TL;DR: In this article, a medical device (1210) comprises a generally cylindrical treatment element (1220) for location between a pair of valve leaflets (1212) situated between an atrium (1214) and a ventricle (1216) of a heart.
Abstract: A medical device (1210) comprises a generally cylindrical treatment element (1220) for location between a pair of valve leaflets (1212) situated between an atrium (1214) and a ventricle (1216) of a heart . The treatment element (1220) supports the valve leaflets (1212) at the region of co-aptation of the valve leaflets (1212) and occludes the valve opening to resist fluid flow in the retrograde direction through the valve opening. The device (1210) comprises a support (1222) to support the treatment element (1210) at the region of co-aptation of the valve leaflets (1212) . The support has an anchor (1224) and a tether (1226) , the tether (1226) being provided at the end of a guide wire (1228) which is initially utilised in the percutaneous insertion of the treatment element (1220) . The anchor (1224) is secured, in use, to a septal wall (1230) , while the guide wire (1228) exits the atrium (1214) through a vein adjacent a rear wall (1224) thereof .
TL;DR: A radially expandable artificial valve prosthesis for regulating fluid flow through a body vessel is provided in this article, which includes a ring frame, at least one valve leaflet attached to the ring frame forming a valve pocket and a support structure adapted to position the ringframe within the bodily passage.
Abstract: A radially expandable artificial valve prosthesis for regulating fluid flow through a body vessel is provided. The prosthesis includes a radially expandable ring frame, at least one valve leaflet attached to the ring frame forming a valve pocket and a support structure attached to the ring frame and adapted to position the ring frame within the bodily passage. The height of the valve pocket is less than the maximum cross sectional dimension of the lumen defined by the expanded ring frame. The valve leaflet is allows fluid flow in a first, antegrade, direction and restricts flow in a second, retrograde direction.
TL;DR: In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.
Abstract: Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V 1 -V 2 , A 1 -A 2 ) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V 1 -V 2 , A 1 -A 2 ) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction. The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A 1 -A 2 , H 1 -H 2 ) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.
TL;DR: V-A is less often longer and more often shorter than A-V and in some patients retrograde pre-excitation and V-A may occur through bypass pathways, functional in the retrograde direction only, which suggest bidirectional conduction through a single common pathway.
Abstract: The purpose of this report was to compare antegrade (atrioventricular [A-V]) and retrograde (ventriculoatrial [V-A]) conduction times in 124 consecutive patients who exhibited bidirectional conduction during diagnostic studies where His bundle recordings were obtained. None of these patients had any evidence of antegrade pre-excitation. The mean age was 64 ± 13 (range 32-89 years). The QRS complex was abnormal (≧ 0.11 sec) in 46 patients. The control mean P-R, A-H, and H-V times were 170 ± 37, 80 ± 21, 49 ± 8 msec, respectively. The A-V and V-A times were measured from local bipolar right ventricular (RV) and right atrial (RA) electrograms obtained via pacing catheters placed in the high RA and RV apex. Both RA and RV were paced at identical cycle lengths and the rate was progressively increased until block developed or to a cycle length of 400-330 msec. The V-A time was longer than A-V in 45 (group A), equal in 11 (group B), and shorter in 68 patients. Of the latter 68 patients (group C) in 49 V-A time was 172 ± 36 as compared to 197 ± 38 msec for A-V time, and while the interval lengthened at higher pacing rates, it remained shorter than A-V time throughout (197 ± 40 versus 261 ± 51 msec). In the remaining 19 patients (group D) the V-A was not only shorter than A-V (176 ± 27 versus 207 ± 49 msec) but remained unchanged up to the highest paced rates, whereas A-V time progressively lengthened 269 ± 81 msec). In group D a constant V-A time in all probability is indicative of retrograde impulse transmission through tissue other than the A-V node, i.e., bypass pathways functioning only in a retrograde direction. Progressively increasing A-V and V-A times in groups A to C suggest bidirectional conduction through a single common pathway. Our data demonstrate that: 1) V-A is less often longer (35%) and more often shorter (56%) than A-V; 2) In some patients retrograde pre-excitation and V-A may occur through bypass pathways, functional in the retrograde direction only. These findings may be of clinical significance.
TL;DR: Axonal transport of the molecular forms of acetylcholinesterase in chick sciatic nerve found that the rapidly mobile fraction of AChE was estimated to constitute 23% of the total enzyme activity present in the nerve, 14% of it moving in an anterograde and 9% in a retrograde direction.
Abstract: :
Acetylcholinesterase (AChE) polymorphism was studied in the sciatic nerve of 4-week-old Leghorn chicks, by sucrose gradient sedimentation analysis. Four main AChE molecular forms were found with sedimentation coefficients of 5S, 7.5S, 11.5S and 20S respectively. Axonal transport of each of these forms was investigated on the basis of the enzyme accumulation kinetics measured on both sides of nerve transections and of the enzyme redistribution kinetics in nerve segments isolated in vivo. After nerve transection, 11.5S and 20S forms accumulated faster in the anterograde than in the retrograde direction and also much faster than 5S and 7.5S forms in the anterograde direction. Retrograde accumulations of 5S and 7.5S were faint or negligible. In addition, 1 h after nerve cutting, the accumulation rates for 11.5S and 20S forms (but not for 5S and 7.5S) fell, in both directions, to about one-third of their initial values, probably owing to reversal of axonal transport at the axotomy site. Local protein synthesis inhibition by cycloheximide did not affect the accumulation of 11.5S and 20S in front of a transection, at least during the first hours, but reduced that of 5S and 7.5S by about 40%. In isolated nerve segments in vivo, the rapidly mobile fraction of AChE was estimated to constitute 23% of the total enzyme activity present in the nerve, 14% of it moving in an anterograde and 9% in a retrograde direction. A small amount of 11.5S molecules (approx. 20%) was in rapid transit (two-thirds in the anterograde and one-third in the retrograde direction), whereas almost all the 20S—about 90%—migrated rapidly (two-thirds forwards and one-third backwards). Anterograde velocities of 408 ± 94 and 411 ± 161 mm/day respectively were estimated for the 11.5S and 20S forms. Their respective retrograde velocities were 175 ± 85 and 145 ± 107 mm/day. Assuming that the totality of 5S and 7.5S molecules are moving in the anterograde direction, their accumulation rates were consistent with the average anterograde velocities of 2.9 ± 1.3 and 5.1 ± 1.4 mm/day, respectively. Couraud J. Y. and Di Giamberardino L. Axonal transport of the molecular forms of acetylcholinesterase in chick sciatic nerve. J. Neurochem. 35, 1053–1066 (1980).