Spastic Vessels Research Articles

Immediate angiographic control after intra-arterial nimodipine administration underestimates the vasodilatory effect

Intra-arterial nimodipine administration is a widely used rescue therapy for cerebral vasospasm. Although it is known that its effect sets in with delay, there is little evidence in current literature. Our aim was to prove that the maximal vasodilatory effect is underestimated in direct angiographic controls. We reviewed all cases of intra-arterial nimodipine treatment for subarachnoid hemorrhage-related cerebral vasospasm between January 2021 and December 2022. Inclusion criteria were availability of digital subtraction angiography runs before and after nimodipine administration and a delayed run for the most affected vessel at the end of the procedure to decide on further escalation of therapy. We evaluated nimodipine dose, timing of administration and vessel diameters. Delayed runs were performed in 32 cases (19 patients) with a mean delay of 37.6 (± 16.6) min after nimodipine administration and a mean total nimodipine dose of 4.7 (± 1.2) mg. Vessel dilation was more pronounced in delayed vs. immediate controls, with greater changes in spastic vessel segments (n = 31: 113.5 (± 78.5%) vs. 32.2% (± 27.9%), p < 0.0001) vs. non-spastic vessel segments (n = 32: 23.1% (± 13.5%) vs. 13.3% (± 10.7%), p < 0.0001). In conclusion intra-arterially administered nimodipine seems to exert a delayed vasodilatory effect, which should be considered before escalation of therapy.

Does the intracoronary pressure differ according to two types (diffuse or focal) of coronary spasm?

Several reports show that two types of coronary vasospasm (diffuse and focal spasm) are associated with the severity or prognosis of coronary spasm in patients with vasospastic angina (VSA). It is unclear whether intracoronary pressure differs between the two spasm types. To investigate such relationships using a pressure wire during the spasm provocation test (SPT) in patients with VSA. Eighty-seven patients with VSA (average age: 67 years; 50 men, 37 women) underwent SPT. During the SPT, a pressure wire was advanced into the distal portion of the right coronary artery and left anterior descending coronary artery, and the ratio of the intracoronary pressure to the aortic pressure (Pd/Pa) was continuously monitored. An SPT was performed using acetylcholine (ACh), and the presence of coronary spasm was defined as the presence of > 90% arterial narrowing in response to an ACh infusion, with the usual chest symptoms and/or ischemic ECG changes. Focal spasm was defined as total or subtotal spasm within one segment of the AHA classification, while diffuse spasm was defined as > 90% spasm with two or more segments. Among 87 patients, the frequencies of metabolic syndrome and having coronary atherosclerosis were higher in the focal group (n = 33) than in the diffuse spasm group (n = 54, P < 0.05). In the vessel analyses, in these 134 spastic segments, diffuse and focal spasms were detected in 100 and 34 vessels, respectively. The Pd/Pa at baseline was similar in both groups (diffuse: 0.96 ± 0.05, focal: 0.95 ± 0.05, P = 0.35); however, the Pd/Pa during coronary spasm was lower in focal spastic vessels (0.66 ± 0.20) than in diffuse spastic vessels (0.76 ± 0.11, P < 0.01), and the reduction in Pd/Pa during an SPT was also lower in focal spastic vessels (-0.29 ± 0.20) than in diffuse spastic vessels (-0.18 ± 0.11, P < 0.01). The presence of focal spasm was a significant factor responsible for reduction in Pd/Pa during SPT. These findings suggest that focal spasm may be more severe than diffuse spasm, judging from the intracoronary pressure during coronary spasm.

Ultrasound-Induced Release of Nimodipine from Drug-Loaded Block Copolymer Micelles: In Vivo Analysis

Nimodipine prevents cerebral vasospasm and improves functional outcome after aneurysmal subarachnoid hemorrhage (aSAH). The beneficial effect is limited by low oral bioavailability of nimodipine, which resulted in an increasing use of nanocarriers with sustained intrathecal drug release in order to overcome this limitation. However, this approach facilitates only a continuous and not an on-demand nimodipine release during the peak time of vasospasm development. In this study, we aimed to assess the concept of controlled drug release from nimodipine-loaded copolymers by ultrasound application in the chicken chorioallantoic membrane (CAM) model. Nimodipine-loaded copolymers were produced with the direct dissolution method. Vasospasm of the CAM vessels was induced by means of ultrasound (Physiomed, continuous wave, 3 MHz, 1.0 W/cm2). The ultrasound-mediated nimodipine release (Physiomed, continuous wave, 1 MHz, 1.7 W/cm2) and its effect on the CAM vessels were evaluated. Measurements of vessel diameter before and after ultrasound-induced nimodipine release were performed using ImageJ. The CAM model could be successfully carried out in all 25 eggs. After vasospasm induction and before drug release, the mean vessel diameter was at 57% (range 44–61%) compared to the baseline diameter (set at 100%). After ultrasound-induced drug release, the mean vessel diameter of spastic vessels increased again to 89% (range 83–91%) of their baseline diameter, which was significant (p = 0.0002). We were able to provide a proof of concept for in vivo vasospasm induction by ultrasound application in the CAM model and subsequent resolution by ultrasound-mediated nimodipine release from nanocarriers. This concept merits further evaluation in a rat SAH model.Graphical abstract

Long-term outcome in pediatric surgical bypass grafting after traumatic injury and tumor resection: retrospective cohort analysis

Vascular bypass surgery in children differs significantly from adults. It is a rarely performed procedure in the setting of trauma and tumor surgery. Besides technical challenges to reconstruct the small and spastic vessels, another concern in bypass grafting is the adequate limb length growth over time. The primary aim of this study was to assess long-term outcome after pediatric bypass grafting, in a single academic center, focusing on potential effects on limb development. In this retrospective cohort analyses we included all pediatric patients undergoing vascular bypass grafting at our department between 2002 and 2017. All patients ≤ 18 years suffered a traumatic injury or underwent a tumor resection of the lower or upper limb. The youngest female patient was 0.4 years, the youngest male patient was 3.5 years. During the observation period, 33 pediatric patients underwent vascular repair, whereby 15 patients underwent bypass grafting. Median overall follow-up was 4.7 years (IQR ± 9). 8 patients (53%) had a traumatic injury (traumatic surgery group) and 7 patients had a planned orthopedic tumor resection (orthopedic surgery group). In 13/15 (87%) a great saphenous vein (GSV) graft and in 2/15 (13%) a Gore-Tex graft was used for bypassing. Both Gore-Tex grafts showed complete occlusion 12 and 16 years after implantation. No patient died in the early postoperative phase (< 30 days), however 3/7 (43%) in the orthopedic group died during follow-up. Revision surgery had to be performed in 1/15 (7%) patients. A functional use of the extremity was reported in all patients. Normal limb length growth according to the contralateral site, and therefore bypass growth, could be documented in 14/15 patients. Children are surgically challenging. In our study, surgery by a specialized vascular surgery team using GSV grafts led to adequate limb length and bypass growth, and we observed no functional restrictions.

First experience with percutaneous arteriovenous fistula creation using the Ellipsys® vascular access system

Abstract Objective Percutaneous creation of arteriovenous fistulae (pAVF) has been developed as an alternative to the creation of an upper arm cephalic or basilic vein fistula. Several studies have shown high technical success rates and comparable time of maturation. To our knowledge, the technique has not been used in Switzerland before. Methods Prospective data collection of the first consecutive patients undergoing the creation of pAVF between April and July 2020 at two vascular surgery centres. Results Seven patients underwent pAVF creation with the Ellipsys® vascular access system under regional anaesthesia for maximum vasodilation. The procedures were performed entirely under sonographic control without the use of fluoroscopy. The cephalic or basilic vein was punctured and the puncture needle advanced under sonographic control through the cubital perforator vein into the proximal radial artery. The Ellipsys® catheter was advanced over a guidewire and activated to create the fistula between the proximal radial artery and the perforator vein. The fistula was further dilated with a 5mm PTA balloon. We achieved technical success in 6 patients. In one patient with small and spastic vessels, the needle could not be advanced into the radial artery. A conventional upper arm cephalic fistula was created during the same procedure. In three patients primary maturation was achieved and the cephalic vein or distal basilic vein could be punctured for dialysis without any adjunct procedures. One patient required three additional procedures before the fistula could be used successfully (additional angioplasty of the fistula, superficialisation of the basilic vein and correction of a cubital vein stenosis by excision and end-to-end anastomosis). One patient required superficialisation of the basilic vein and one patient transposition of the arterialised brachial vein. Maturation was achieved in six pAVF after a mean of 158 days with a mean fistula flow of 920 ml/ min. Conclusion We achieved high technical success and maturation rates in our first patients undergoing pAVF creation with the Ellipsys® system. Prerequisites are suitable anatomy of the cubital perforator vein and good skills in sonography and endovascular techniques. We believe that pAVF is a promising alternative to the creation of a conventional upper arm fistula in patients unsuitable for a distal radio-cephalic fistula.

Novel Treatment of Cerebral Vasospasm Using Solitaire Stent Retriever−Assisted Angioplasty: Case Series

Endovascular procedures such as intraarterial (IA) vasodilator injection and balloon angioplasty are used to treat medically refractory cerebral vasospasm. The effects of IA therapy may be short lived and thus require multiple treatments. Balloon angioplasty also has limitations including transient occlusion of the spastic blood vessel, possible endothelial injury, and limited access to proximal vessels. We aim to demonstrate a novel technique using a stent retriever for the management of medically refractory vasospasm, especially in distal vessels. Compared with balloon angioplasty, stent retrievers provide a passive, self-limiting expansion of blood vessels. Other benefits over balloon angioplasty include 1) ability to simultaneously inject IA vasodilators, 2) limited contact and damage to vessel wall, 3) nonocclusive expansion, and 4) technical ease. Fourteen blood vessels from 6 patients with symptomatic vasospasm after subarachnoid hemorrhage were identified. We injected 5 mg of IA vasodilator medication into the vasospastic segments without radiographic improvement in vessel diameter and blood flow. The stent retriever was deployed for 2-5 minutes in each vasospastic segment. Distal anterior and posterior circulation segments were easily accessible with the stent retriever system. It resulted in improved vessel diameter and blood flow with subsequent improvement in neurologic examination. All patients demonstrated radiographic resolution of vasospasm. No procedural-related complications were noted. We demonstrate the safety and efficacy of a novel technique for the treatment of medically refractory cerebral vasospasm using stent retriever angioplasty in distal vessels. Stent angioplasty can be used as an additional tool in the management of subarachnoid hemorrhage-induced cerebral vasospasm.

P3579Clinical characteristics of an intracoronary erosion and thrombus in patients with vasospastic angina

Abstract Background Intracoronary erosion and thrombus are sometimes detected in patients with vasospastic angina (VSA) through intracoronary imaging modalities. However, the clinical characteristics of these intracoronary findings remain unclear. Therefore, we assessed the clinical and lesion characteristics of these intracoronary abnormalities in patients with VSA. Methods We included 48 patients with VSA who underwent coronary angiography (CAG), spasm provocation test (SPT), and coronary angioscopy (CAS). In all patients, acetylcholine was infused in the left and right coronary arteries. The vessels were classified into spastic vessels (SVs) and non-spastic vessels (NSVs) based on SPT results. SVs that could not be observed using CAS were excluded from the study. CAG and SPT findings were evaluated for the presence of atherosclerotic lesions (%stenosis &lt;30%) and types of spasm (segmental or diffuse). Two experts examined the presence of an intracoronary erosion and thrombus on CAS. Other serious symptoms such as cold sweating or syncope were also assessed. Results Among the 48 patients, intracoronary erosion and thrombus were detected in 11 (23%) and 10 (21%) patients, respectively, and total intracoronary abnormalities were observed in 17 (35%) patients. Male sex (p&lt;0.05), smoking (p&lt;0.05), and presence of other serious symptoms (p&lt;0.01) were associated with the presence of intracoronary abnormalities. The logistic regression analysis showed the presence of other serious symptoms to be the only factor associated with the presence of intracoronary abnormalities (p&lt;0.05). In the lesion analyses, among the 72 vessels, intracoronary abnormalities were observed only in SVs (17/53, 33%) but not in NSVs (0/19, 0%, p&lt;0.01). Among the 53 SVs, the presence of atherosclerotic lesions (p&lt;0.05) and segmental spasm type (p&lt;0.05) were found to be associated with the presence of intracoronary abnormalities. Conclusions Intracoronary erosion and thrombus were observed in approximately 35% of patients with VSA. Such intracoronary abnormalities may be partly affected by the forms of the coronary artery and coronary spasm, leading to the onset of serious symptoms of VSA.

The Effects of Cerebral Vasospasm on Cerebral Blood Flow and the Effects of Induced Hypertension: A Mathematical Modelling Study

Background: Induced hypertension has been used to promote cerebral blood flow under vasospastic conditions although there is no randomised clinical trial to support its use. We sought to mathematically model the effects of vasospasm on the cerebral blood flow and the effects of induced hypertension. Methods: The Anatomically Detailed Arterial Network (ADAN) model is employed as the anatomical substrate in which the cerebral blood flow is simulated as part of the simulation of the whole body arterial circulation. The pressure drop across the spastic vessel is modelled by inserting a specific constriction model within the corresponding vessel in the ADAN model. We altered the degree of vasospasm, the length of the vasospastic segment, the location of the vasospasm, the pressure (baseline mean arterial pressure [MAP] 90 mm Hg, hypertension MAP 120 mm Hg, hypotension), and the presence of collateral supply. Results: Larger decreases in cerebral flow were seen for diffuse spasm and more severe vasospasm. The presence of collateral supply could maintain cerebral blood flow, but only if the vasospasm did not occur distal to the collateral. Induced hypertension caused an increase in blood flow in all scenarios, but did not normalise blood flow even in the presence of moderate vasospasm (30%). Hypertension in the presence of a complete circle of Willis had a marginally greater effect on the blood flow, but did not normalise flow. Conclusion: Under vasospastic condition, cerebral blood flow varies considerably. Hypertension can raise the blood flow, but it is unable to restore cerebral blood flow to baseline.

The unexplained success of stentplasty vasospasm treatment : Insights using Mechanistic Mathematical Modeling.

Cerebral vasospasm (CVS) following subarachnoid hemorrhage occurs in up to 70% of patients. Recently, stents have been used to successfully treat CVS. This implies that the force required to expand spastic vessels and resolve vasospasm is lower than previously thought. We develop amechanistic model of the spastic arterial wall to provide insight into CVS and predict the forces required to treat it. The arterial wall is modelled as acylindrical membrane using aconstrained mixture theory that accounts for the mechanical roles of elastin, collagen and vascular smooth muscle cells (VSMC). We model the pressure diameter curve prior to CVS and predict how it changes following CVS. We propose astretch-based damage criterion for VSMC and evaluate if several commercially available stents are able to resolve vasospasm. The model predicts that dilatation of VSMCs beyond athreshold of mechanical failure is sufficient to resolve CVS without damage to the underlying extracellular matrix. Consistent with recent clinical observations, our model predicts that existing stents have the potential to provide sufficient outward force to successfully treat CVS and that success will be dependent on an appropriate match between stent and vessel. Mathematical models of CVS can provide insights into biological mechanisms and explore treatment approaches. Improved understanding of the underlying mechanistic processes governing CVS and its mechanical treatment may assist in the development of dedicated stents.

Effect of Intra-arterial Nimodipine on Cerebral Oxygen Saturation and Systemic Hemodynamic Indices in Patients With Cerebral Vasospasm: A Prospective Cohort Study.

Intra-arterial nimodipine (IaN) is used in the management of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). The impact of IaN therapy on regional cerebral oxygen saturation (rScO2) assessed by near infra-red spectroscopy, and dynamic cardiac indices, is currently unknown. This study assessed the effect of IaN on rScO2 and systemic hemodynamic indices during IaN therapy for cerebral vasospasm after aSAH. This prospective cohort study was conducted in 20 patients over sixteen month period after ethics committee approval and informed consent. Patients with angiographic evidence of vasospasm received IaN 3mg over 30 minutes in the spastic vessels. Data regarding rScO2 heart rate (HR), mean blood pressure (MBP) cardiac index (CI), stroke volume index (SVI), stroke volume variation (SVV), and total peripheral resistance index (TPRI) were collected during IaN treatment. The primary outcome measure was change in rScO2 after IaN therapy. There was no significant change from baseline in ipsilateral and contralateral rScO2 after IaN administration (mean difference [MD], 0.2; 95% confidence interval [CI], -2.1 to 1.6; P=0.804, and 1.3; -1.1 to 3.8; P=0.276, respectively). There was a significant decrease in MBP and TPRI (MD, -12.4; 95% CI, -6.6 to -18.2; P<0.001, and -674.3; -374.9 to -973.7; P<0.001, respectively) and increase in SVI and CI (MD, 7.5; 95% CI, 14.4 to 0.6; P=0.035 and 0.7; 0.9 to 0.4; P<0.001, respectively) after IaN therapy. HR and SVV were unchanged. IaN for aSAH-related cerebral vasospasm did not improve rScO2 but was associated with significant systemic hemodynamic effects, including a decrease in MBP and TPRI. These hemodynamic changes might offset any potential effects of IaN to improve rScO2.

Identification of OPN, TNC and E-selectin as potential recognition proteins in cerebral vasospasm after subarachnoid hemorrhage

Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious and significant health problem in the worldwide. There are still no effective therapies for treatment of CVS in patients suffering from SAH. Our early studies have demonstrated that the expression of connexin43 (Cx43, a member of gap junctional proteins) in cerebral spastic vessel is significantly up-regulated, and knocking down Cx43 with specific siRNA interference can significantly alleviate CVS after SAH. Therefore, Cx43 in cerebral vessel is a potential target in the treatment of CVS. However, Cx43 is widely distributed in many organs, particularly in the heart, and plays an important role in the physiological function. This study is aimed at identify whether OPN, TNC or E-selectin can be used as a target protein to be recognized in spastic cerebral vessels, then we can produce a carrier containing Cx43 siRNA or other inhibitors as a new potential treatment for CVS. Twenty eight male Sprague Dawley rats (weighing 300–350 g) were randomly divided into either SAH (n = 16) or sham group (n = 12). The double hemorrhage model was performed on day 0 and 1. All animals were sacrificed after performing India ink angiography on day 5. Initially, the expression of E-selectin, TNC and OPN in cerebral arteries, thoracic aorta and abdominal aorta were analyzed respectively by immunohistochemical staining, western blot in both groups. Then, only those with less expression in thoracic aorta, abdominal aorta and normal cerebral arteries, but higher expression in cerebral spastic arteries were further detected in the spinal cord, heart, kidney, liver, spleen, lung, pancreas, mesenteric and pulmonary arteries, retina and brain tissue, respectively. TNC, OPN and E-selectin were markedly elevated in the spastic cerebral arteries in SAH group but not in control group. The expression of TNC, but not OPN and E-selectin, is abundant in both groups of thoracic aorta and abdominal aorta. Further study demonstrated that expression of OPN, but not E-selecting, in both groups is relatively rich in brain tissue, kidney, pancreas, mesenteric artery, spinal cord and retina, but in heart, liver, lung and pulmonary artery. However, the positive expression of E-selectin was detected in spleen in both groups. TNC is highly expressed in thoracic aorta and abdominal aorta, so it is unsuitable for being a recognition protein. Although OPN, unlike TNC, does not express much in vascular system, but it expresses in many other organs or tissues. However, E-selecting could be considered as a potential recognition protein because it is not so widely distributed in the organs or tissues detected.

Is intra arterial nimodipine really beneficial in vasospasm following aneurysmal subarachnoid haemorrhage?

Object/Background: Vasospasm is a common cause of mortality and morbidity following rupture of intracranial aneurysm. Hemodynamic therapy instituted in these patients in the past has been replaced by direct manipulation of the spastic vessels by angioplasty and intra-arterial infusion of vasodilators. However, no case control studies exist proving its superiority. The purpose of our study was to compare the efficacy of intra-arterial nimodipine (IAN) to that of hemodynamic therapy in patients with vasospasm following aSAH. Material and methods: Fifty-three patients who developed vasospasm following aSAH were included in the study. IAN was instilled in addition to hemodynamic therapy in 39 patients and 14 patients (who refused to give consent for IAN) were continued on hemodynamic therapy alone and served as controls. The response to IAN was studied on angiogram. The clinical response was assessed in both the groups at regular intervals. IAN was repeated if necessary. The outcome (GOS) at discharge and at 3 months after discharge was compared. Results: Thirty-six (92.3%) out of 39 patients showed immediate angiographic reversal of vasospasm.28 of them showed clinical response, of which only 11 had lasting response. 11(28.2%) of 39 patients who received IAN had a good outcome at discharge and 23(58.9%) had a favourable outcome at 3 months follow up. In those who received hemodynamic therapy alone, 4 out of 14(28.6%) patients had a good outcome at discharge and 8 (57.1%) a favourable outcome at 3 months. Conclusions: Angiographic reversal of vasospasm is seen in majority of the patients following IAN. However, this does not necessarily translate into a long lasting clinical response. The final outcome in patients who received hemodynamic therapy is comparable to those who received additional IAN. IAN does not appear to provide a major added advantage over the conventional hemodynamic therapy.

Numerical analysis of hemodynamics in spastic middle cerebral arteries

Cerebral vasospasm (CVS) is the most common serious complication of subarachnoid hemorrhage. Among the many factors that are associated with the pathogenesis of CVS, hemodynamics plays an important role in the initiation and development of CVS. Numerical simulation was carried out to obtain the flow patterns and wall shear stress (WSS) distribution in spastic middle cerebral arteries. The blood was assumed to be incompressible, laminar, homogenous, Newtonian, and steady. Our simulations reveal that flow velocity and WSS level increase at the stenosis segment of the spastic vessels, but further downstream of stenosis, the WSS significantly decreases along the inner wall, and flow circulation and stagnation are observed. The hydrodynamic resistance increases with the increase of vessel spasm. Moreover, the change of flow field and hydrodynamic forces are not linearly proportional to the spasm level, and the rapid change of hemodynamic parameters is observed as the spasm is more than 50%. Accordingly, in the view of hemodynamic physiology, vessels with less than 30% stenosis are capable of self-restoration towards normal conditions. However, vessels with more than 50% stenosis may eventually lose their capacity to adapt to differing physiologic conditions due to the extreme non-physilogic hemodynamic environment, and the immediate expansion of the vessel lumen might be needed to minimize serious and non-reversible effects.

Effects of iodinated contrast media in a novel model for cerebral vasospasm.

We developed an in vitro model for vasospasm post subarachnoid hemorrhage that was suitable for investigating brain vessel autoregulation. We further investigated the effects of iodinated contrast medium on the vascular tone and the myogenic response of spastic cerebral vessels. We isolated and perfused the superior cerebellar arteries of rats. The vessels were pressurized and studied under isobaric conditions. Coagulated blood was used to simulate subarachnoid hemorrhage. The contrast medium iodixanol was applied intraluminally. Vessels exposed to blood developed significantly stronger myogenic tone (65.7 ± 2.0% vs 77.1 ± 1.2% of the maximum diameter, for the blood and the control group, respectively) and significantly decreased myogenic response, compared with the control groups. The contrast medium did not worsen the myogenic tone or the myogenic response in any group. Our results show that deranged myogenic response may contribute to cerebral blood flow disturbances subsequent to subarachnoid hemorrhage. The contrast medium did not have any negative influence on vessel tone or myogenic response in this experimental setting.

Cerebral vasospasm patterns following aneurysmal subarachnoid hemorrhage: an angiographic study comparing coils with clips

Background and purposeCerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) results in significant morbidity due to ischemia. Subarachnoid hematoma evacuation during aneurysm clipping reduces the incidence of vasospasm. However, studies comparing...

Effects of iodinated contrast media on a novel model of vasospasm due to subarachnoid hemorrhage (LB504)

Objective: Application of iodinated contrast media (CM) in patients with vasospasm after subarachnoid haemorrhage (SAH) may influence the vascular function of spastic brain vessels, with possible consequences for SAH morbidity and mortality. We developed an in vitro model of vasospasm post SAH to investigate the effects of CM on spontaneous myogenic tone and myogenic response of brain vessels.Methods: We used a model of isolated, pressurized rat superior cerebellar arteries. Coagulated blood was deployed in the chamber of a perfusion myograph to simulate SAH. Either vehicle or iodixanol was applied intraluminally. Vessel diameter was monitored in stable conditions and during controlled changes of intraluminal pressure. The myogenic response was quantified as the change in the diameter after each change in intraluminal pressure.Results: Vessels treated with coagulated blood developed a stronger spontaneous myogenic tone compared to the control groups (65.7% and 62.1% in comparison to 77.8% and 78.6% of initial diameter), as well as a significant decrease of the myogenic response. CM did not worsen the myogenic tone and the myogenic response. However, the myogenic response was significantly less impaired for higher pressure changes in vessels exposed to coagulated blood and CM in comparison to coagulated blood alone. The variability of the myogenic response was decreased in the groups receiving CM.Conclusion: Our in vitro model of cerebral vasospasm reflects the clinical evidence that the autoregulation of cerebral blood flow may be impaired after SAH. CM had no negative influence on vessel spontaneous myogenic tone and myogenic response in this model.

Cerebral Vasospasm after Subarachnoid Hemorrhage and Tadalafil-Nimodipine Hypothesis

Cerebral vasospasm following subarachnoid hemorrhage (SAH) is a common reaction induced by multiple factors with unclear mechanisms. This complication is difficult to treat and puts patient at risk for developing a delayed ischemic neurological deficit that can lead to substantial morbidity and mortality. Although numerous strategies have been suggested for the treatment and prevention of cerebral vasospasm following SAH, no definitive effect has been concluded in this regard. In this paper, we hypothesize that phosphodiesterase-5 inhibitors, tadalafil, can be used together with nimodipine, a calcium channel blocker, to prevent vasospasm in patients with subarachnoid hemorrhage. With synergic effects, the proposed drugs can promote relaxation of smooth muscles in spastic vessels.

E-005 Super-selective pre-operative embolization of juvenile angiofibromas

PurposeJuvenile angiofibromas (JNAs) are hypervascular, locally destructive tumors best treated by complete surgical resection. They occur predominantly in teenage boys and originate at the posterior pedicle of the middle turbinate...

Intra-arterial colforsin daropate for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Cerebral vasospasm (CV) remains a major cause of mortality and morbidity in patients with subarachnoid hemorrhage (SAH). Here, we examined the effectiveness and safety of intra-arterial injection of colforsin daropate hydrochloride (CDH). A consecutive series of 29 patients with angiographically confirmed CV received intra-arterial CDH (IAC) therapy. Angiographic changes in spastic vessels and the cerebral circulation time (CCT) were assessed before and after IAC treatment, together with the change in clinical status. IAC treatment was performed in 53 procedures in 29 patients. Angiographic improvement was observed following all procedures (100%), and clinical improvement was observed following 36 of 42 procedures (86%) in symptomatic cases. CCT improved significantly. At the 3-month follow-up, 19 patients (66%) showed good recovery or moderate disability on the Glasgow Outcome Scale. Major adverse effects were headache and increased heart rate. IAC treatment was effective and safe for the treatment of CV after SAH.

Relationship between vasospasm, cerebral perfusion, and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

IntroductionVasospasm after aneurysmal subarachnoid hemorrhage (SAH) is thought to cause ischemia. To evaluate the contribution of vasospasm to delayed cerebral ischemia (DCI), we investigated the effect of vasospasm on cerebral perfusion and the relationship of vasospasm with DCI.MethodsWe studied 37 consecutive SAH patients with CT angiography (CTA) and CT perfusion (CTP) on admission and within 14 days after admission or at time of clinical deterioration. CTP values (cerebral blood volume, cerebral blood flow (CBF) and mean transit time), degree of vasospasm on CTA, and occurrence of DCI were recorded. Vasospasm was categorized as follows: no spasm (0–25% decrease in vessel diameter), moderate spasm (25–50% decrease), and severe spasm (>50% decrease). The correspondence of the flow territory of the most spastic vessel with the least perfused region was evaluated, and differences in perfusion values and occurrence of DCI between degrees of vasospasm were calculated with 95% confidence intervals (95% CI).ResultsFourteen patients had no vasospasm, 16 were moderate, and seven were severe. In 65% of patients with spasm, the flow territory of the most spastic vessel corresponded with the least perfused region. There was significant CBF (milliliters per 100 g per minute) difference (−21.3; 95% CI, −37 ↔ −5.3) between flow territories of severe and no vasospasm. Four of seven patients with severe, six of 16 with moderate, and three of 14 patients with no vasospasm had DCI.ConclusionVasospasm decreases cerebral perfusion, but corresponds with the least perfused region in only two thirds of our patients. Furthermore, almost half of patients with severe vasospasm do not have DCI. Thus, although severe vasospasm can decrease perfusion, it may not result in DCI.