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[Angioplasty with stenting for intracranial vertebral and basilar artery stenosis: three technical case reports and literature review].

Patients with intracranial vertebral artery (VA) or basilar artery (BA) stenosis have been mainly treated with medication. However, it has been reported that about 10% of patients experience restroke in the VBA territory, with a high rate of morbidity and mortality. Percutaneous transluminal angioplasty (PTA) is regarded as one of the treatments although it carries the risk of restenosis, recoil or dissection. Stent placement is, therefore, considered to be a further option for the treatment of intracranial artery stenosis since it can prevent the restenosis. We report three medical refractory cases of intracranial VA (2 cases) or BA stenosis (1 case) treated with stenting, none of which had complications and their symptoms disappeared or diminished. Angioplasty with the use of a stent device is regarded as a useful treatment for intracranial artery stenosis, but its risk and long-term result need to be investigated further.

Aged↗

Imaging in acute basilar artery thrombosis.

The aim of this study was to review the imaging features in acute (< 24 h) basilar artery thrombosis. CT and MR studies in 11 patients with clinical diagnosis of acute basilar artery thrombosis were retrospectively reviewed. MR angiography was obtained in 4 patients. Correlation with clinical symptoms was performed. Multiple cranial nerve palsies and hemiparesis were the most common clinical symptoms at presentation. CT revealed hyperdense basilar arteries (n = 7) and hypodensities in the posterior circulation territory (n = 8). In one instance, the infarction was hemorrhagic. MR imaging showed absence of flow void within the basilar in 6 patients and MRA (using both PC and TOF techniques) confirmed absence of blood flow in 4 basilar arteries. One week after presentation, 5 patients died. Autopsy was obtained in 1 case and confirmed the diagnosis of basilar artery thrombosis. Basilar artery thrombosis has fairly typical imaging features by both CT and MR. MRA may be used to confirm the diagnosis. Prompt recognition may lead to early thrombolytic treatment and may improve survival.

Acute Disease↗

Effect of diabetes mellitus on flow-mediated and endothelium-dependent dilatation of the rat basilar artery.

BACKGROUND AND PURPOSE: Diabetes mellitus may impair endothelium-dependent responses in cerebral arterioles. The basilar artery dilates in response to increases in blood flow. The goal of this study was to examine effects of diabetes mellitus on "flow-mediated" and endothelium-dependent dilatation of the basilar artery. METHODS: Diabetes was induced in rats with 50 mg/kg streptozotocin. Six months later, vessel diameter and velocity of blood flow through the basilar artery were measured using a cranial window in anesthetized rats under baseline conditions and during occlusion of the carotid arteries. Changes in vessel diameter were also measured during topical application of acetylcholine and sodium nitroprusside. RESULTS: With aortic pressure maintained at baseline levels, blood flow velocity through the basilar artery increased similarly in control and diabetic rats during unilateral common carotid artery occlusion and during bilateral occlusion. In control and diabetic rats, diameter of the basilar artery increased by 10 +/- 2% and 10 +/- 4% during unilateral occlusion and by 27 +/- 5% and 31 +/- 4% during bilateral occlusion, respectively. Thus, diabetes did not impair flow-mediated dilatation of the basilar artery. In contrast, dilatation in response to 10(-5) M topical acetylcholine was less in diabetic rats (13 +/- 2%) than in control rats (45 +/- 8%) (p less than 0.05). Dilator responses to nitroprusside were not impaired by diabetes. CONCLUSIONS: The findings suggest that diabetes produces impairment of endothelium-dependent responses to acetylcholine, but not flow-mediated dilatation, in the basilar artery.

Acetylcholine↗

Thromboaspiration in the basilar artery: report of two cases.

Recanalization of the basilar artery is not always achieved with intraarterial fibrinolysis. We report two cases of thromboaspiration in the basilar artery in which recanalization with fibrinolysis was successful. Thromboaspiration requires favorable anatomy and a fresh nonadhesive clot. It reduces the time for recanalization, has no hemorrhagic risk, and may prevent distal clot migration. Thromboaspiration may be attempted as an adjunct or alternative to intraarterial fibrinolysis for basilar artery recanalization.

Adult↗

Responses of the basilar artery to products released by platelets during chronic hypertension.

The goal of this study was to determine whether responses of the basilar artery to products released by platelets are altered during chronic hypertension. The diameter of the basilar artery was measured using intravital microscopy in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (6-8 months old) in response to adenosine 5'-diphosphate (ADP), serotonin, and the thromboxane analogue, U-46619. Dilatation of the basilar artery in response to nitroglycerin was also examined in WKY and SHR. Topical application of ADP (10 and 100 microM) produced only minimal changes in diameter of the basilar artery in WKY (3 +/- 1% and 1 +/- 1%, respectively) and SHR (-0.5 +/- 2% and -2 +/- 3%, respectively) (P greater than 0.05 vs WKY). Nitroglycerin, however, produced potent vasodilatation in WKY and SHR. Constriction of the basilar artery in response to serotonin was potentiated in SHR compared to WKY. Serotonin (0.1 and 1.0 microM) constricted the basilar artery by 11 +/- 2% and 20 +/- 2%, respectively, in WKY and by 29 +/- 3% and 40 +/- 3%, respectively, in SHR (P less than 0.05 vs WKY). In contrast, the thromboxane analogue (U-46619) (0.1 and 1.0 microM) produced similar constriction of the basilar artery in WKY (13 +/- 1% and 18 +/- 2%, respectively) and in SHR (14 +/- 3% and 21 +/- 6%, respectively). Thus, augmented vasoconstriction during chronic hypertension was specific for serotonin. Next, we examined the role of the cyclooxygenase pathway in responses of the basilar artery to ADP and serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Flow dynamics in a fatal aneurysm of the basilar artery.

PURPOSE: To examine the flow dynamics in a fatal aneurysm of the basilar artery in humans. METHODS: We made transparent elastic replicas of the vertebrobasilar arteries of an elderly patient who died of a ruptured aneurysm in the basilar artery. Using non-Newtonian fluid, physiological pulsatile flow volumes and profiles, and isobaric dyes and particles, we observed and recorded the slipstreams as they entered the aneurysm while changing relative flow in the vertebral arteries. Finally, we placed clips on the aneurysm, leaving residuals (or dog-ears), and observed the slipstreams. RESULTS: The aneurysm originated laterally from the greater curvature of a tortuous basilar artery, measured 19 x 11 x 12 mm, and had a Murphy's teat at the apex, the rupture site. The neck measured 10 x 4 mm, about the diameter of the basilar artery. Slipstreams joined at the confluence of the vertebral arteries, formed helical flow patterns, and entered the aneurysm violently, striking the apex. They then passed proximally around the sac walls, then centrally, and finally reentered the basilar artery to pass distally. Altering the relative flows in the vertebral arteries could modify and prevent slipstream flow into the aneurysm. When a dog-ear was created by incorrect placement of an aneurysm clip, slipstreams entered only dog-ears that lay distal to the clip. Correctly placed clips excluded the aneurysm from the circulation, but did not return the flow dynamics to normal. CONCLUSION: High-velocity slipstreams strike aneurysms at their rupture site and have an impact on distal but not proximal dog-ears. Modifying relative flow may prevent aneurysmal filling. Further, a knowledge of flow dynamics may allow us to predict which aneurysms are at risk of enlarging and rupturing, and may help guide proper therapy.

Aged↗

Zygomatic temporopolar approach for basilar artery aneurysms.

For surgery of upper basilar artery aneurysms, we have modified the temporopolar approach proposed by Sano by detaching the zygomatic arch to obtain a wide, shallow operating field. This approach seems to be suitable for anteriorly protruding, high-positioned, or large aneurysms of the upper basilar artery. We have used this zygomatic temporopolar approach in 4 patients with such aneurysms and obtained satisfactory results. In this paper, we detail the operative procedure and emphasize certain technical points to minimize temporal lobe retraction and to prevent oculomotor and facial nerve injuries.

Aged↗

Two actions of gamma-aminobutyric acid on the responses of the isolated basilar artery from the rabbit.

1 In the isolated basilar artery of the rabbit, gamma-aminobutyrate acid (GABA) (ED50 +/- s.e. mean, 2.4 +/- 1.1 x 10(-5) M) produced a relaxation, if the tone had been increased with 5-hydroxytryptamine (5-HT). 2 3-Aminoproprane sulphonic acid (3-APS) produced a similar, but smaller relaxation, while baclofen had no effect. The relaxation produced by GABA was inhibited by bicuculline. 3 Transmural electrical stimulation produced a reproducible contraction of the isolated basilar artery. In 9 out 14 preparations GABA (ED50 +/- s.e. mean, 5.6 +/- 2.1 x 10(-7) M) caused a reduction of the response, with a maximum of 49.2 +/- 4.3%. Bicuculline did not inhibit these responses to GABA. 4 Baclofen (ED50 +/- s.e. mean, 6.8 +/- 1.4 x 10(-7) M) produced a similar inhibition (47.4 +/- 3.2% maximum) but 3-APS had no effect. 5 GABA (10(-4) M) had no effect on the tone of isolated mesenteric or internal carotid arteries from the rabbit, whether or not the tone was increased with 5-HT. Similarly, GABA (10(-4) M) did not produce any change in the responses to transmural stimulation in isolated mesenteric or internal carotid arteries. 6 These findings are consistent with the presence of two types of GABA receptor on the rabbit basilar artery.

Animals↗

Effects of Iskedyl and its two constituents raubasine and dihydroergocristine on the release of [3H]noradrenaline and [3H]serotonin in canine basilar arteries.

In strips of isolated canine basilar arteries, previously labeled with 3 X 10(-7) M of either [3H]noradrenaline or [3H]serotonin, three consecutive periods of electrical stimulation (2 Hz) evoked a reproducible overflow of the respective [3H]amine. Increasing concentrations of raubasine (7.5 X 10(-7)-7.5 X 10(-6) M) did not influence the spontaneous 3H efflux but increased the stimulation-induced 3H overflow in a concentration-dependent way. The highest concentration of raubasine used (2.5 X 10(-5) M) caused an increased spontaneous 3H efflux but no longer augmented the stimulation-induced 3H overflow. Dihydroergocristine (5.4 X 10(-8)-1.8 X 10(-6) M) did not affect the spontaneous 3H efflux; the compound slightly but significantly reduced the stimulation-evoked 3H overflow concentration dependently. High concentrations of Iskedyl (mixtures of raubasine and dihydroergocristine in a 14:1 molar ratio) augmented the spontaneous 3H efflux and moderately decreased the stimulation-induced 3H overflow. Although some quantitative differences were noted, the compounds exerted similar effects on arteries labeled with either [3H]noradrenaline or [3H]serotonin. The most important difference detected was that DHEC decreased the stimulation-induced release of [3H]serotonin more than that of [3H]noradrenaline. Our results allow a comparison of [3H]noradrenaline and [3H]serotonin release in the dog basilar artery: the basal fractional release of [3H]serotonin was higher than that of [3H]noradrenaline while the stimulation-induced overflow was equal in both groups of tissues. The constituents of Iskedyl can profoundly affect the release of the neurotransmitters. Raubasine, a presynaptic alpha-receptor antagonist, increases the stimulation-induced release of the neurotransmitters and both DHEC, a presynaptic receptor agonist, and the combination of the compounds, Iskedyl, decrease the release of the neurotransmitters.

Animals↗

Segmental duplication of the basilar artery with thrombosis.

Duplication or fenestration of the basilar artery, a result of an embryologic malformation, has an incidence of up to 5.3% in the general population. The most common complication of this anomaly is the formation of aneurysms. Thrombosis of a partially duplicated basilar artery developed in a 43-year-old man who complained of visual disturbances followed by seizures and coma, and who eventually died. Autopsy showed a partially organized thrombus occluding both halves of a duplicated portion of the basilar artery, old infarcts in the calcarine cortices, and a recent large infarct in the basis pontis. There was only minimal atherosclerosis of other intracranial arteries, including the vertebral arteries. Hemodynamic disturbances and turbulent blood flow at the site of fenestration may be the cause of the thrombosis that occurred in this artery.

Adult↗

Detection of basilar artery thrombosis by computed tomography.

Thrombosis of the basilar artery is not uncommon and occurs in the elderly as well as in younger patients. The clinical diagnosis may be supported by the appearance on computed tomography enabling appropriate investigations and therapeutic measures to be taken which may lead to a favourable outcome. Four cases of basilar artery thrombosis are described in which the clinical diagnosis was assisted by computed tomography. The basilar artery, which is normally isodense in unenhanced studies, was seen as a hyperdense structure. Follow-up scans demonstrated a decrease in the density and size of the vessel consistent with resolution of a thrombus.

Adult↗

Effects of VA-045, a novel apovincaminic acid derivative, on rabbit basilar artery.

We investigated the effects of VA-045, an apovincaminic acid derivative, on isolated basilar artery of the rabbit. In basilar artery precontracted with histamine (10(-6) M), VA-045 (10(-9) to 10(-5) M) produced a concentration-dependent relaxation, but VA-045-induced relaxation was significantly reduced when the tonus of the mesentery was raised by isotonic high K+ (30 or 65 mM) or histamine (10(-6) M) with 15 mM K+. VA-045-induced relaxations of the basilar artery were not affected by 10 mM tetraethylammonium (TEA), 10(-6) M 4-aminopyridine, 10(-6) M charybdotoxin, 10(-7) M apamin and 10(-6) M glybenclamide. VA-045-induced relaxation was not influenced by 10(-5) M methylene blue. These results suggest that increased open probability of potassium channels, which are not Ca(2+)-dependent K(+)-channels or TEA- or ATP-sensitive K(+)-channels, may be involved in VA-045-induced relaxation of basilar artery.

Animals↗

Interaction between the L-type Ca2+ channel and the Ca(2+)-activated K+ channel in the fluctuating myogenic contraction in the rabbit basilar artery.

Ring preparations of the rabbit basilar artery spontaneously developed a fluctuating contraction that was not inhibited by the removal of the endothelium or by blockade of the synthesis or action of neurotransmitters and prostanoids. Nifedipine greatly relaxed the spontaneously-developed contraction. Charybdotoxin, an antagonist of the Ca(2+)-activated K+ channel, converted the fluctuating contraction to a tonic contraction, whereas the ATP-sensitive K+ channel blocker, glibenclamide, had no effect. These results indicate that the increased Ca2+ influx via the L-type Ca2+ channel in the rabbit basilar artery may induce myogenic contraction and consequently activate the Ca(2+)-activated K+ channel, which might lead to the fluctuation of the contraction by feedback regulation of the Ca2+ channel.

Animals↗

Massive pontine hemorrhagic infarction associated with embolic basilar artery occlusion.

We report here an autopsy case of massive pontine hemorrhagic infarction secondary to embolic basilar artery occlusion. A large embolus appeared to have traversed the vertebral artery into the basilar artery as a result of basilarization of the vertebral artery due to severe stenosis of the contralateral vertebral artery. Extensive ischemia due to embolic occlusion of the entire length of the basilar artery, and migration of the embolus are assumed to have resulted in a massive pontine hemorrhagic infarction.

Aged↗

Superoxide dismutase ameliorates impaired nitric oxide synthase-dependent dilatation of the basilar artery during chronic alcohol consumption.

The goals of this study were to determine whether chronic alcohol consumption impairs nitric oxide synthase-dependent reactivity of the basilar artery and to determine a potential mechanism which might account for the effects of alcohol on the basilar artery. Sprague-Dawley rats were fed liquid diets with or without alcohol for 8 weeks. Using intravital microscopy, we measured the diameter of basilar artery in response to nitric oxide synthase-dependent agonists (acetylcholine and bradykinin) and a nitric oxide synthase-independent agonist (nitroglycerin). Topical application of acetylcholine (0.1 and 1 microM) and bradykinin (1 and 10 nM) produced dose-related dilatation of the basilar artery in non-alcohol-fed and alcohol-fed rats. However, the magnitude of vasodilatation in response to acetylcholine and bradykinin was significantly less in alcohol-fed rats compared to non-alcohol-fed rats. Dilatation of the basilar artery in response to nitroglycerin was similar in non-alcohol-fed and alcohol-fed rats. Next, we examined whether impaired responses of the basilar artery in alcohol-fed rats in response to acetylcholine and bradykinin may be related to the production of oxygen radicals. We found that topical application of superoxide dismutase (150 U/ml) significantly improved impaired receptor-mediated nitric oxide synthase-dependent dilatation of basilar artery in alcohol-fed rats. However, superoxide dismutase did not alter responses of the basilar artery to nitroglycerin in alcohol-fed rats, and did not alter responses of the basilar artery to nitric oxide synthase-dependent or -independent agonists in non-alcohol-fed rats. Our findings suggest that chronic consumption of alcohol impairs nitric oxide synthase-dependent dilatation of a large cerebral artery which may be related to the receptor-mediated release of oxygen radicals to inactivate nitric oxide.

Acetylcholine↗

Bilateral segmental absence of the internal carotid artery with rete compensation associated with absence of basilar artery: case report.

BACKGROUND: Bilateral ICA absence is a rare lesion. Collateral circulation to the middle and anterior cerebral arteries in the absence of one or both ICAs may develop transcranial anastomoses from the external carotid system, a so-called CRM. Very rarely, theses arterial channels are observed in humans. CASE DESCRIPTION: In the following case study, a 38-year-old man presented himself. He had a headache and scalp laceration after having had an accident. A right external carotid angiography identified anastomoses to distal intracranial vessel through the internal maxillary artery, but the intracranial vessels were only faintly visible. A right ascending pharyngeal arteriography showed an abnormal course and anastomoses with the intracranial vessel. The right ICA was absent. The left external carotid angiography demonstrated a network of tortous arteries in the region of the cavernous and petrous portion of ICA. The plexus of vessels on the left side communicated with the proximal part of the cavernous segment of the ICA. Both vertebral angiographies demonstrated a sudden diminution in caliber at the level of vertebrobasilar junction. There was an anomalous arterial collateral circulation originating from vertebral muscular and meningeal branch. There was also an absence of the basilar artery (BA). CONCLUSION: This is the first case with CRM associated with bilateral segmental ICA and BA absence. The cause of this bilateral segmental ICA and BA absence may be maldevelopment of vessel connective tissue or extracellular matrix.

Arteriovenous Anastomosis↗

Vascular responsiveness of isolated, perfused basilar arteries in dogs and monkeys.

A new model of isolated basilar arterial preparation was developed in the dog and monkey. Isolated arteries were perfused at a constant flow rate with Krebs solution and suspended in a bath at 37 degrees C. By inserting the steel cannula into the artery, the space between the luminal wall of the artery and the cannula was narrowed enough to obtain a suitable perfusion pressure during the perfusion. The resting perfusion pressure was maintained at a constant level of 50-100 mmHg. The drug solution was intraluminally administered, and the response was obtained as changes in the perfusion pressure. Responses to 6 vasoactive substances (norepinephrine, 5-HT, PGF2 alpha, histamine, ATP and KCl) were compared between simian and canine basilar arteries. It was demonstrated that in simian arteries, PGF2 alpha was the strongest but 5-HT and norepinephrine induced slight vasoconstriction to the same degree, and in canine basilar arteries, 5-HT induced the strongest constriction but norepinephrine did not produce significant vasoconstriction, and KCl induced marked constriction to the same degree at extremely large doses in both species. It was demonstrated that the cannula inserting method is useful to observe the responses of isolated basilar arteries.

Adenosine Triphosphate↗