Vertebral and Basilar Arteries: Transcranial Color-Coded Duplex Ultrasonography versus Conventional TCD in Detection of Narrowings.

We prospectively compared the accuracies of conventional transcranial Doppler ultrasound (TCD) and transcranial color-coded duplex sonography (TCCS) in the diagnosis of narrowing of the basilar (BA) and vertebral arteries (VA). Fifty-six consecutive patients (mean age 55.8 years; 34 women) after subarachnoid hemorrhage (n=46), stroke or transient ischemic attack (n=5), and for other reasons (n=5) underwent on the same day TCD, TCCS and the intra-arterial digital subtraction angiography (DSA) - the reference standard. The accuracy of peak-systolic (VPS), mean (VM), and end-diastolic velocities (VED) in detection of any arterial narrowing was estimated using the receiver operator characteristic (ROC) curve methodology and the total area (Az) under the curve. Accuracy of TCCS in detection of VA narrowing based on VPS and VM measurements was significantly higher than accuracy of TCD (Az=0.65 for VPS and Az=0.62 for VM versus Az=0.51 and Az=0.50, respectively, p<0.05 for both). Accuracy of TCCS in detection of BA narrowing was also higher than accuracy of TCD based on VPS measurements (Az=0.69 versus Az=0.50, respectively), with a trend toward significant difference, p=0.085. The accuracy of TCCS is superior to accuracy of TCD in detection of narrowings of vertebral and basilar arteries, thus TCCS should be preferred in routine clinical practice.

The role of time-resolved 3D contrast-enhanced MR angiography in the assessment and grading of cerebral arteriovenous malformations.

PURPOSE: To assess the role of three-dimensional (3D) contrast-enhanced, time-resolved MR angiography (CE TR MRA) in patients with intracranial arteriovenous malformations (AVMs). METHODS: We studied 12 patient with intracranial AVMs on a 3.0T MR imaging system (Magentom TIM Trio, Siemens Medical Solutions, Erlangen, Germany) using 3D CE TR MRA with autocalibrating partially parallel acquisitions and echo sharing schemes, which provided temporal resolution of 0.58 or 1.7s and near isotropic voxels. We qualitatively assessed image quality of the 3D CE TR MRA and compared the grading of the AVMs based on modified Spetzler-Martin system for 3D CE TR MRA and catheter digital subtraction angiography (DSA). RESULTS: CE TR MRA provided good quality images in the 3 standard orthogonal planes, and good arterial-venous separation in all cases. All AVMs were correctly graded by CE TR MRA when compared with DSA. 3D CE TR MRA provides a non-invasive alternative to DSA for the evaluation of cerebral AVMs.

Restenosis after carotid endarterectomy: incidence and endovascular management.

SUMMARY: Surgical procedures designed to restore vascular patency for a recurrent stenosis following carotid endarterectomy (CEA) are burdened with technical difficulties as well as with the possibility of serious neurological complications. An endovascular approach employing transluminal percutaneous angioplasty and stenting (PTAS) is a promising solution to these problems. We aimed to evaluate the incidence of carotid artery restenosis following CEA, and to evaluate the safety and efficacy of treating post-CEA restenosis with an endovascular technique (PTAS). One hundred and two patients who underwent CEA for symptomatic and asymptomatic stenosis were included in the analysis. Clinical and sonographic follow-up examinations identified carotid artery restenosis in 16 patients, who fulfilled our criteria for endovascular treatment. Carotid PTAS was performed on symptomatic patients with a stenosis over 60% of the artery lumen (n=7) and in asymptomatic patients with a stenosis over 80% (n=9). The post-PTAS patients were evaluated by duplex sonography every three months over a 24 month follow-up period for evidence of restenosis. The cumulative incidence of post-CEA carotid restenosis qualifying for PTAS was 9.3% during an average 12-month follow-up interval. The average time from CEA to carotid PTAS was 11 months. All 16 endovascular procedures were technically successful. All of the carotid arteries were widely patent following PTAS. There were no immediate perioperative complications. One patient died two days after carotid PTAS from a cerebral hemorrhage. Thirteen of the 16 patients remained asymptomatic and had no sonographic evidence of significant restenosis during the 24- month post-PTAS follow-up period. One patient developed a symptomatic 80% restenosis proximal to the stent six months after carotid PTAS. Another patient developed an asymptomatic 60% restenosis proximal to the stent at 24 months. One patient was lost to follow-up. Following CEA, there is a significant risk of developing a symptomatic or high-grade carotid artery restenosis requiring correction. Endovascular treatment (PTAS) of a recurrent stenosis after CEA is a safe and effective alternative to repeat carotid surgery.

Cerebrovascular angioplasty and stenting for the prevention of stroke.

Until recently, stroke preventive strategies have focused on either medical regimens aimed at antagonizing or reversing atherosclerosis, or surgical intervention for revascularization of the cerebrovascular system. However, with the advent of rapidly emerging microcatheterization techniques and technology, endovascular surgical revascularization of the brain is rapidly emerging as a powerful therapeutic modality. In particular, significant advances already have been made in revascularization of the extracranial carotid artery and many common anatomic sites of intracranial athero-occlusive disease, using special adaptations of conventional percutaneous angioplasty and stenting techniques. This paper reviews the cumulative experience with these emerging techniques, with a particular emphasis on clinical outcomes and future directions. It also reports the substantial cumulative institutional experience of the authors over the past 18 months with both extracranial carotid and intracranial artery stent-assisted carotid angioplasty.

Expandable intravascular catheter: percutaneous use for endoluminal retrievals.

Percutaneous use of an expandable vascular access catheter that can be deployed to temporarily occlude the entry vessel during retrieval of embolic material is described. The catheter was used to facilitate removal of two intraarterial objects, a postangioplasty free atheroma fragment and a displaced Gianturco coil. The expanded catheter end was equal to the arterial lumen, thus preventing distal embolization. The large distal lumen also facilitated plaque or foreign body removal by allowing deployment of various endovascular tools.

Renal arterial rupture complicating transluminal angioplasty: successful conservative management.

Vessel rupture complicating transluminal angioplasty is an uncommon event, especially in the renal artery. The authors report such a case, which was treated with immediate balloon tamponade and did not require surgical intervention. Possible causes and appropriate management are discussed, as well as the need for reporting angioplasty-related complications to a registry being developed by the Society of Cardiovascular and Interventional Radiology.

Functional reconstitution of the purified sodium channel protein from rat sarcolemma.

The purified saxitoxin (STX) binding component of the rat sarcolemmal sodium channel (SBC) has been reconstituted into phospholipid vesicles. The reconstituted SBC displays the pharmacological properties and the ability to control sodium fluxes expected of a functional sodium channel. Batrachotoxin (BTX) increases 22Na+ influx into reconstituted SBC vesicles by greater than 100% over control at early time points. The BTX-stimulated 22Na+ influx is specifically and quantitatively blocked by STX. Veratridine and aconitine also stimulate Na+-flux--although less effectively than BTX--in the order: BTX greater than veratridine greater than aconitine. The logarithmic dose--response curves for BTX and veratridine are sigmoidal with a K0.5 of 1.5 microM and 35 microM, respectively. Vesicles containing the reconstituted SBC demonstrate 3H-labeled STX binding to a single class of high affinity sites witha Kd of 5--7 nM at 0 degrees C; the thermal stability of the STX receptor is markedly enhanced by reconstitution. Our results confirm that the purified STX binding component from rat sarcolemma constitutes the sodium channel itself and contains at least those components sufficient for channel activation, transmembrane ion movement, and inhibition by STX.

Ultraviolet irradiation produces loss of saxitoxin binding to sodium channels in rat synaptosomes.

Ultraviolet irradiation (UV) has been shown to cause an electrophysiologically measured inactivation of the rapid, transient sodium conductance system in nerve. Tritiated saxitoxin ([3H]STX) was used as a structural probe to assess the possibility of a corresponding perturbation in the conformation of the STX binding site. UV irradiation caused an irreversible decrease in the total number of high-affinity [3H]STX binding sites in rat synaptosomes, while the dissociation constant of the remaining sites did not change. The receptor loss followed first-order kinetics, and the rate of loss was independent of temperature. The action spectrum for binding loss indicated a peak in spectral sensitivity near 280 nm. A22Na flux assay in irradiated synaptosomes directly demonstrated that [3H]STX binding sites and veratridine-stimulated, STX-blocked 22Na efflux had similar sensitivities to UV radiation. We conclude that the UV inactivation of functional channels includes a modification of the STX binding-site structure.

Characteristics of saxitoxin binding to the sodium channel of sarcolemma isolated from rat skeletal muscle.

1. The characteristics of saxitoxin (STX) binding to the mammalian Na channel have been studied in purified sarcolemma isolated from rat skeletal muscle. 2. STX binds specifically to isolated sarcolemma with a Kd of 1.43 x 10(-9) M and Bmax of 7-8 p-mole STX bound/mg membrane protein at 0 degrees C in the presence of 140 mM-NaCl. In rat muscle homogenate under the same conditions the corresponding values are Kd = 1.53 x 10(-9) M and Bmax = 0.15-0.20 p-mole/mg protein (18-20 p-mole/g wet wt.). Membrane purification produced a fortyfold increase in STX binding site concentration per milligram protein. Calculated binding site density in isolated sarcolemma was about 30 sites/micron 2 of membrane surface. 3. Denervation (10-14 days) results in a 43% reduction in the density of high-affinity STX binding sites in purified sarcolemma, but the Kd for this class of sites is not changed. 4. In sarcolemma, the apparent Kd for STX binding is dependent on temperature pH and ionic strength. The Q10 for Kd between 0 and 40 degrees C is 1.3. Protonation of a group having a pK of 6.0 markedly raises Kd without affecting Bmax. Apparent Kd increases eightfold when ionic strength is raised from 20 to 600 mM. 5. Dissociation and association rate constants for STX binding are temperature dependent with Q10 of 2.6 and 1.9 respectively between 0 and 20 degrees C. 6. STX binding is competitively inhibited by monovalent and divalent cations under conditions of constant total ionic strength. An affinity sequence of Tl+ greater than Li+ greater than Na+ greater than K+ greater than Rb+ greater than Cs+ is seen for the monovalent cation-binding site. 7. The STX binding site is relatively stable to heat and to enzymic degradation. A specific modifier of carboxyl residues inactivates subsequent STX binding. This process can be prevented by the presence of STX during the reaction. 8. Characteristics of the STX binding site in isolated sarcolemma are compared to those reported for other isolated excitable membranes and for studies of whole muscle and muscle homogenate. Sarcolemma provides a potential source of enriched Na channels for further purification efforts in a mammalian system.

Muscle surface membranes: preparative methods affect apparent chemical properties and neurotoxin binding.

Considerable disagreement exists between results reported by various authors for lipid composition and enzyme activity in purified muscle membrane fractions presumed to be sarcolemma, although an explanation for these discrepancies has not been presented. We have prepared muscle light surface membrane fractions of comparable density (1.050--1.120) by a low-salt sucrose method and by an LiBr-KCl extraction procedure and compared them for density profile, total lipid and cholesterol content, protein composition and ATPase activity. In addition, sodium channels characteristic of excitable membranes have been quantitated in each preparation using [3H]saxitoxin binding assays, and the density of acetylcholine receptors determined in fractions from control and denervated muscle using alpha-[125I]bungarotoxin. Although both fractions contain predominantly surface membrane, the LiBr fraction consistently shows the higher specific activity of p-nitrophenylphosphatase, higher free cholesterol content, and higher density of sodium channels and acetylcholine receptors. The density distribution of sodium channels appears uniform throughout both fractions. Quantitative differences were seen between sodium dodecyl sulfate polyacrylamide gel electrophoresis patterns of membrane proteins from the two preparations although most bands are represented in both. A majority of the low-salt sucrose light membrane proteins were accessible in varying degrees to labelling with diazotized diiodosulfanylic acid in intact muscle. These results suggest that light surface membrane fractions may be mixtures of sarcolemma and T-tubular membranes. Using our preparative methods, the LiBr fraction may contain predominantly sarcolemma while low-salt sucrose light membranes may be enriched in T-tubular elements.