A system for delivering and deploying a self-expandable heart valve to a site of implantation such as the aortic annulus includes a deployment mechanism that engages the valve and regulates the rate of expansion of both the proximal and distal ends thereof. The heart valve may be a rolled-type valve and the deployment mechanism may include a plurality of distal fingers and a plurality of proximal fingers that engage the outer layer of the heart valve. Controlled radial movement of the fingers regulates the unwinding of the rolled heart valve. The fingers may be removed prior to inflation of a balloon to fully expand the valve, or the fingers may be repositioned to the inside of the valve for this purpose. The deployment mechanism may include an umbrella structure that forces the rolled valve outward into its fully expanded configuration. Alternatively, a gear shaft that engages one or more gear tracks on the valve may be utilized to regulate expansion of the valve. A stabilization balloon may be used to axially and radially locate the deployment mechanism relative to the site of implantation. Methods of operation of the delivery and deployment mechanism include regulating the rate of self-expansion of the valve and forcing the valve outward into its fully expanded configuration utilizing the same or different means.

Methods and apparatuses for deploying minimally-invasive heart valves

The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Embodiments of the present disclosure provide a prosthetic heart valve and a heart valve delivery apparatus for delivery of the prosthetic heart valve to a native valve site via the human vasculature. The delivery apparatus is particularly suited for advancing a prosthetic valve through the aorta (i.e., in a retrograde approach) for replacing a diseased native aortic valve. In one embodiment, a self-expanding valve comprises an expandable stent that is shaped to maintain the valve in the aortic annulus against axial without anchors or retaining devices that engage the surrounding tissue. A delivery apparatus for delivering s self-expanding prosthetic valve can be configured to allow controlled and precise deployment of the valve from a valve sheath so as to minimize or prevent jumping of the valve from the valve sheath.

Prosthetic heart valve and delivery apparatus

A folding apparatus (200) for use in mounting a prosthetic valve (102) on a stent (104), the valve having an expanded diameter, the apparatus configured to fold the valve into an undulated shape having multiple folds and a diameter that is less than the expanded diameter. The apparatus comprises: a base (202); a plurality of stationary posts (204) connected to the base at fixed locations, nd a plurality of moveable posts (206) connected to the base and moveable relative to the base radially inwardly toward each other and the center point and radially outwardly away from each other and the center point; wherein when the valve (102) is placed around the posts with the valve extending around outer sides of the stationary posts and inner sides of the moveable posts, moving the moveable posts radially inwardly toward each other folds the valve.

Implantable prosthetic valve assembly and method for making the same

Embodiments of prosthetic valves for implantation within a native mitral valve are provided. A preferred embodiment of a prosthetic valve includes a radially compressible main body and a one-way valve portion. The prosthetic valve further comprises at least one ventricular anchor coupled to the main body and disposed outside of the main body. A space is provided between an outer surface of the main body and the ventricular anchor for receiving a native mitral valve leaflet. The prosthetic valve preferably includes an atrial sealing member adapted for placement above the annulus of the mitral valve. Methods and devices for delivering and implanting the prosthetic valve are also described.

Prosthetic valve for replacing mitral valve

Increasing doses of adenosine were given by rapid intravenous bolus to seven patients with spontaneous supraventricular tachycardia. Adenosine restored sinus rhythm in 10 of 14 episodes of narrow complex tachycardia. In those patients in whom adenosine produced only transient ventricular slowing the underlying rhythm was atrial flutter. Transient dyspnoea occurred in all patients. In two patients taking dipyridamole the mean dose of adenosine which produced an electrophysiologic effect (restoration of sinus rhythm or ventricular slowing to under 100 beats min-1) was 1.0 +/- 0.52 mg, whereas in other patients the mean dose was 8.8 +/- 2.6 mg, suggesting potentiation of the action of adenosine by dipyridamole.

Intravenous adenosine in the treatment of supraventricular tachycardia: a dose-ranging study and interaction with dipyridamole

Adenosine is an endogenous nucleoside which stimulates respiration in man and other mammals. In animals adenosine appears to initiate respiratory stimulation within the carotid body, but whether this is the site of action in man is not known. We administered adenosine by intra-aortic infusion to 12 subjects undergoing cardiac catheterisation. When adenosine was infused at three sites proximal to the carotid circulation, minute ventilation was significantly higher than baseline values or those during adenosine infusion at a more distal site. These results support the hypothesis that adenosine-induced respiratory stimulation in man is mediated in the carotid body.

/pdf/adenosine-induced-respiratory-stimulation-in-man-depends-on-4zb7usrw70.pdf

Adenosine-induced respiratory stimulation in man depends on site of infusion. Evidence for an action on the carotid body?

The effects on respiration of intravenous infusions of the endogenous nucleoside adenosine and its deaminated metabolite, inosine, administered in random order, single-blind, were compared in six healthy volunteers. The infusion rate of each nucleoside was initially 3.1 mg min-1 and was increased stepwise every 2 min, as tolerated, up to a possible maximum of 23.4 mg ml-1. The maximum dose rates received by all subjects were 8.5 mg min-1 for adenosine and 16.8 mg min-1 for inosine. Adenosine infusion at rates of 6.1 mg min-1 and above caused a significant increase in minute ventilation, principally due to an increase in tidal volume, with an associated significant fall in end-tidal Pco2. Mean inspiratory flow rate increased and expiratory duration decreased during adenosine infusion, but there was no change in inspiratory duration. Adenosine infusion also caused a significant increase in heart rate and a slight, but significant increase in systolic blood pressure. Infusion of inosine at dose rates up to 16.8 mg min-1 produced no pharmacological effects. This study shows that adenosine by infusion produces sustained respiratory stimulation in man and demonstrates that it does not depend on prior conversion of adenosine to inosine or related metabolites and that it is not secondary to systemic hypotension.

/pdf/intravenous-infusion-of-adenosine-but-not-inosine-stimulates-1n17gsoqyv.pdf

Intravenous infusion of adenosine but not inosine stimulates respiration in man.

Amiodarone is a useful antiarrhythmic agent whose pharmacokinetics are incompletely characterised. In order to optimise efficacy of an antiarrhythmic drug, information regarding plasma concentrations achieved during use of the drug is necessary. We report plasma amiodarone and desethylamiodarone concentrations in eight patients following intravenous infusion at a rate of 175 mg h-1 for the first 2 h, followed by infusion at a rate of 50 mg h-1 for a further 46 h a regimen very similar to that recommended by the manufacturers. In at least three of eight patients plasma concentrations were below the suggested therapeutic range of 1.0-2.5 mg l-1 from 3 to 16 h after the infusion was started. Our data suggests that larger doses of intravenous amiodarone than those previously recommended may be necessary to obtain optimal benefit from the drug.

/pdf/plasma-amiodarone-concentrations-during-intravenous-infusion-18tfoye5h6.pdf

Plasma amiodarone concentrations during intravenous infusion.

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Papers

Intravenous adenosine in the treatment of supraventricular tachycardia: a dose-ranging study and interaction with dipyridamole

Adenosine-induced respiratory stimulation in man depends on site of infusion. Evidence for an action on the carotid body?

Intravenous infusion of adenosine but not inosine stimulates respiration in man.

Plasma amiodarone concentrations during intravenous infusion.