression of protective collateral blood flow induced by thrombosis, (2) Serotonin is an important factor in this depression of collateral blood flow, and (3) Isolation of the factors responsible for collateral inhibition could permit the development of therapeutic interventions.

Platelet Inhibitory Drugs Improve Collateral Blood Flow After Aortic Thrombosis

1981 ◽  
Author(s):  
R Schaub ◽  
C Helenski ◽  
K Gates ◽  
R Roberts
Keyword(s):  
Blood Flow ◽  
Contrast Media ◽  
Blood Vessels ◽  
Platelet Activation ◽  
Treated Group ◽  
Collateral Blood Flow ◽  
Clotting Factors ◽  
Iliac Arteries ◽  
Platelet Counts ◽  
Intermediate Response

Complete occlusion of the feline caudal aorta with a thrombus inhibits opening of collateral blood vessels to the hindlimbs. Our previous studies suggest this inhibition results from platelet activation. To test this hypothesis we evaluated the effect of indomethacin (I), aspirin (ASA), and prostacyclin (PGI) on collateral inhibition. Prothrombin times (OSPT), thromboplastin times (PTT), fibrin monomer (FM), and platelet counts were measured in 20 cats before the aortas were occluded by thrombosis. Five cats were untreated. Treatment of the others was started 1 hour prior to thombosis. Five cats received I (20 mg/kg i.v.), 6 cats received ASA (650 mg orally), and 4 cats received an i.v. infusion of PGI (50 ug/kg/hr). Cats were maintained 3 hours post-operatively. Coagulation parameters were measured after the 3 hour period and calculated as a percent of pre-thrombosis values. Collateral circulation was assessed as the time necessary for contrast media to appear in the iliac arteries caudal to the thrombus during aortography. All treated groups were statistically compared to the non-treated group. The OSPT, PTT, and FM values were not significantly changed in any group except for a prolonged PTT in the ASA group. Platelet counts were significantly reduced in non- treated cats (66 ± 4%) compared to treated cats I (96 ± 3%), ASA (97 ± 10), and PGI (97 ± 9%). Contrast media did not appear in the iliac arteries of non-treated cats until 8 seconds injection. In 4 I treated and all ASA treated cats contrast media appeared in the iliac arteries within 2 seconds after injection. The PGI treated cats had an intermediate response. Contrast media appeared in the iliac arteries 4 seconds after injection. These results suggest: (1) Some consequences of arterial thrombosis may be due to humoral inhibition of collateral blood flow. (2) This inhibition is related to platelet activation with release of vasoactive and aggregating agents and not to gross alteration of other clotting factors. (3) Platelet thromboxane A2 maY be the factor promoting collateral inhibition since prostaglandin synthesis inhibitors and antagonists are effective. (4) Inhibition of platelet function prior to thombosis could reduce ischemic damage by enhancing development of collateral blood vessels.

scholarly journals Augmenting Collateral Blood Flow during Ischemic Stroke via Transient Aortic Occlusion

2013 ◽  
Vol 34 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Ian R Winship ◽  
Glenn A Armitage ◽  
Gomathi Ramakrishnan ◽  
Bin Dong ◽  
Kathryn G Todd ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Collateral Circulation ◽  
Aortic Occlusion ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Flow Through ◽  
Transient Aortic Occlusion

Collateral circulation provides an alternative route for blood flow to reach ischemic tissue during a stroke. Blood flow through the cerebral collaterals is a critical predictor of clinical prognosis after stroke and response to recanalization, but data on collateral dynamics and collateral therapeutics are lacking. Here, we investigate the efficacy of a novel approach to collateral blood flow augmentation to increase collateral circulation by optically recording blood flow in leptomeningeal collaterals in a clinically relevant model of ischemic stroke. Using high-resolution laser speckle contrast imaging (LSCI) during thromboembolic middle cerebral artery occlusion (MCAo), we demonstrate that transiently diverting blood flow from peripheral circulation towards the brain via intra-aortic catheter and balloon induces persistent increases in blood flow through anastomoses between the anterior and middle cerebral arteries. Increased collateral flow restores blood flow in the distal middle cerebral artery segments to baseline levels during aortic occlusion and persists for over 1 hour after removal of the aortic balloon. Given the importance of collateral circulation in predicting stroke outcome and response to treatment, and the potential of collateral flow augmentation as an adjuvant or stand-alone therapy for acute ischemic stroke, this data provide support for further development and translation of collateral therapeutics including transient aortic occlusion.

Depression of Collateral Blood Flow Following Arterial Thrombosis

1977 ◽  
Vol 38 (04) ◽  
pp. 0850-0862 ◽  
Author(s):  
Robert G. Schaub ◽  
Ronald Sande ◽  
Kenneth M. Meyers
Keyword(s):  
Blood Flow ◽  
Arterial Thrombosis ◽  
Hind Limb ◽  
Therapeutic Interventions ◽  
Collateral Blood Flow ◽  
Serotonin Antagonist ◽  
Limb Perfusion ◽  
Clinical Consequences ◽  
Collateral Vessels ◽  
Iliac Bifurcation

SummaryPermanent ligation of the feline aorta at the iliac bifurcation is followed by rapid opening of pre-existing collateral blood vessels. However, if ligation is combined with formation of a clot, these protective collateral vessels do not function. This study was undertaken to determine if drugs which alter serotonin function can improve collateral blood flow after arterial thrombosis. Permanent ligations were placed at the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. A clot was produced in the aorta of 27 cats by injection of 0.1 ml of thromboplastin. Ligated clot-occluded cats were untreated (10); had blood serotonin depleted using a single dose of reserpine (0.1 mg/kg i. m.) followed by para-chlorophenylanine (p-CPA) (100 mg/kg orally) every 3 days (9) ; or were treated prior to surgery with a serotonin antagonist cinanserin HC1 (4 mg/kg i. v.) (8). Control cats (18) were acutely ligated. 9 of these cats were untreated, 5 were cinanserin HC1-treated, and 4 were reserpine/p-CPA-treated. Extent of collateral development was assessed by aortograms 3 days after occlusion and by neurologic rating. Aortograms of acutely ligated cats indicated a significant collateral blood flow around the segment of ligated aorta, while ligated clot-occluded cats had a severely depressed hind-limb perfusion. Reserpine/p-CPA-treated ligation clot-occluded cats had aortograms similar to acutely ligated cats. The cinanserin HC1-treated ligation clot-occluded cats had aortograms which indicated hind-limb perfusion was not as adequate as the acutely ligated cats. However, the perfusion of these animals was improved over untreated ligation clot-occluded cats. Neurologic rating correlated with aortograms. These results suggest: 1) the clinical consequences of arterial thrombosis cannot be entirely attributed to mechanical occlusion of an artery, but may be due to depression of protective collateral blood flow induced by thrombosis, 2) serotonin is an important factor in this depression of collateral blood flow, and 3) isolation of the factors responsible for collateral inhibition could permit the development of therapeutic interventions.

Abstract T P83: Strain Differences In Leptomeningeal Collateral Flow Dynamics Correlate With Differences In Stroke Outcome

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yasuo Nishijima ◽  
Yosuke Akamtsu ◽  
Chih Cheng Lee ◽  
Jialing Liu
Keyword(s):  
Blood Flow ◽  
Acute Phase ◽  
Collateral Circulation ◽  
Artery Occlusion ◽  
Flow Dynamics ◽  
Mouse Strains ◽  
Collateral Flow ◽  
Doppler Flowmetry ◽  
Collateral Arteries ◽  
Retrograde Filling

Introduction: Emerging evidences suggest that the collateral circulation plays a key role in the risk of stroke and the severity of infarction. The current study aimed to investigate the effect of the brain collateral circulation in acute phase of stroke and outcome in two inbred mouse strains that differ markedly in anatomical collateralization. Methods: Male C57BL/6 and Balb/C mice were subjected to permanent unilateral common carotid artery occlusion (CCAO) or temporary distal middle cerebral artery occlusion (dMCAo). Regional cerebral blood flow (rCBF) was assessed by laser doppler flowmetry. In vivo imaging of collateral blood flow and flow velocity was evaluated by doppler optical coherence tomography (DOCT). Infarct size and motor function was assessed at 24 hours and 1 week after dMCAo, respectively. DiI-labeling was used to reveal anastomoses and to determine vessel diameter. Results: The diameters of the ICA and ACA on the ischemic side in both strains markedly decreased at 24 hours after CCAO but recovered at 7 days, although the diameters of ICA, MCA and ACA are larger in the Balb/C compared to the C57BL/6 strain before and after CCAO. Balb/C mice exhibited significantly less leptomeningeal connecting collateral arteries compared to C57BL/6 (0.6±0.3 vs 11.3±0.4, p<0.001), coincided with a larger infarction and worse neurological outcomes after dMCAo compared to C57BL/6. During the acute phase of occlusion of the CCA or MCA, C57BL/6 mice also demonstrated a much more robust retrograde filling of several distal branches of the MCA from ACA compared to Balb/C mice. Conclusion: Our results demonstrate that anatomical insufficiency of the leptomeningeal collateralization is associated with an impaired collateral flow dynamics, resulting in reduced rCBF during the acute phase of MCA stroke, which might in part, contribute to the larger infarction observed in the Balb/C strain.

Abstract 1122‐000181: Collateral Circulation in Ischemic Stroke is Not Determined by Anatomical Variants of the Cerebral Arteries

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Karolina Brzegowy ◽  
Bernard Solewski ◽  
Paweł Brzegowy ◽  
Agata Musiał ◽  
Tadeusz Popiela ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Collateral Circulation ◽  
Cerebral Arteries ◽  
Anatomical Variations ◽  
Detailed Knowledge ◽  
Collateral Blood Flow ◽  
Posterior Portion ◽  
Cortical Vein ◽  
Anatomical Variants

Introduction : In acute ischemic stroke, collateral circulation determines tissue fate and treatment results. The aim of this study was to evaluate the role of anatomical variations of the Circle of Willis (CoW) in formation of cerebral collateral blood flow in patients with acute M1 occlusion. Methods : This study was a retrospective assessment of radiological examinations of patients with stroke due to middle cerebral artery M1 segment occlusion. All patients underwent mechanical thrombectomy from January 2015 until March 2021. The anatomy of the CoW was assessed on initial CT‐angiography and DSA. CTA was utilized to grade cranial collateral vasculature status and cortical vein opacification score (COVES). Non‐contrast CT scans and ASPECTS scores (using RAPID software) were used to determine the ischemic area. Results : A total of 100 patients were included in the analysis (58 females and 42 males, mean age: 71.6 +/‐ 13.9). We classified the anatomy of the CoW according to its continuity as a full circle. Patients with fully continuous CoW (n = 19) had worse COVES scores than those with CoW incomplete at both anterior and posterior portion (n = 9) (89% vs 68% with COVES 0–2, p = 0.179). No statistically significant results were found when comparing the enhancement of collaterals between these two groups (p = 0.390). The COVES scores were similar for patients with complete and incomplete anterior portions of CoW (77% vs 80% with COVES 0–2, p = 0.812). Patients with incomplete posterior portions of CoW had lower COVES scores than those with complete (80% vs 67% with COVES 0–2, p = 0.206). No statistically significant differences were discovered when comparing different types of the posterior communicating artery (adult, transitional and fetal). Analysis of ischemic areas determined as ASPECTS scores pre‐ and post‐thrombectomy yielded no significant differences between any of the groups. Conclusions : Although certain variants of the CoW have been reported to increase the risk of ischemic stroke, our results show that the anatomy of CoW has no large effect on collateral blood flow during acute M1 occlusion. We presume that the greater role is played by pial arterioles than anatomical variants of major cerebral arteries in cerebral collateral circulation formation. Detailed knowledge about the factors that influence collateral blood flow is crucial as it may aid in identification of patients prone to worse outcomes of ischemic stroke. Anatomical variants of CoW do not play a major role in formation of cerebral collaterals.

5-Hydroxytryptamine dominates over thromboxane A2 in reducing collateral blood flow by activated platelets

1993 ◽  
Vol 265 (1) ◽  
pp. H158-H164 ◽  
Author(s):  
W. Loots ◽  
F. De Clerck
Keyword(s):  
Blood Flow ◽  
Platelet Activation ◽  
Perfusion Defect ◽  
Activation Process ◽  
Collateral Blood Flow ◽  
Peripheral Vascular ◽  
Similar Extent ◽  
Receptor Antagonism ◽  
Prostaglandin Endoperoxide ◽  
Activated Platelets

Intra-aortic infusion of collagen (100 micrograms/kg in 1 min) elicited an extensive platelet activation and transient but marked reductions of blood flow and increases of peripheral vascular resistance, both responses being more pronounced in collaterals than in normal arterial beds in feline hind legs. Blockade of 5-hydroxytryptamine (5-HT) subtype 2 (5-HT2) receptors for 5-HT (ketanserin or ritanserin, 0.63 mg/kg iv, -10 min) or amine depletion (reserpine, 0.1 mg/kg im, -10 days, + parachlorophenylalanine 100 mg/kg sc daily for 3 days), but not cyclooxygenase inhibition (indomethacin, 5 mg/kg iv) or thromboxane (Tx) A2/prostaglandin endoperoxide receptor antagonism (sulotroban, 2.5 mg/kg iv), largely prevented the collagen-induced perfusion defect without interfering substantially with the platelet activation process. TxA2 synthase inhibition, alone (dazoxiben, 5 mg/kg iv) or combined with TxA2-prostaglandin endoperoxide receptor antagonism (ridogrel, 2.5 mg/kg iv), partially reduced the collagen-induced perfusion defect and limited to a similar extent the initial platelet aggregation and release of 5-hydroxyindoles and TxB2 while increasing plasma levels of prostacyclin. These results suggest that platelet-derived 5-HT dominates over TxA2 in reducing blood flow in collateral-dependent tissue of the cat hindlimb.

Effects of time on volume and distribution of coronary collateral flow

1976 ◽  
Vol 230 (2) ◽  
pp. 279-285 ◽  
Author(s):  
ML Marcus ◽  
RE Kerber ◽  
J Ehrhardt ◽  
FM Abboud
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Coronary Occlusion ◽  
Marked Decrease ◽  
Relative Proportion ◽  
Collateral Flow ◽  
Coronary Vascular Resistance ◽  
Collateral Blood Flow ◽  
Coronary Collateral Flow ◽  
Hemodynamic Measurements

Changes in the volume and distribution of collateral blood flow were studied during the 1st h after coronary occlusion in nine open-chest dogs. Labeled microspheres (7-10 mum) were injected into the left atrium prior to and 20 s, 5 min, and 60 min after acute occlusion of the midcircumflex coronary artery so that myocardial perfusion to small segments of the entire left ventricle could be measured. The segmental perfusions were classified as normally perfused, severely hypoperfused, moderately hypoperfused, and borderline hypoperfused. Standard hemodynamic measurements were obtained and relative coronary vascular resistance to the normally perfused and hypoperfused zones was calculated. The principal conclusions of the study are as follows: 1) during the 1st h after coronary occlusion the collateral flow to the hypoperfused myocardium increases substantially; 2) the increase in collateral flow is distributed fairly evenly to various hypoperfused zones and is associated with a marked decrease in coronary vascular resistance; and 3) as a result of this influx in collateral flow the size of the hypoperfused area decreases and the relative proportion of severely hypoperfused segments within the hypoperfused area decreases.

scholarly journals Effects of Adenosine and 2-Chloroadenosine on Cerebral Collateral Vessels

1995 ◽  
Vol 15 (6) ◽  
pp. 1075-1081 ◽  
Author(s):  
Michael G. Muhonen ◽  
Christopher M. Loftus ◽  
Donald D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Topical Application ◽  
Collateral Circulation ◽  
Arterial Occlusion ◽  
Collateral Flow ◽  
Cortical Layers ◽  
Area At Risk ◽  
Collateral Vessels ◽  
Cerebral Vasodilator

Adenosine is a potent cerebral vasodilator. We tested the hypothesis that dilatation of collateral vessels in cerebrum, in response to topical adenosine and 2-chloroadenosine (2-CAD), would increase blood flow to collateral-dependent cerebrum. In dogs anesthetized with halothane, a branch of the middle cerebral artery (MCA) was occluded proximally and cannulated distally. The collateral-dependent area at risk for infarction was perfused from a reservoir with microsphere-free blood, and blood flow to normal cerebrum and to cerebrum dependent on collateral flow was measured with radioactive microspheres injected into the left ventricle through a femoral artery catheter. Perfusion through the cannulated MCA branch was stopped, and flow to normal and collateral-dependent cerebrum was measured after adenosine (10−2 M) or 2-CAD (10−4 M) was added to the superfusate over the cerebrum. In normal cerebrum, topical application of adenosine increased flow to outer but not inner layers. Topical application of adenosine had little effect on flow to collateral-dependent tissue. In normal cerebrum, 2-CAD increased flow to outer layers, whereas flow to inner layers tended to increase. During 2-CAD, flow to outer cortical layers of collateral-dependent cerebrum increased from 140 ± 20 ml/100 g/min (mean ± SD) to 231 ± 68, whereas flow to the inner collateral-dependent tissue did not change. The findings indicate that, after occlusion of a cerebral artery, topical 2-CAD increases blood flow to outer layers of collateral-dependent and normal cerebrum. The findings suggest also that, after arterial occlusion, collateral circulation to cerebrum has dilator reserve, and flow to tissues that are dependent on collaterals may be augmented.

scholarly journals Relationship between haemodynamic impairment and collateral blood flow in carotid artery disease

2017 ◽  
Vol 38 (11) ◽  
pp. 2021-2032 ◽  
Author(s):  
Nolan S Hartkamp ◽  
Esben T Petersen ◽  
Michael A Chappell ◽  
Thomas W Okell ◽  
Maarten Uyttenboogaart ◽  
...  
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Carotid Artery Disease ◽  
Tissue Level ◽  
Cerebrovascular Reactivity ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Ischaemic Damage ◽  
Before And After ◽  
Artery Disease

Collateral blood flow plays a pivotal role in steno-occlusive internal carotid artery (ICA) disease to prevent irreversible ischaemic damage. Our aim was to investigate the effect of carotid artery disease upon cerebral perfusion and cerebrovascular reactivity and whether haemodynamic impairment is influenced at brain tissue level by the existence of primary and/or secondary collateral. Eighty-eight patients with steno-occlusive ICA disease and 29 healthy controls underwent MR examination. The presence of collaterals was determined with time-of-flight, two-dimensional phase contrast MRA and territorial arterial spin labeling (ASL) imaging. Cerebral blood flow and cerebrovascular reactivity were assessed with ASL before and after acetazolamide. Cerebral haemodynamics were normal in asymptomatic ICA stenosis patients, as opposed to patients with ICA occlusion, in whom the haemodynamics in both hemispheres were compromised. Haemodynamic impairment in the affected brain region was always present in symptomatic patients. The degree of collateral blood flow was inversely correlated with haemodynamic impairment. Recruitment of secondary collaterals only occurred in symptomatic ICA occlusion patients. In conclusion, both CBF and cerebrovascular reactivity were found to be reduced in symptomatic patients with steno-occlusive ICA disease. The presence of collateral flow is associated with further haemodynamic impairment. Recruitment of secondary collaterals is associated with severe haemodynamic impairment.

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