scholarly journals Use of the Cascade expandable net to treat cerebral vasospasm – initial clinical experience from a single centre with in vitro benchside tests

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
P. Bhogal ◽  
T. Simpanen ◽  
K. Wong ◽  
D. Bushi ◽  
M. A. Sirakov ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Retrospective Review ◽  
Average Diameter ◽  
Radial Force ◽  
Use Of Self ◽  
Single Centre ◽  
Delayed Cerebral Vasospasm ◽  
Ischemic Complications ◽  
Initial Results

Abstract Background The use of self-expanding stents to treat post-hemorrhagic cerebral vasospasm was recently described. We sought to determine the clinical efficacy of the Cascade device to treat delayed cerebral vasospasm (DCV). We performed benchside tests to determine the chronic outward force exerted by the Cascade in comparison to the Solitaire. Methods The chronic outward force (COF) of the Cascade M agile and Cascade L Agile was tested with equivalent tests of the Solitaire 4x20mm. Further tests to determine the forces generated in pre-formed tubes of 1.5–6 mm were performed using both fully and partially unsheathed Cascades. A retrospective review to identify all patients with aSAH and DCV treated with a Cascade device between January 2020 and July 2021. We recorded the treatment arterial vessel diameters and hemorrhagic or ischemic complications. Results In vitro the Cascade generated greater radial force than the Solitaire. The force generated by the Cascade M Agile at 1.5 mm was approximately 64% higher than the Solitaire 6x40mm and approximately 350% higher than the Solitaire 4x20mm. 4 patients with DCV were identified all of whom were treated with a cascade device. In all cases there was a significant improvement in the diameter of the vasospastic vessels treated with an average diameter increase of approximately 300%. There were no complications from the Cascade. Delayed CT angiography showed persistent dilatation of the segments treated with the Cascade at 24 h. Conclusion The Cascade is a safe and effective device when used to treat DCV secondary to aSAH. Larger studies are required to validate our initial results.

Treatment of cerebral vasospasm with self-expandable retrievable stents: proof of concept

2016 ◽  
Vol 9 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Pervinder Bhogal ◽  
Yince Loh ◽  
Patrick Brouwer ◽  
Tommy Andersson ◽  
Michael Söderman
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
High Volume ◽  
Radial Force ◽  
Proof Of Concept ◽  
Stent Angioplasty ◽  
Delayed Cerebral Vasospasm ◽  
Stent Retrievers ◽  
Cerebral Vasodilation ◽  
Standard Techniques

ObjectiveTo report our preliminary experience with the use of stent retrievers to cause vasodilation in patients with delayed cerebral vasospasm secondary to subarachnoid hemorrhage.MethodsFour patients from two different high volume neurointerventional centers developed cerebral vasospasm following subarachnoid hemorrhage. In addition to standard techniques for the treatment of cerebral vasospasm, we used commercially available stent retrievers (Solitaire and Capture stent retrievers) to treat the vasospastic segment including M2, M1, A2, and A1. We evaluated the safety of this technique, degree of vasodilation, and longevity of the effect.ResultsStent retrievers can be used to safely achieve cerebral vasodilation in the setting of delayed cerebral vasospasm. The effect is long-lasting (>24 hours) and, in our initial experience, carries a low morbidity. We have not experienced any complications using this technique although we have noted that the radial force was not sufficient to cause vasodilation in some instances. The vasospasm did not return in the vessel segments treated with stent angioplasty in any of these cases. In two of our cases stent angioplasty resulted in the reversal of focal neurological symptoms.ConclusionsStent retrievers can provide long-lasting cerebral vasodilation in patients with delayed cerebral vasospasm.

scholarly journals Bilirubin Production and Oxidation in CSF of Patients with Cerebral Vasospasm after Subarachnoid Hemorrhage

2005 ◽  
Vol 25 (8) ◽  
pp. 1070-1077 ◽  
Author(s):  
Gail J Pyne-Geithman ◽  
Chad J Morgan ◽  
Kenneth Wagner ◽  
Elizabeth M Dulaney ◽  
Janice Carrozzella ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Spinal Fluid ◽  
Spinal Fluid ◽  
Oxidation Products ◽  
Mortality And Morbidity ◽  
Delayed Cerebral Vasospasm ◽  
And Oxidative Stress

Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) remains a significant cause of mortality and morbidity; however, the etiology is, as yet, unknown, despite intensive research efforts. Research in this laboratory indicates that bilirubin and oxidative stress may be responsible by leading to formation of bilirubin oxidation products (BOXes), so we investigated changes in bilirubin concentration and oxidative stress in vitro, and in cerebral spinal fluid (CSF) from SAH patients. Non-SAH CSF, a source of heme oxygenase I (HO-1), and blood were incubated, and in vitro bilirubin production measured. Cerebrospinal fluid from SAH patients was collected, categorized using stimulation of vascular smooth muscle metabolism in vitro, and information obtained regarding occurrence of vasospasm in the patients. Cerebral spinal fluid was analyzed for hemoglobin, total protein and bilirubin, BOXes, malonyldialdehyde and peroxidized lipids (indicators of an oxidizing environment), and HO-1 concentration. The formation of bilirubin in vitro requires that CSF is present, as well as whole, non-anti-coagulated blood. Bilirubin, BOXes, HO-1, and peroxidized lipid content were significantly higher in CSF from SAH patients with vasospasm, compared with nonvasospasm SAH CSF, and correlated with occurrence of vasospasm. We conclude that vasospasm may be more likely in patients with elevated BOXes. The conditions necessary for the formation of BOXes are indeed present in CSF from SAH patients with vasospasm, but not CSF from SAH patients without vasospasm.

Individual variations in response of human cerebral arterioles to vasoactive substances, human plasma, and CSF from patients with aneurysmal SAH

1981 ◽  
Vol 55 (3) ◽  
pp. 431-437 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt
Keyword(s):  
Human Plasma ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Vessel ◽  
Content Type ◽  
Vasoactive Substances ◽  
Delayed Cerebral Vasospasm ◽  
Prostaglandin F ◽  
Cerebral Arterioles

✓ The capricious appearance of delayed cerebral vasospasm in some but not all patients with an aneurysmal subarachnoid hemorrhage (SAH) was the stimulus for studying the reactivity of human cerebral arterioles in vitro to various vasoactive agents (prostaglandin F2a, noradrenaline, serotonin, human plasma, and cerebrospinal fluid from patients with aneurysmal SAH). There was a marked variability in response between arterioles from different individuals. The finding of a markedly individual profile in terms of reactivity toward vasoactive substances emphasizes the importance of a human cerebral vessel wall factor in the pathogenesis of cerebral vasospasm.

Prevention of subarachnoid hemorrhage—induced cerebral vasospasm by oral administration of endothelin receptor antagonists

1996 ◽  
Vol 84 (3) ◽  
pp. 503-507 ◽  
Author(s):  
Mario Zuccarello ◽  
Giovanni B. Soattin ◽  
Adam I. Lewis ◽  
Volker Breu ◽  
Hussein Hallak ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Oral Administration ◽  
Receptor Antagonist ◽  
Cerebral Vasospasm ◽  
Oral Treatment ◽  
Specific Treatment ◽  
Receptor Antagonists ◽  
Content Type ◽  
Delayed Cerebral Vasospasm

✓ The purpose of this study was to investigate the effectiveness of oral treatment with the endothelin (ET)A/B receptor antagonist Ro 47-0203, 4-tert-butyl-N-[6-(hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2′-bipyrimidin-4-yl]-benzenesulfonamide (bosentan), and the ETA receptor antagonist 2-benzo[1,3]dioxol-5-yl-3-benzyl-4-(4-methoxy-phenyl)-4-oxobut-2-enoic acid monosodium salt (PD155080), in the prevention of subarachnoid hemorrhage (SAH)—induced delayed cerebral vasospasm. Double hemorrhage in the rabbit constricted the basilar artery to 34% of control as determined by angiography. Oral bosentan and PD155080 administration after the initial SAH decreased the magnitude of constriction to 9% and 16% of control, respectively. Plasma and cerebrospinal fluid bosentan levels and plasma PD155080 levels were consistent with concentrations reported to inhibit ET-1 constriction of blood vessels in vitro. These results support the use of oral administration of ETA/B and ETA receptor antagonists as potential specific treatment for vasospasm resulting from SAH in humans.

scholarly journals Effects of Histidine-Rich Glycoprotein on Cerebral Blood Vessels

2013 ◽  
Vol 33 (9) ◽  
pp. 1373-1375 ◽  
Author(s):  
Samantha M Steelman ◽  
Travis W Hein ◽  
Amy Gorman ◽  
Gregory J Bix
Keyword(s):  
Cerebral Vasospasm ◽  
Hemorrhagic Stroke ◽  
Blood Clot ◽  
Cerebral Blood Vessels ◽  
Delayed Cerebral Vasospasm ◽  
Vasoactive Factors ◽  
Cerebral Arterioles ◽  
Cerebrovascular Endothelial Cells ◽  
Subarachnoid Blood

Delayed cerebral vasospasm is thought to be caused by factors released from a subarachnoid blood clot. Because vasospasm occurs several days after hemorrhage, we hypothesized that clotted blood releases vasoactive factors as it ages. Targeted proteomics identified histidine-rich glycoprotein (HRG) as a potentially vasoactive factor released within the first 72 hours of clot formation. In vitro studies revealed that HRG caused moderate (~30%) dilation of cannulated cerebral arterioles and proliferation of cerebrovascular endothelial cells. We conclude that HRG released from clotted blood, while unlikely to contribute to cerebral vasospasm, might provide important vasodilatory or angiogenic stimuli after hemorrhagic stroke.

Characteristics of clover primary leaf necrosis virus, a new spherical isolate from Trifolium pratense

1977 ◽  
Vol 55 (15) ◽  
pp. 2122-2136 ◽  
Author(s):  
H. W. J. Ragetli ◽  
M. Elder
Keyword(s):  
Trifolium Pratense ◽  
Red Clover ◽  
Average Diameter ◽  
Primary Leaf ◽  
Antigenic Determinants ◽  
Necrosis Virus ◽  
Virus Propagation ◽  
Crimson Clover ◽  
Leaf Necrosis

An unknown virus was isolated from a young red clover plant (Trifolium pratense) with a bright yellow leaf mottle and subsequently was isolated from five other field clover plants with milder symptoms growing in three locations. In the laboratory, red clover became systemically infected by the virus only when the plants were kept between 10 and 16 °C after inoculation, and symptoms were mild. Crimson clover (T. incarnatum) was readily invaded at room temperature, and survivors of the initial shock reaction were severely mottled. White clover (T. repens) and Alsike clover (T. hybridum) did not become systemically infected under either temperature regime. The symptom common to all four species, necrotic spots in the inoculated primary leaves, suggested the name clover primary leaf necrosis virus. Among the nine leguminous and six non-leguminous host species, bean (Phaseolus vulgaris) was best suited for virus propagation, and cucumber (Cucumis sativus) was best suited for quantitative assay and detection.The virus was characterized by a single sedimenting species of spherical nucleoprotein particles with a sedimentation value, S20.w, of 136–137, an average diameter of 36 nm, and a specific extinction, E260 nm1%, 1 cm, of 58.15. The nucleic acid was of the ribose type and constituted 21% of the weight of the virion. Activity was lost from crude juice at 65 °C and from purified suspensions at 85 °C, with about 10% activity persisting between 60–70 °C. Two electrophoretic components were isolated from purified preparations. They induced identical symptoms in three hosts, but one replicated both components in bean and had more antigenic determinants than the other, which replicated itself only. The virus was weakly antigenic inducing an antiserum with titer of 128. Some of its in vitro properties were similar to those of carnation ringspot virus, but the two viruses were serologically unrelated. Nor was this virus serologically related to any of 15 other spherical viruses tested.

scholarly journals Application of the 1-µsec pulsed-dye laser to the treatment of experimental cerebral vasospasm

1991 ◽  
Vol 75 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Atsushi Teramura ◽  
Robert Macfarlane ◽  
Christopher J. Owen ◽  
Ralph de la Torre ◽  
Kenton W. Gregory ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Laser Energy ◽  
Autologous Blood ◽  
Preliminary Investigation ◽  
Dye Laser ◽  
Pulsed Dye Laser ◽  
Content Type

✓ Laser energy of 480 nm was applied in 1-µsec pulses varying between 2.2 and 10 mJ to in vitro and in vivo models of cerebral vasospasm. First, the pulsed-dye laser was applied intravascularly via a 320-µm fiber to basilar artery segments from six dogs. The segments were mounted in a vessel-perfusion apparatus and constricted to, on average, 70% of resting diameter by superfusion with dog hemolysate. Immediate increase in basilar artery diameter occurred to a mean of 83% of control. In a second model, the basilar artery was exposed transclivally in the rabbit. In three normal animals, superfusion of the artery with rabbit hemolysate resulted in a reduction of mean vessel diameter to 81% of control. Following extravascular application of the laser, vessels returned to an average of 106% of the resting state. In six rabbits, the basilar artery was constricted by two intracisternal injections of autologous blood, 3 days apart. Two to 4 days after the second injection, the basilar artery was exposed. Extravascular laser treatment from a quartz fiber placed perpendicular to the vessel adventitia resulted in an immediate 53% average increase in caliber to an estimated 107% of control. No reconstriction was observed over a period of up to 5 hours. Morphologically, damage to the arterial wall was slight. This preliminary investigation suggests that the 1-µsec pulsed-dye laser may be of benefit in the treatment of cerebral vasospasm.

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