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The study sought to compare the acute gain and two-year follow-up late lumen loss (LLL) between the Absorb bioresorbable vascular scaffold (BVS) and the analogous everolimus-eluting metallic stent (EES). The current analysis included all the patients recruited in the ABSORB Cohort B and SPIRIT II trials implanted with a single 3.0×18 mm device (Absorb BVS or EES) who underwent serial angiographic examinations at baseline and at two-year follow-up. The acute gain was defined as the difference between post- and preprocedural minimal lumen diameter (MLD). The in-stent/scaffold LLL was calculated as the difference in stent/scaffold segment between the post-procedural MLD and follow-up MLD. Thirty-three patients (33 lesions) implanted with the Absorb BVS, and 26 patients (28 lesions) implanted with the EES were studied. The acute gain was similar in the Absorb BVS group (1.23±0.38 mm) compared to the EES group (1.32±0.26 mm, p=0.29). The in-stent/scaffold LLL at two-year follow-up in the Absorb BVS group (0.26±0.19 mm) was also similar compared to the EES group (0.22±0.22 mm, p=0.29). Although the two groups had similar two-year clinical outcomes (major adverse cardiac events: Absorb BVS: 6.1% vs. EES: 0.0%), patients treated with the Absorb BVS exhibited a significantly lower two-year in-stent/scaffold MLD compared to the EES (2.02±0.26 mm vs. 2.22±0.34 mm, p=0.01). Although BVS and EES demonstrated similar two-year clinical outcomes, patients treated with the Absorb BVS exhibited a significantly lower two-year in-stent/scaffold MLD compared to patients treated with the EES. Appropriately powered randomised trials are necessary to confirm these exploratory results and evaluate their prognostic and clinical significance.
Part 1 Innervation of the Airways: Neuropeptides and Classic Innervation - Neural Structures in Human Airways Functional Autonomic Innervation of the Airways - The Cholinergic and Adrenergic Systems Neuropeptides in the Lower Airways Investigated by Modem Microscopy Neural Control of the Upper Respiratory Tract Peptide Biosynthesis and Secretion - Some Recent Developments and Unresolved Issues Vasoactive Intestinal Polypeptide in the Respiratory Tract Neuropeptide Y in the Airways Sensory Nerves and Tachykinins Pulmonary Endocrine Cells In Vivo and In Vitro Molecular Characterization of Autonomic and Neuropeptide Receptors Autonomic Receptors in the Upper and Lower Airways Tachykinin Receptor Antagonists Pulmonary Peptidases - General Principles of Peptide Metabolism and Molecular Biology of Angiotensin Converting Enzyme, Neutral Endopeptidase 24.11, and Carboxypeptidase M Peptidases in the Respiratory Tract - The Localization and Actions of Carboxypeptidase M. Part 2 Physiological Functions of Neuropeptides in the Airways: The Concept of Neurogenic Inflammation in the Respiratory Tract Modulation of Neurogenic Inflammation by Peptidase Control of Airway Vascular Beds Basophil and Mast Cell Activation - Neuropeptides and Nerves Inositol Triphosphate and Smooth Muscle Function Neuropeptides and Airway Macromolecule Secretion ATP as Neurally Released Modulator of Human Airway Ion Transport Effects of Neuropeptides on Neurotransmission in the Airways. Part 3 Pathophysiological Contribution of Neuropeptides to Disease: Neuropeptides and Asthma Inflammatory Mechanisms in Cystic Fibrosis Lung Disease Allergic Rhinitis Neuropeptides in Small Cell Lung Carcinoma Neuroregulation of Pulmonary Immunity - The Roles of Substance P and Vasoactive Intestinal Peptide Sensory Neuropeptides in an Animal Model of Hyperpnoea-induced Bronchoconstriction Nitric Oxide and Guanylyl Cyclases - Correlation with Neuropeptides Neuropeptides in Bronchoalveolar Lavage in Allergic Asthma Morphology of Neurogenic lnflammation in the Airways - Plasma Protein Movement Across the Airway Mucosa and Epithelium.
No abstract is provided for this article.
GATA-3 is a transcription factor that is specifically expressed in T helper 2 (Th2) cells and plays a critical role in the differentiation of Th2 cells from uncommitted CD4+ lymphocytes. In addition GATA-3 is essential for the gene expression of the cytokines IL-4, IL-5 and IL-13 that mediate allergic inflammation. In human T lymphocytes GATA-3 is normally localized to the cytoplasm, but on activation by antigen-presenting cells via the T cell receptor (CD3) and co-stimulatory receptor CD28 GATA-3 is phosphorylated by p38 MAP kinase and translocates to the nucleus via the nuclear import protein importin-α. Corticosteroids bound to glucocorticoid receptors inhibit GATA-3 function by competing for nuclear entry via importin-α and also by inhibiting p38 MAP kinase through the induction of MAP kinase phosphatase-1. GATA-3 is inhibited by the Th1 master regulatory transcription T-bet but in turn inhibits STAT-4 and thus T-bet so that Th2 polarization is maintained. Since GATA-3 appears to be a critical transcription factor for allergic inflammation it is an obvious target for inhibition. However, direct inhibition by inhaled specific oligonucleotides or interference RNA is not yet possible. Corticosteroids act as indirect inhibitors and in patients with corticosteroid resistance p38 MAP kinase inhibitors may also prove to be useful in the future.
Background: Optical Coherence Tomography (OCT) is a high resolution imaging technique capable of accurate assessment of polymeric struts, changes in luminal and scaffold dimensions, and quantificat...
Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory disorders of the respiratory tract that are characterized by airflow limitation. They are distinct conditions with different causes, structural changes, and immunopathology. The pathophysiology in asthma and COPD involves not only the proximal large airways, but also the distal small airways, and thus the small airways are an important therapeutic target in the treatment of both diseases. The assessment of diseased distal small airways is challenging. Extensive disease can be present in the small airways with little abnormality in conventional pulmonary function tests. Recent advances in imaging technologies have led to better spatial resolution to assess small airways morphology non-invasively. New physiological tests have been developed to detect disease and response to therapy in regional airways. Improving the efficiency of existing aerosolized therapy to direct drug to the appropriate lung regions may improve clinical efficacy. Approaches to target distal lung regions include developing new drug formulations with smaller aerosol particle size or using inhaler devices that emit aerosolized drug at slow inhalation flows. Large studies are needed to determine whether better distal lung deposition leads to improvements in small airways function that are translated into clinically significant patient outcomes.
No abstract is provided for this article.
Objectives The primary objective of this study was to evaluate the safety and effectiveness of the Mirage (Manli Cardiology, Singapore) bioresorbable microfiber sirolimus-eluting scaffold compared with the Absorb (Abbott Vascular, Santa Clara, California) bioresorbable vascular scaffold in the treatment of stenotic target lesions located in native coronary arteries, ranging from ≥2.25 to ≤4.0 mm in diameter. Secondary objectives were to establish the medium-term safety, effectiveness, and performance of the Mirage device. Background The current generation of bioresorbable scaffolds has several limitations, such as thick square struts with large footprints that preclude their deep embedment into the vessel wall, resulting in protrusion into the lumen with microdisturbance of flow. The Mirage sirolimus-eluting bioresorbable microfiber scaffold is designed to address these concerns. Methods In this prospective, single-blind trial, 60 patients were randomly allocated in a 1:1 ratio to treatment with a Mirage sirolimus-eluting bioresorbable microfiber scaffold or an Absorb bioresorbable vascular scaffold. The clinical endpoints were assessed at 30 days and at 6 and 12 months. In-device angiographic late loss at 12 months was quantified. Secondary optical coherence tomographic endpoints were assessed post–scaffold implantation at 6 and 12 months. Results Median angiographic post-procedural in-scaffold minimal luminal diameters of the Mirage and Absorb devices were 2.38 mm (interquartile range [IQR]: 2.06 to 2.62 mm) and 2.55 mm (IQR: 2.26 to 2.71 mm), respectively; the effect size (d) was −0.29. At 12 months, median angiographic in-scaffold minimal luminal diameters of the Mirage and Absorb devices were not statistically different (1.90 mm [IQR: 1.57 to 2.31 mm] vs. 2.29 mm [IQR: 1.74 to 2.51 mm], d = −0.36). At 12-month follow-up, median in-scaffold late luminal loss with the Mirage and Absorb devices was 0.37 mm (IQR: 0.08 to 0.72 mm) and 0.23 mm (IQR: 0.15 to 0.37 mm), respectively (d = 0.20). On optical coherence tomography, post-procedural diameter stenosis with the Mirage was 11.2 ± 7.1%, which increased to 27.4 ± 12.4% at 6 months and remained stable (31.8 ± 12.9%) at 1 year, whereas the post-procedural optical coherence tomographic diameter stenosis with the Absorb was 8.4 ± 6.6%, which increased to 16.6 ± 8.9% and remained stable (21.2 ± 9.9%) at 1-year follow-up (Mirage vs. Absorb: dpost-procedure = 0.41, d6 months = 1.00, d12 months = 0.92). Angiographic median in-scaffold diameter stenosis was significantly different between study groups at 12 months (28.6% [IQR: 21.0% to 40.7%] for the Mirage, 18.2% [IQR: 13.1% to 31.6%] for the Absorb, d = 0.39). Device- and patient-oriented composite endpoints were comparable between the 2 study groups. Conclusions At 12 months, angiographic in-scaffold late loss was not statistically different between the Mirage and Absorb devices, although diameter stenosis on angiography and on optical coherence tomography was significantly higher with the Mirage than with the Absorb. The technique of implantation was suboptimal for both devices, and future trials should incorporate optical coherence tomographic guidance to allow optimal implantation and appropriate assessment of the new technology, considering the novel mechanical properties of the Mirage.
