Treatment of a Symptomatic Severe Basilar Artery Stenosis with Balloon Dilatation (NeuroSpeed) Followed by the Implantation of a Self-Expanding Stent (Credo) with Good Clinical Outcome and Follow-Up
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Keywords:
Balloon dilatation
Stroke
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Self-expanding metal stents (SEMS) seem to be the optimal choice for benign esophageal disorders, especially those not associated with a stricture, such as anastomotic leaks, iatrogenic perforations, and fistulas. On the other hand stent embedding can be an important limitation of SEMS placement, because this precludes safe stent removal [1]. In fact, in the literature there are only a few case series reporting the stent-in-stent technique using SEMS to remove embedded stents (14 – 189 days from the placement of the first stent) [2] [3].
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OBJECTIVE Endothelin (ET)-1 may be involved in the regulation of cerebrovascular resistance under pathological conditions, most notably during the development of vasospasm after subarachnoid hemorrhage. Blocking ET-converting enzyme activity may be a promising approach to the prevention of cerebral vasospasm after subarachnoid hemorrhage. METHODS In this study, the effects of several putative ET-converting enzyme inhibitors were investigated after intracisternal application in rabbits, to inhibit basilar artery contractions induced by big ET-1 (2 × 10−6 mol/L). RESULTS In the group pretreated with [d-Val22]big ET-1[16–38] (2 × 10−5 mol/L) (n = 8), the angiographically measured diameter of the basilar artery changed from 0.63 ± 0.12 mm to 0.66 ± 0.12 mm. In the control group (n = 8), the diameter of the basilar artery decreased from 0.71 ± 0.13 mm to 0.57 ± 0.15 mm. These results corresponded to an increase in vessel diameter of 5 ± 10% in the treatment group and a decrease in vessel diameter of 20 ± 16% in the control group (P = 0.014). In the group pretreated with captopril (2 × 10−4 mol/L) (n = 8), the angiographically measured diameter of the basilar artery changed from 0.64 ± 0.11 mm to 0.71 ± 0.10 mm. These results corresponded to an increase in vessel diameter of 14 ± 19% in the treatment group, compared with a decrease in vessel diameter of 20 ± 16% in the control group (P = 0.014). CONCLUSION These results demonstrate that [d -Val22]big ET-1[16–38] and captopril act as highly potent ET-converting enzyme inhibitors, affecting big ET-1-induced contraction of the rabbit basilar artery.
Cerebral Vasospasm
Captopril
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SUMMARY 1. Previous studies have suggested the involvement of arginine vasopressin (AVP) and inflammation in the development of cerebral vasospasm after subarachnoid haemorrhage (SAH). The aim of the present study was to clarify the role of AVP in the arterial narrowing following cerebral haemorrhage by examining the effect of SR 49059 (a V 1 receptor antagonist) on the diameter of rat basilar artery exposed to SAH. The effect of the 5‐lipoxygenase inhibitor ZM 230487 on AVP‐induced contraction of rat basilar arteries was also investigated. 2. After 1 h and 2 days from SAH induction, brains were removed and pictures of the basilar arteries were taken. The external diameter of the basilar artery was measured in the presence and absence of SR 49059 (1 mg/kg, i.v.). For in vitro experiments, the basilar arteries isolated from control and SAH rats (at 1 h and at 2 days from SAH induction) were cut into spiral preparations and the AVP (0.3 nmol/L)‐induced contraction in the presence of ZM 230487 was investigated. Each group analysed (i.e. control, SAH 1 h and SAH 2 days) consisted of eight rats. 3. The diameter of rat basilar arteries decreased by 43 and 25% at 1 h and 2 days from SAH induction, respectively, compared with control. The administration of SR 49059 significantly reduced cerebral vasospasm. After SAH induction, the diameter of the basilar artery in SR 49059‐treated groups decreased by only 22% (at 1 h) and by 3% (at 2 days) compared with the control group ( P < 0.01). In basilar arterial strips, ZM 230487 attenuated the vasopressin‐induced contraction in both control and SAH groups. However, SAH groups showed a significant resistance of the AVP‐induced contraction in the presence of ZM 230487 compared with control ( P < 0.05). 4. The results suggest that the cerebral vasospasm in SAH rats is due, at least in part, to endogenous AVP and may involve an increase in the activity of 5‐lipoxygenase. SR 49059 may represent a potential therapeutic strategy for the treatment of cerebral vasospasm.
Cerebral Vasospasm
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Endothelin (ET)-1 may be involved in the regulation of cerebrovascular resistance under pathological conditions, most notably during the development of vasospasm after subarachnoid hemorrhage. Blocking ET-converting enzyme activity may be a promising approach to the prevention of cerebral vasospasm after subarachnoid hemorrhage.In this study, the effects of several putative ET-converting enzyme inhibitors were investigated after intracisternal application in rabbits, to inhibit basilar artery contractions induced by big ET-1 (2 x 10(-6) mol/L).In the group pretreated with [D-Val22]big ET-1[16-38] (2 x 10(-5) mol/L) (n = 8), the angiographically measured diameter of the basilar artery changed from 0.63 +/- 0.12 mm to 0.66 +/- 0.12 mm. In the control group (n = 8), the diameter of the basilar artery decreased from 0.71 +/- 0.13 mm to 0.57 +/- 0.15 mm. These results corresponded to an increase in vessel diameter of 5 +/- 10% in the treatment group and a decrease in vessel diameter of 20 +/- 16% in the control group (P = 0.014). In the group pretreated with captopril (2 x 10(-4) mol/L) (n = 8), the angiographically measured diameter of the basilar artery changed from 0.64 +/- 0.11 mm to 0.71 +/- 0.10 mm. These results corresponded to an increase in vessel diameter of 14 +/- 19% in the treatment group, compared with a decrease in vessel diameter of 20 +/- 16% in the control group (P = 0.014).These results demonstrate that [D-Val22]big ET-1[16-38] and captopril act as highly potent ET-converting enzyme inhibitors, affecting big ET-1-induced contraction of the rabbit basilar artery.
Cerebral Vasospasm
Captopril
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Objective
To explore the basilar artery morphology and pathology after hemodynamic changes of basilar artery.
Methods
New Zealand white rabbits were subjected to bilateral common carotid artery ligation to produce compensatory vertebrobasilar artery flow increase. The basilar artery flow velocity was monitored by transcranial Doppler before the procedure and at 1 day, 1 week and 2 weeks after the procedure. DSA was performed at 1 week and 2 weeks after the procedure respectively and the basilar artery diameter and the extent of tortuosity were measured. The basilar artery tissues were harvested at 1 week and 2 weeks after the procedure and examined histologically by EVG and Masson staining.
Results
The basilar artery flow velocity of New Zealand white rabbit was increased significantly subjected to common carotid artery ligation (10.99 ml/min vs 36.53 ml/min, P<0.001). One or two weeks after surgery, the basilar artery diameter was expanded (0.60 mm vs 0.82 mm; 0.73 mm vs 1.03 mm, P<0.001), and the artery was curved. The internal elastic layer of artery was intact with smooth muscle cells proliferation in response to high flow and shear stress. The basilar artery was bent to the left side in 57.1% of all rabbits and there was significant difference compared with that of preoperation.
Conclusions
The hemodynamic increasing of the basilar artery after bilateral common carotid artery ligation of New Zealand white rabbits resulted in expansion and tortuosity of the basilar artery.
Key words:
Basilar artery; Hemodynamic; Vascular remodeling; Angiography
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Restenosis after successful balloon angioplasty remains problematic. Early elastic response after angioplasty is significant when considering the possible development of restenosis. The purpose of this study was to compare early elastic recoil within 10 minutes after successful percutaneous transluminal coronary angioplasty and early lumen loss at 24 hours after angioplasty in a cutting balloon group and a conventional balloon group.Extent of early elastic recoil was quantitatively measured as the difference of mean balloon diameter at maximal inflation pressure and minimal luminal diameter after angioplasty in 82 cutting balloon-treated lesions and 51 conventional balloon-treated lesions.Reference diameter and balloon/artery ratio were similar between the cutting balloon and conventional balloon groups (2.89 0.47 mm vs. 2.88 0.60 mm; 1.19 0.11 vs. 1.19 0.13, respectively). Early elastic recoil after angioplasty was significantly smaller in the cutting balloon than the conventional balloon group (0.96 0.40 mm vs. 1.12 0.37 mm, respectively; p = 0.04). Also, the mean amount of lumen loss from 10 minutes after angioplasty to 24 hours after was significantly smaller in the cutting balloon than the conventional balloon group (0.08 0.28 mm vs. 0.20 0.33 mm, respectively; p = 0.02).There is significantly less early elastic recoil in the cutting balloon angioplasty than in the conventional balloon angioplasty group. The efficacy of cutting balloon continues 24 hours after angioplasty.
Elastic recoil
Cutting balloon
Lumen (anatomy)
Recoil
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Objective: To establish an in vivo observation method of basilar artery in rat.Methods: The basilar artery of the rat was exposed by a cranial window opened via clivus approach.The basilar artery and the related vascular structure were observed using a visual microscope and the screen of a computer.Results: The basilar artery and the related vascular structure including the microvasculature could be clearly viewed.Conclusion: An easy-to-use observation method of basilar artery in rat was successfully established.
Clivus
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Studies in vitro suggest that the basilar artery has distinctive responses to endothelium-dependent stimuli. Our first goal was to examine the effects of acetylcholine on diameter of the basilar artery in vivo. Because aggregating platelets may have important effects on cerebral arteries, our second goal was to examine the effects on the basilar artery of products that are released by platelets (thromboxane, serotonin, and adenosine 5'-diphosphate). Diameter of the basilar artery was measured through a cranial window in anesthetized rats (n = 25). Baseline diameter of the basilar artery was 247 +/- 10 microns mean +/- SEM. Topical application of acetylcholine at 10(-6) and 10(-5) M dilated the basilar artery by 13 +/- 2% and 19 +/- 2%, respectively. The thromboxane analogue U46619 at 10(-8) and 10(-7) M reduced the diameter of the basilar artery by 18 +/- 5% and 29 +/- 4%, respectively. At 10(-8) and 10(-7) M, serotonin had little effect on pial arterioles on the cerebrum but constricted the basilar artery by 18 +/- 2% and 29 +/- 4%, respectively. At 10(-6) and 10(-5) M, adenosine 5'-diphosphate produced marked dilatation of pial arterioles on the cerebrum (9 +/- 2% and 20 +/- 3%, respectively) but had little effect on the basilar artery (increased diameter by 4 +/- 2% and 6 +/- 2%, respectively). Thus, in contrast to some studies of the basilar artery in vitro, acetylcholine produces dilatation of the basilar artery in vivo. Potent constrictor responses to thromboxane and serotonin, in combination with the minimal dilator effect of adenosine 5'-diphosphate, suggest that release of these products during platelet aggregation would favor constriction of the basilar artery.
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Objective.
Black Africans currently experience a distinctly low frequency of atherosclerotic cardiovascular disease. Whether this protection persists in those with rheumatoid arthritis (RA) is unknown. We compared the carotid atherosclerosis burden and its relationships with cardiovascular (CV) risk factors between Africans with RA from a developing black and developed CV population.Methods.
We performed high resolution B-mode ultrasonography and assessed CV risk factors in 243 patients with established RA, of whom 121 were black and 122 white. Data were analyzed in age, sex, and healthcare center-adjusted regression models.Results.
The mean ± SD common carotid intima-media thickness (cIMT) was 0.694 ± 0.097 mm in black and 0.712 ± 0.136 mm in white patients (adjusted p = 0.8). Plaque prevalence was also similar in black compared to white cases (35.5% and 44.3%, respectively; adjusted OR 0.83, 95% CI 0.32–2.20, p = 0.7). Interactions between population grouping and several CV risk factors were independently associated with cIMT and plaque. In stratified analysis, that is, in each population group separately, risk factors associated with cIMT or/and plaque comprised the systolic blood pressure (p = 0.02), serum cholesterol/high-density lipoprotein cholesterol ratio (p = 0.004), C-reactive protein concentrations (p = 0.01), and the presence of extraarticular manifestations (p = 0.01) in whites but, contrastingly, the Arthritis Impact Measurement Scales tension score (p = 0.04) and use of nonsteroidal antiinflammatory agent (p = 0.03) in black patients. The Framingham score was significantly associated with atherosclerosis only in whites (p < 0.0001).Conclusion.
The carotid atherosclerosis burden is similar in black compared to white Africans with RA, but relationships between modifiable CV risk factors and atherosclerosis vary substantially among Africans with RA.Recoil
Elastic recoil
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