Background Stent restenosis is an infrequent but poorly understood clinical problem in the drug-eluting stent era. The aim of the study was to evaluate the morphologic characteristics of stent restenosis by optical coherence tomography (OCT). Methods Patients (n = 24, 25 vessels) presenting with angiographically documented stent restenosis were included. Quantitative OCT analysis consisted of lumen and stent area measurement and calculation of restenotic tissue area and burden. Qualitative restenotic tissue analysis included assessment of tissue structure, backscattering and symmetry, visible microvessels, lumen shape, and presence of intraluminal material. Results By angiography, restenosis was classified as diffuse, focal, and at the margins in 9, 11, and 5 vessels, respectively. By OCT, restenotic tissue structure was layered in 52%, homogeneous in 28%, and heterogeneous in 20%. The predominant backscatter was high in 72%. Microvessels were visible in 12%. Lumen shape was irregular in 28% and there was intraluminal material in 20%. The mean restenotic tissue symmetry ratio was 0.58 ± 0.19. Heterogeneous and low scattering restenotic tissue was more frequent in focal (45.5% and 54.5%, respectively) than in diffuse (0 and 11.1%) and margin restenosis (0 and 0%) (P = .005 for heterogeneous, P = .03 for low scattering). Restenosis patients with unstable angina symptoms presented more frequently irregular lumen shape (60 vs 6.7%, P = .007). Stents implanted ≤12 months ago had more frequently restenotic tissue with layered appearance (84.6% vs 16.7%, P = .003). Conclusions We demonstrate the ability of OCT to identify differential patterns of restenotic tissue after stenting. This information could help in understanding the mechanism of stent restenosis.
No abstract is provided for this article.
A pesar de los avances que se han efectuado en el tratamiento de los pacientes con enfermedad coronaria, los cuadros de muerte súbita por causa cardíaca tienen todavía una prevalencia inaceptable. Los pacientes con cardiopatía isquémica requieren habitualmente la combinación de distintas formas de tratamiento (fármacos e intervención coronaria), a pesar de lo cual pueden seguir presentando sintomatología. Recientemente, se han desarrollado numerosas formas de tratamiento mediante intervención percutánea y distintas herramientas diagnósticas que permiten la detección de las placas vulnerables y el tratamiento del elevado número de pacientes que presentan isquemia miocárdica. La investigación actual respecto al uso de endoprótesis con capacidad de liberación de fármacos, bypass coronario efectuado con catéteres (abordajes percutáneos en los que se utiliza la circulación venosa adyacente para revascularizar la arteria obstruida, así como el abordaje mediante endoprótesis para la conexión entre el ventrículo y la arteria coronaria), los abordajes terapéuticos de angiogénesis y miogénesis, y las técnicas intracoronarias para la detección de la vulnerabilidad y la composición de las placas (placas ateromatosas con abundante core lipídico, cubierta fibrosa fina y remodelado positivo), puede facilitar opciones diagnósticas y terapéuticas adicionales en los pacientes con enfermedad coronaria. Despite the advances in the treatment of patients with coronary artery disease, sudden cardiac death is still unacceptably prevalent. Patients with ischemic heart disease usually require a combination of therapies (drugs and coronary intervention) and may continue to experience symptoms. Recently, numerous percutaneous interventional treatments and diagnostic tools have been developed to diagnose the vulnerable plaque and to treat the large number of patients with myocardial ischemia. Ongoing research on the use of drug eluting stents, catheter based bypass graft (percutaneous approaches that use the adjacent venous circulation to bypass an obstructed artery and stent-based approach for ventricle to coronary artery bypass), therapeutic angiogenesis and myogenesis, and the catheter based devices to detect the plaque vulnerability and composition (lipid-rich atheromatous core, thin fibrous cap, and expansive vessel remodeling) may result in additional diagnostic and therapeutic options for patients with coronary artery disease.
Conference Abstract| February 01 1982 The Effects of Almitrine on Resting Ventilation and Hypoxic and Hypercapnic Drives to Ventilation in Normal Subjects J.R. Stradling; J.R. Stradling 1Department of Medicine, Hammersmith Hospital, Royal Postgraduate Medical School London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar S. L. Turner; S. L. Turner 1Department of Medicine, Hammersmith Hospital, Royal Postgraduate Medical School London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar P. Barnes; P. Barnes 1Department of Medicine, Hammersmith Hospital, Royal Postgraduate Medical School London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar N. B. Pride N. B. Pride 1Department of Medicine, Hammersmith Hospital, Royal Postgraduate Medical School London W12 OHS Search for other works by this author on: This Site PubMed Google Scholar Author and article information Publisher: Portland Press Ltd Online ISSN: 1470-8736 Print ISSN: 0143-5221 © 1982 The Biochemical Society and the Medical Research Society1982 Clin Sci (Lond) (1982) 62 (2): 6P. https://doi.org/10.1042/cs062006P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation J.R. Stradling, S. L. Turner, P. Barnes, N. B. Pride; The Effects of Almitrine on Resting Ventilation and Hypoxic and Hypercapnic Drives to Ventilation in Normal Subjects. Clin Sci (Lond) 1 February 1982; 62 (2): 6P. doi: https://doi.org/10.1042/cs062006P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1982 The Biochemical Society and the Medical Research Society1982 Article PDF first page preview Close Modal You do not currently have access to this content.
No abstract is provided for this article.
We present a grey-scale map of a portion of the Orion Nebula made at a wavelength of 2.2 µm. Spatial chopping was not employed, so the map includes a true representation of the extended emission as well as the dense cluster of point infrared sources, Several features not previously recorded can be seen in this map. The nature of the point sources is discussed in relation to their near-infrared colours, and their magnitude distribution. We also describe our DC mapping technique and discuss its potential.
Chronic obstructive pulmonary disease (COPD) is a major and increasing global health problem that is now a leading cause of death. COPD is associated with a chronic inflammatory response, predominantly in small airways and lung parenchyma, which is characterized by increased numbers of macrophages, neutrophils, and T lymphocytes. The inflammatory mediators involved in COPD have not been clearly defined, in contrast to asthma, but it is now apparent that many lipid mediators, inflammatory peptides, reactive oxygen and nitrogen species, chemokines, cytokines, and growth factors are involved in orchestrating the complex inflammatory process that results in small airway fibrosis and alveolar destruction. Many proteases are also involved in the inflammatory process and are responsible for the destruction of elastin fibers in the lung parenchyma, which is the hallmark of emphysema. The identification of inflammatory mediators and understanding their interactions is important for the development of anti-inflammatory treatments for this important disease.
Peter Barnes is Professor of Thoracic Medicine at the National Heart and Lung Institute (London, UK), Head of Respiratory Medicine at Imperial College (London, UK) and Honorary Consultant Physician at Royal Brompton Hospital (London, UK). He qualified at Cambridge and Oxford Universities (first class honours [Cambridge, UK and Oxford, UK, respectively]) and was appointed to his present posts in 1987. He has published over 1000 peer-reviewed papers on asthma, chronic obstructive pulmonary disorder (COPD) and related topics and has written or edited over 50 books. He is also among the top 50 most highly cited researchers in the world and has been the most highly cited clinical scientist in Europe and the most highly cited respiratory researcher in the world over the last 20 years. He was elected a Fellow of the Royal Society in 2007, the first respiratory researcher for over 150 years. He is currently a member of the Scientific Committee of global guidelines on asthma and COPD. He also serves on the Editorial Board of over 30 journals and is currently an Associate Editor of several respiratory publications. He has given several prestigious lectures, including the Amberson Lecture at the American Thoracic Society, the Sadoul Lecture at the European Respiratory Society and the Croonian Lecture at the Royal College of Physicians, London. He has been received honorary MD degrees from the Universities of Ferrara (Italy), Athens (Greece), Tampere (Finland) and Leuven (Belgium). He is a NIHR Senior Investigator and was elected a Master Fellow of the American College of Chest Physicians in 2012. He is President Elect of the European Respiratory Society. He co-founded an Imperial spin-out company RespiVert, which was acquired by Johnson & Johnson and has developed novel inhaled treatments for COPD and severe asthma. Interview conducted by Hannah Coaker, Assistant Commissioning Editor.
The release of neurotransmitters may exacerbate the inflammatory response. Such neurogenic inflammation has been documented in a number of inflammatory diseases. Neurogenic inflammation due to release of neuropeptides from sensory nerves has been demonstrated in airways of several species, particularly rodents, and may contribute to the inflammatory response in asthmatic airways. Tachykinins (substance P and neurokinin A) released from airway sensory nerves may cause bronchoconstriction, vasodilatation, plasma exudation, and mucus secretion, whereas another sensory neuropeptide, calcitonin gene-related peptide, may contribute to hyperemia of inflammation. Airway epithelial damage in asthma exposes sensory nerves which may become sensitized by inflammatory products (including prostaglandins and cytokines) so that neuropeptides are released via a local reflex trigger such as bradykinin, resulting in exaggerated inflammation. The effects of tachykinins may be amplified further by loss of the major degrading enzyme, neutral en-dopeptidase, from epithelial cells. Direct evidence for neurogenic inflammation in asthma is still awaited, however. Several strategies for reducing neurogenic inflammation are possible, particularly inhibition of neuropeptide release from sensory nerves by stimulating prejunctional receptors such as μ-opioid receptors.
No abstract is provided for this article.
No abstract is provided for this article.
