Introduction: The appreciable rise in percutaneous valve procedures has been pursued by a wave of development in advanced technology to help guide straightforward, streamlined and safe intervention. This review article aims to highlight the adjunctive devices, tools and techniques currently used in transcatheter aortic valve implantation procedures to avoid potential pitfalls.
Areas covered: The software and devices featured here are at the forefront of technological advances, most of which are not yet in widespread use. These products have been discussed in national and international structural intervention conferences and the authors felt it important to showcase particularly well designed adjuncts that improve procedural efficacy and safety. Whilst vascular pre-closure systems are used routinely and are an integral part of these complex cardiovascular procedures, these have been well summarised elsewhere and are beyond the scope of this article.
Expert commentary: The rising volume of patients with aortic stenosis who are treatable with TAVI means that this exponential increase in procedures must be accompanied by a steady decline in procedural complications. This section provides an overview of our current perspective, and what we feel the direction of travel will be. 相似文献
Previous studies have shown that alloantigen-activated spleen T cells produce a soluble factor which suppresses mixed lymphocyte reaction proliferative responses, and that the interaction between suppressor and responder cells is controlled by genes of the H-2 complex. However a defect in the expression of suppressor activity was identified in the mouse strain C57BL/6J. Factor prepared from alloactivated B6 spleen cells failed to suppress MLR responses of syngeneic or H-2 compatible responder cells. Unimpaired suppressor factor production by other H-2 (b) strains and failure of suppressor factor production by a B6 congenic strain, B6.C-H-2(d) isolated the defective gene to the non-H-2 portion of the genome. In addition, the defect appeared to be related specifically to inability to produce an active factor, while the capacity to respond to suppressor molecules was unimpaired. The genetic character of the non-H-2 gene action was identified in F1 hybrid studies. Initially F(1) hybrids of the nondefective histoincompatible strains were studied. Suppressor factor from F1 cells suppressed the responses of both parental strains, and parental factors each suppressed the response of F(1) cells. Adsorption of F(1) factor with Con A-activated thymocytes of either parental strain removed suppressor activity specific for that strain, leaving activity against the other parental strain intact. The data support cedominant expression and production of distinct, parental H-2 haplotype-specific suppressor molecules by F(1) suppressor cells. An F(1) hybrid of the defective B6 strain with nondefective BALB/c produced suppressor factor which was also capable of suppressing both parental strains. Production of a suppressive B6-reactive factor by F(1) cells was verified by adsorption studies. Thus it appears that non-H-2 genes of the BALB/c parent acted in a genetically dominant fashion to provide the function required for expression of B6 suppressor molecules. We conclude that multiple genes control the expression of alloactivated suppressor cell activity, with at least one gene mapped to the I-C subregion of the murine major histocompatibility complex and one or more genes mapped to the non-H-2 gene complement. 相似文献
Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 μg (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with doses of 1-2/μg (20-40 ng/kg). A marked increase in arterial blood pressure invariably accompanied the onset of fever; the latency of responses to the higher and lower doses of endotoxins averaged 26 min and 42 min, respectively. Prostaglandin (PG) assays of plasma from the carotid artery and jugular vein during fever episodes revealed a surge of PGE and PGF coincident with the pressor response and the first phase of fever, but PG were not detected in plasma samples taken throughout the second phase of fever. PG measurements of arterial and venous plasma collected at a distal site (hind limb) showed a similar surge of PGE and PGF in association with the early fever response, indicating that intravascular PG synthesis and release represents a generalized systemic response to circulating endotoxin. Carotid arterial infusions of PGE(2) produced immediate monophasic fevers and pressor responses, whereas PGD(2) infusions produced an immediate pressor effect but no fever. Infusions of PGF(2α) or prostacyclin, however, evoked neither fever nor pressor effects. Intracarotid infusions of leukocyte pyrogen (LP) caused monophasic fevers with latent periods of 15-20 min but pressor responses were not seen and neither PGE nor PGF were detected in plasma samples from the carotid artery or jugular vein before or during fever. Indomethacin, a potent inhibitor of arachidonic acid metabolism, blocked fever responses to endotoxin and to LP. These findings implicate PGE as the mediator of the early phase of endotoxin fever and imply a role for another pyrogenic metabolite ofarachidonic acid in the mediation of the second phase of fever, i.e., the phase associated with circulating LP. It is possible that both pyrogenic metabolites are generated within the vascular compartment, reaching thermoregulatory centers of the brain by transfer across the blood-brain interface. 相似文献
Among Hong Kong Chinese blood donors, 99.71 percent were found to be D+. Of these, 55.02 percent were of the phenotype CCDee. The Du phenotype was found to be present in 0.016 percent. Among the 0.27 percent who were apparently D-, 0.079 percent were of the Del phenotype, while the remaining 0.19 percent were "true D-," as defined by a nonreactive eluate obtained by an adsorption and elution procedure using anti-D. The ccdee phenotype constitutes 56.77 percent of the "apparent D-" and 80.24 percent of the true D-. Data show that anti-D rarely occurs in Hong Kong Chinese, and it is postulated that this could be due to the presence of a very weak form of the D antigen among many of those who appear to be D-. 相似文献