Relevant bibliographies by topics / Arteriopathy

Academic literature on the topic 'Arteriopathy'

Author: Grafiati
Published: 7 July 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Arteriopathy":

1

Chen, Alan M., Kunal B. Karani, J. Michael Taylor, Bin Zhang, Andrew Furthmiller, Gabriel De Vela, James L. Leach, Sudhakar Vadivelu, and Todd A. Abruzzo. "Cervicocerebral quantitative arterial tortuosity: a biomarker of arteriopathy in children with intracranial aneurysms." Journal of Neurosurgery: Pediatrics 24, no. 4 (October 2019): 389–96. http://dx.doi.org/10.3171/2019.5.peds1982.

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OBJECTIVEAlthough intracranial arterial aneurysms (IAAs) of childhood are usually idiopathic, it is possible that underlying arteriopathy escapes detection when using conventional diagnostic tools. Quantitative arterial tortuosity (QAT) has been studied as a biomarker of arteriopathy. The authors analyzed cervicocerebral QAT in children with idiopathic IAAs to assess the possibility of arteriopathy.METHODSCases were identified by text-string searches of imaging reports spanning the period January 1993 through June 2017. QAT of cervicocerebral arterial segments was measured from cross-sectional studies using image-processing software. Other imaging and clinical data were confirmed by retrospective electronic record review. Children with idiopathic IAAs and positive case controls, with congenital arteriopathy differentiated according to aneurysm status (with and without an aneurysm), were compared to each other and to healthy controls without vascular risk factors.RESULTSCervicocerebral QAT was measured in 314 children: 24 with idiopathic IAAs, 163 with congenital arteriopathy (including 14 arteriopathic IAAs), and 127 healthy controls. QAT of all vertebrobasilar segments was larger in children with IAAs (idiopathic and arteriopathic forms) (p < 0.05). In children with congenital arteriopathy without an aneurysm, QAT was decreased for the distal cervical vertebral arteries and increased for the supraspinal vertebral artery relative to healthy children. QAT of specific cervicocerebral segments correlated with IAA size and rupture status.CONCLUSIONSCervicocerebral QAT is a biomarker of arteriopathy in children with IAA, even in the absence of other disease markers. Additional findings suggest a correlation of cervicocerebral QAT with IAA size and rupture status and with the presence of IAA in children with congenital arteriopathy.
2

Rafay, Mubeen F., Kevin A. Shapiro, Ann-Marie Surmava, Gabrielle A. deVeber, Adam Kirton, Heather J. Fullerton, Catherine Amlie-Lefond, et al. "Spectrum of cerebral arteriopathies in children with arterial ischemic stroke." Neurology 94, no. 23 (May 26, 2020): e2479-e2490. http://dx.doi.org/10.1212/wnl.0000000000009557.

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ObjectiveTo determine that children with arterial ischemic stroke (AIS) due to an identifiable arteriopathy are distinct from those without arteriopathy and that each arteriopathy subtype has unique and recognizable clinical features.MethodsWe report a large, observational, multicenter cohort of children with AIS, age 1 month to 18 years, enrolled in the International Pediatric Stroke Study from 2003 to 2014. Clinical and demographic differences were compared by use of the Fisher exact test, with linear step-up permutation min-p adjustment for multiple comparisons. Exploratory analyses were conducted to evaluate differences between cases of AIS with and without arteriopathy and between arteriopathy subtypes.ResultsOf 2,127 children with AIS, 725 (34%) had arteriopathy (median age 7.45 years). Arteriopathy subtypes included dissection (27%), moyamoya (24.5%), focal cerebral arteriopathy–inflammatory subtype (FCA-i; 15%), diffuse cerebral vasculitis (15%), and nonspecific arteriopathy (18.5%). Children with arteriopathic AIS were more likely to present between 6 and 9 years of age (odds ratio [OR] 1.93, p = 0.029) with headache (OR 1.55, p = 0.023), multiple infarctions (OR 2.05, p < 0.001), sickle cell anemia (OR 2.9, p = 0.007), and head/neck trauma (OR 1.93, p = 0.018). Antithrombotic use and stroke recurrence were higher in children with arteriopathy. Among arteriopathy subtypes, dissection was associated with male sex, older age, headache, and anticoagulant use; FCA-i was associated with hemiparesis and single infarcts; moyamoya was associated with seizures and recurrent strokes; and vasculitis was associated with bilateral infarctions.ConclusionSpecific clinical profiles are associated with cerebral arteriopathies in children with AIS. These observations may be helpful indicators in guiding early diagnosis and defining subgroups who may benefit most from future therapeutic trials.
3

Joyal, France, and Pascal Margaroli. "Calcific Arteriopathy." New England Journal of Medicine 352, no. 26 (June 30, 2005): e24. http://dx.doi.org/10.1056/nejmicm040777.

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4

Wagenvoort, C. A. "Plexogenic arteriopathy." Thorax 49, Suppl (September 1, 1994): S39—S45. http://dx.doi.org/10.1136/thx.49.suppl.s39.

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Mitchell, Richard N. "Allograft arteriopathy." Cardiovascular Pathology 13, no. 1 (January 2004): 33–40. http://dx.doi.org/10.1016/s1054-8807(03)00108-x.

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Gupta, R. K. "Transplant Arteriopathy." Transplantation Proceedings 39, no. 3 (April 2007): 763–65. http://dx.doi.org/10.1016/j.transproceed.2007.01.068.

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Smith, Edward R. "Moyamoya Arteriopathy." Current Treatment Options in Neurology 14, no. 6 (August 3, 2012): 549–56. http://dx.doi.org/10.1007/s11940-012-0195-4.

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Kothur, Kavitha, Christopher Troedson, Richard Webster, Sushil Bandodkar, Stephanie Chu, Louise Wienholt, Alun Pope, Mark T. Mackay, and Russell C. Dale. "Elevation of cerebrospinal fluid cytokine/chemokines involved in innate, T cell, and granulocyte inflammation in pediatric focal cerebral arteriopathy." International Journal of Stroke 14, no. 2 (September 13, 2018): 154–58. http://dx.doi.org/10.1177/1747493018799975.

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Aim To determine the role of inflammation in pediatric transient focal cerebral arteriopathy using cerebrospinal fluid cytokine/chemokines as biomarkers. Methods We measured 32 cytokine/chemokines in acute cerebrospinal fluid collected from children with stroke due to focal cerebral arteriopathy (n = 5) using multiplex immunoassay and compared with two patients with arterial ischemic stroke due to other causes (non-focal cerebral arteriopathy group, vertebral dissection, n = 1; cryptogenic, n = 1), pediatric encephalitis (n = 43), and non-inflammatory neurological disease controls (n = 20). Results Median age in the focal cerebral arteriopathy group was 9.3 years (range, 2.8–13 years). In the focal cerebral arteriopathy group (n = 5), four patients had middle cerebral ± distal carotid arteriopathy; one patient had posterior circulation arteriopathy. The median time from symptom onset to cerebrospinal fluid sampling was four days (range, 0.6–7 days). Only IL-6, IL-8, CXCL1, and CXCL10 levels were significantly higher in the acute cerebrospinal fluid of focal cerebral arteriopathy patients compared to non-inflammatory neurological disease controls and non-focal cerebral arteriopathy stroke. In contrast to focal cerebral arteriopathy, a broad array of Th1, Th2, Treg, Th17, B-cell related, and other broad spectrum cytokine/chemokines were elevated in encephalitis. Conclusion The elevated cerebrospinal fluid cytokine/chemokines support innate, T cell, and granulocyte inflammatory mechanisms in children with focal cerebral arteriopathy. This warrants larger cohort studies to discriminate primary inflammatory signals of the arteriopathy from secondary inflammation due to the stroke itself.
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Cuoco, Joshua A., Christopher M. Busch, Brendan J. Klein, Michael J. Benko, Rachel Stein, Andrew D. Nicholson, and Eric A. Marvin. "ACTA2 Cerebral Arteriopathy: Not Just a Puff of Smoke." Cerebrovascular Diseases 46, no. 3-4 (2018): 159–69. http://dx.doi.org/10.1159/000493863.

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Background: Missense mutations in the gene that codes for smooth muscle actin, ACTA2, cause diffuse smooth muscle dysfunction and a distinct cerebral arteriopathy collectively known as multisystemic smooth muscle dysfunction syndrome (MSMDS). Until recently, ACTA2 cerebral arteriopathy was considered to be a variant of moyamoya disease. However, recent basic science and clinical data have demonstrated that the cerebral arteriopathy caused by mutant ACTA2 exhibits genetic loci, histopathology, neurological sequelae, and radiographic findings unique from moyamoya disease. We conducted a literature review to provide insight into the history, clinical significance, and neurosurgical management of this recently described novel cerebral arteriopathy. Summary: We performed a literature search using PubMed with the key words “ACTA2 mutation,” “ACTA2 cerebral arteriopathy,” and “multisystemic smooth muscle dysfunction syndrome.” Case reports with confirmed ACTA2 mutations and cerebral arteriopathy were included in our review. Our literature search revealed 15 articles (58 cases) of confirmed ACTA2 cerebral arteriopathy. Distinctive features of this arteriopathy included an aberrant internal carotid circulation with dilatation of the proximal segments, occlusive disease at the distal segments, and dolichoectasia. As such, mutant ACTA2 predisposed patients to ischemic strokes as children. Direct and indirect cerebral revascularization procedures are the mainstay treatment options with varying degrees of success. Key Messages: ACTA2 cerebral arteriopathy is a recently described novel cerebrovascular disease seen in patients with MSMDS. Patients currently diagnosed with moyamoya disease who also have dysfunction of smooth muscle organs may benefit from reevaluation by a medical geneticist and ACTA2 genotyping.
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Olivero, Juan Jose, Juan Jorge Olivero, Peter Nguyen, and Anna Kagan. "Nephrogenic Calcific Arteriopathy." Methodist DeBakey Cardiovascular Journal 7, no. 4 (October 1, 2011): 33. http://dx.doi.org/10.14797/mdcvj.304.

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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Arteriopathy":

1

Hayashino(Miyagawa), Aya. "Arteriopathy in chronic allograft rejection in liver transplantation." Kyoto University, 2005. http://hdl.handle.net/2433/144489.

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Quesada, Sabaté Miquel. "Arteriopatia perifèrica assimptomàtica: prevalença, detecció i tractament." Doctoral thesis, Universitat de Girona, 2017. http://hdl.handle.net/10803/457149.

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Background There is few epidemiological data of peripheral arterial disease (PAD) in our environment. The recommendation of screening with ankle brachial index (ABI) in asymptomatic individuals is controversial. Evidence is lacking about the effectiveness of risk reduction interventions in patients with asymptomatic peripheral arterial disease (PAD). Aims 1) To determine the prevalence of ankle-brachial index (ABI)<0.9 and symptomatic peripheral arterial disease (PAD), association with cardiovascular risk factors (CVRF), and impact of adding ABI measurement to coronary heart disease (CHD) risk screening 2) to develop and validate a pre-screening test to select candidates for ABI measurement in the Spanish population 50-79 years old, and to compare its predictive capacity to current Inter-Society Consensus (ISC) screening criteria. 3) to assess whether statin therapy was associated with a reduction in major cardiovascular events (MCE) and mortality in this population
Introducció Existeix poca informació epidemiològica de la malaltia arterial perifèrica (MAP) al nostre medi, la recomanació de cribratge amb índex turmell-braç (ITB) en individus asimptomàtics és objecte de controvèrsia i es desconeix l'efectivitat de les intervencions de reducció de risc amb estatines en pacients amb MAP asimptomàtica. Objectius Els objectius de la present tesi són: 1) Determinar la prevalença d'ITB <0,9 i de MAP asimptomàtica, la seva associació amb factors de risc cardiovascular (FRCV) en la població de 35-79 anys i estimar l'impacte d'afegir la mesura d'ITB a la predicció de risc cardiovascular 2) Desenvolupar i validar una funció de risc per seleccionar els millors candidats pel cribratge de MAP amb ITB en la població de 50-79 anys d'edat 3) Avaluar si la teràpia amb estatines s'associa a una reducció d'esdeveniments cardiovasculars (ECV) i de mortalitat en aquesta població
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Joseph, Emlyn Clive. "Pathogenesis of arteriopathy induced by PDE III inhibitors in the rat and dog." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307684.

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Low, Wee Chuang Roger. "Molecular pathology of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and hereditary multi-infarct dementia." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417546.

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Martin, Roswell James. "CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) : clinical features and approaches to genetic screening in the UK." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609947.

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Cowan, Bryce John. "Elafin inhibition of fibronectin synthesis and inflammatory cell proliferation, and reduction of post-cardiac transplant coronary arteriopathy and myocardial necrosis, in vitro and in vivo mechanisms." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0003/NQ35133.pdf.

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FELISATTI, Michele. "Compressione pneumatica intermittente negli stadi avanzati di arteriopatia periferica: studio delle modificazioni emodinamiche e della perfusione distale indotte da un dispositivo originale e confronto con uno strumento disponibile sul mercato." Doctoral thesis, Università degli studi di Ferrara, 2011. http://hdl.handle.net/11392/2389232.

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Introduction: Intermittent pneumatic compression (IPC) is a technique based on the application of pressure at the level of various points of the inferior limb, aimed at provoking haemodynamic modifications starting from the treatment zone. IPC devices, that are mainly used in the area of venous-lymphatic pathologies to reduce edema and for the prevention of venous thromboembolism, have also been applied for treatment of peripheral arterial occlusive disease (PAOD). An IPC device, “Gradient Pump” (GP), based on new haemodynamic concept and technical solutions, has been recently developed by the Vascular Diseases Center of the University of Ferrara-Italy. Aim of the present study in PAOD patients is a) to evaluate the effects of GP on haemodynamic parameters and foot perfusion during a single operative cycle and during a therapeutic cycle and b) to compare efficacy and compliance to the treatment of GP versus a traditional device for PAOD available on the market. Subjects and Methods: In the study were enrolled and evaluated a) 7 patients (12 diseased legs) with PAOD at III-IV Fontaine’s stage and b) 12 patients (21 diseased legs, 12 out of them affected by critical ischemia). The GP device is composed of a single inflatable cuff to be positioned at the thigh, including a rigid element to apply a proper pressure to the femoral vein. The cuff is connected to a compressor which produces periodic sequences of pressure at 1 operative cycle/minute (20 sec of compression, 40 sec of decompression). The therapeutic cycle is composed by a 5min working period followed by a 5min resting period repeated for 3-4 times, modifiable by a manual electromechanical timer. The pressure of cuff inflation is set by a manual pressure regulator to patient’s blood systolic pressure – 20 mmHg with maximal value at 120 mmHg. For the phase A of the study, haemodynamic measurements as Time Average Velocity (TAV) and Blood Flow (BF) were performed by Echo color doppler (ECD) at the femoral vein at different phases of the operative cycle, at rest (basal level), early compression (In1), full compression (In) and full decompression (Out). The haemodynamic measurements during a therapeutic cycle were performed before the start of the first working cycle (basal level), at the end of the second cycle and at the end of the last working period, during the phase Out of both operative cycles. The study of tissue perfusion at the foot was performed using a Near Infrared Spectroscopy (NIRS) device, in order to detect variations in total (tHb), oxygenated (O2Hb) and deoxygenated haemoglobin by means of probes positioned on the dorsum of the foot. The changes of these parameters were recorded and quantified by the calculation of the areas under the curve (AUC). Measurements were performed continuously for a 5min period before the treatment and for the whole treatment. For the phase B of the study, GP was compared to a device available on the market (Art Assist ACI Medical, LLC San Marcos, CA), with cuffs to be positioned at foot and calf sequentially inflating (foot cuff first and calf cuff after 3 seconds, 20 seconds of rest). The device operates for 3 cycles/min at a fixed pressure of inflation of 120 mmHg. Outcome measures: a) Ankle-Brachial Index (ABI) measured according to the standard at rest and after treatment b) Haemodynamic measurements by ECD, including TAV e BF evaluation at femoral vein and at popliteal artery, performed before treatment, after 30 min in the decompression phase of the operative cycle and at the end of the treatment c) Evaluation of Foot perfusion by NIRS device as above described, by measurements performed continuously for a 5 min period before the treatment and for the whole treatment with both devices.4) Compliance, measured by a properly developed questionnaire proposed to the patients before and after the treatment with both devices to evaluate symptoms reduction and satisfaction. The effects of the AA instrument and GP device were measured in the same subjects in supine position in two different days with an interval of 48 ± 2 hours between the two treatments and an alternate order for each device. AA was tested for two consecutive hours of treatment and GP for 35 minutes. Results: A): the treatment with GP was well tolerated, without reported negative symptoms. During a single operative cycle BF and TAV at the femoral vein significantly increased during In e In1 phases (p>0.01). During a therapeutic cycle (25 min) BF and TAV slightly increased during the phase “out” from the beginning to the end of the treatment (p=0,10 n.s.). The foot perfusion was improved, with a significant increase both of tHbAUC and HbO2AUC (p<0.005), correlated to the TAV variations from the basal level recorded at femoral vein during the phase “out” (p<0.05). B): all patients completed the treatment with GP, while three out of them interrupted the treatment for painful symptoms at the foot. ABI increased from the baseline after treatment with GP (n=21, p=0.005), being unmodified after treatment with AA. After 30min of GP treatment the ECD parameters (TAV e BF) increased significantly at the femoral vein (n=21, p<0.05) as well BF at popliteal artery (p=0.011), while no variations were observed after AA treatment. Following compression with GP an improved foot perfusion was observed, with increase of tHbAUC (p<0.0001) and Hb O2AUC (p=0.001) that instead decreased after AA treatment (p=0.03). Compared to the AA treatment, the compression therapy with GP obtained a higher score for compliance, reduction of symptoms, easy use of the device and patients’ satisfaction (p<0.0001). Conclusions: GP, a new device for IPC in PAOD, evokes favourable haemodynamic changes with increased foot perfusion. Haemodynamic changes, distal perfusion and compliance with GP are more relevant than those observed after treatment with a traditional IPC device available on the market.
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Ait, Hmad Zouhair. "Lp(a) et arteriopathie obliterante des membres inferieurs." Strasbourg 1, 1994. http://www.theses.fr/1994STR15001.

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Lanéelle, Damien. "Hémodynamique cérébrale et périphérique dans un contexte de variation de pression de perfusion d'origine environnementale ou pathologique." Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMC430.

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L’hémodynamique occupe une place centrale dans la prise en charge des maladies vasculaires et en physiologie gravitationnelle. Les travaux présentés ici explorent l’analyse spectrale du signal doppler (ou sonogramme) dans l’artériopathie et l’effet de la microgravité sur l’hémodynamique cérébrale. La reproductibilité de l’analyse de sonogramme est faible quelle que soit la classification utilisée (κ=0.522 [0.520-0.523], p < 0.005 avec 4 catégories, κ=0.546 [0.544-0.547], p < 0.001 avec 13 catégories), indépendamment du diplôme ou de l’expérience. La classification à 13 catégories a un taux de déviance faible par rapport aux autres (5% contre 82 à 88%). Ces résultats encouragent à identifier une méthode d’analyse du sonogramme plus reproductible. Les transitions gravitationnelles sont associées à une augmentation des biomarqueurs de rupture de la barrière hémato-encéphalique ainsi que du stress oxydant et nitrosant (augmentation des protéines GFAP et S100ß, augmentation des radicaux libres et réduction du monoxyde d’azote biodisponible, p < 0,05). La microgravité entraine une augmentation sélective rapide du débit sanguin de l’artère carotide externe ( ̇��ECA, 46% ; p = 0,030, mesuré en échodoppler) alors que le débit sanguin cérébral (DSC) reste identique. Les variations de DSC liées à l’hypercapnie (+ 29% ±18) ou à l’hypovolémie simulée (- 11% ±10) ainsi que la distribution de ce DSC (entre les circulations cérébrales antérieure et postérieure, mesuré en angiographie de flux par résonance magnétique) sont indépendantes de l’anatomie artérielle intracrânienne. Ces résultats encouragent à évaluer l’effet combiné de l’hypoxie et de la microgravité sur le ̇��ECA ainsi que le lien avec les troubles neuro-oculaires associés aux vols spatiaux. La perspective commune est l’étude des résistances vasculaires périphériques afin d’une part de standardiser les conditions d’acquisition des sonogrammes dans le cadre de l’artériopathie ; et d’autre part, d’étudier les potentielles contre-mesures permettant une régulation des débits artériels dans le cadre de la physiologie gravitationnelle
The work presented here explore the spectral analysis of the sonogram and the impact of microgravity on cerebral hemodynamics. The reproducibility of sonogram analysis by classification is low (κ=0.522 [0.520-0.523], p<0.005 with 4 categories, κ=0.546 [0.544-0.547], p<0.001 with 13 categories) independently of the professional’s diploma or experience. The 13-category classification had a low deviance rate (5% compared with 82% to 88%). Gravitational transitions can promote a minor rupture of the blood-brain barrier (significant increase in specific biomarkers, p < 0.05). Microgravity causes a selective increase in external carotid artery blood flow ( ̇��ECA, 46%; p = 0.030) while cerebral blood flow (CBF) remains unchanged. The variations in CBF associated with hypercapnia (+29% ±18) or simulated hypovolemia (-11% ±10) and the distribution of this CBF were independent of intracranial arterial anatomy. These results encourage us to evaluate the combined effect of hypoxia and microgravity on the ̇��ECA as well as the link with the spaceflight associated neuro-ocular syndrome. The common perspective is to study the control of peripheral vascular resistance in order, on the one hand, to standardize the conditions for acquiring sonograms in the context of arteriopathy and, on the other hand, to study potential countermeasures for regulating the arterial flow in the context of gravitational physiology
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Ombredane, Marie-Pierre. "L'endofibrose de l'artere iliaque externe : une arteriopathie du cycliste de competition." Angers, 1988. http://www.theses.fr/1988ANGE1080.

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Books on the topic "Arteriopathy":

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Clausell, Nadine. Increased fibronectin regulated by cytokines is associated with the development of a coronary arteriopathy post-cardiac transplantation. 1993.

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2

Molossi, Silvana. Cytokine-mediated fibronectin production in cardiac allograft arteriopathy: Functional role related to transendothelial trafficking of immune-inflammatory cells. 1994.

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Chang, Yonmee, and Andrew J. Matisoff. Williams-Beuren Syndrome. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0011.

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Williams-Beuren syndrome, also known as Williams syndrome (WS) is a genetic disorder involving the elastin gene on chromosome 7q11.23. Elastin is important for elasticity of vascular walls, and its deficiency can lead to widespread arteriopathy, most notably supravalvar aortic stenosis of the ascending aorta and coronary artery stenosis. Because of these cardiac defects, patients with WS are at high risk for cardiac arrest under anesthesia with a documented incidence around 5%. Appropriate perioperative management of all anesthetics includes a multidisciplinary approach to risk stratification, precise anesthetic management, and disaster planning. This chapter reviews the etiology, pathogenesis, diagnosis, and manifestations of WS. The authors also discuss the preoperative workup and anesthetic implications of WS, as well as issues related to cardiac arrest and extracorporeal cardiopulmonary resuscitation.
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Cowan, Bryce John. Elafin inhibition of fibronectin synthesis and inflammatory cell proliferation, and reduction of post-cardiac transplant coronary arteriopathy and myocardial necrosis: In vitro and in vivo mechanisms. 1998.

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Book chapters on the topic "Arteriopathy":

1

Vamvakopoulos, Joannis, Einari Aavik, Daniel du Toit, Pekka Häyry, and Minnie Sarwal. "Transplant Arteriopathy." In Principles of Molecular Cardiology, 243–70. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1007/978-1-59259-878-6_15.

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Bonnet, Damien. "Pathophysiology of Williams Syndrome Arteriopathy." In Cardiovascular Development and Congenital Malformations, 285–86. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch70.

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Brodmann, Marianne, and Marco De Carlo. "Treatment of Peripheral Arteriopathy in Women." In Percutaneous Treatment of Cardiovascular Diseases in Women, 219–27. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39611-8_17.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy." In Encyclopedia of Molecular Mechanisms of Disease, 307. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7380.

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Stirling, John W. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)." In Diagnostic Electron Microscopy - A Practical Guide to Interpretation and Technique, 269–75. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118452813.ch9.

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Chabriat, Hugues. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)." In Stroke Genetics, 93–103. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56210-0_6.

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Kim, Nick H. "Evaluation of Small-Vessel Arteriopathy in Chronic Thromboembolic Pulmonary Hypertension." In Textbook of Pulmonary Vascular Disease, 1261–67. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-87429-6_89.

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Alexander, Sheila A. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)." In Evidence-Based Nursing Care for Stroke and Neurovascular Conditions, 185–93. West Sussex, UK: John Wiley & Sons, Inc.,, 2013. http://dx.doi.org/10.1002/9781118704950.ch8.

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Chabriat, Hugues. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)." In Stroke Genetics, 117–37. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-41777-1_6.

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Kim, Yerim. "Cerebral Autosomal Dominant Arteriopathy with Subcortical Ischemic Strokes and Leukoencephalopathy (CADASIL)." In Stroke Revisited: Pathophysiology of Stroke, 95–102. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-10-1430-7_8.

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Conference papers on the topic "Arteriopathy":

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Tello Mena, Sandra, Lucía Huidobro Bringas, Víctor M. Mora Cuesta, K. Fabiola Escobar Ramírez, Sheila Izquierdo Cuervo, Guido E. Andretta Juárez, Joy Selene Osorio Chávez, et al. "Incidence rate of coronary arteriopathy in lung transplant candidates." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1101.

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Dhillon, Navneet, Fang Li, Ossama Tawfik, Paul Cheney, and Amy O'Brien-Ladner. "Enhanced Pulmonary Arteriopathy In SIV-infected Macaques Exposed To Morphine." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6318.

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Gunther, Sven, David Montani, Sophie Maitre, Xavier Jais, Olaf Mercier, Elie Fadel, Vincent de Montpreville, et al. "Venous Remodeling And Distal Pulmonary Arteriopathy Are Frequently Present In CTEPH." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1913.

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Vatca, A., KE Maduemem, and N. McSweeney. "G324(P) Childhood stroke due to cerebral arteriopathy; a pandora’s box?" In Royal College of Paediatrics and Child Health, Abstracts of the Annual Conference, 13–15 March 2018, SEC, Glasgow, Children First – Ethics, Morality and Advocacy in Childhood, The Journal of the Royal College of Paediatrics and Child Health. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2018. http://dx.doi.org/10.1136/archdischild-2018-rcpch.314.

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Predescu, S. A., S. Qin, M. Patel, P. Drazkowski, B. Ganesh, and D. N. Predescu. "Pulmonary Artery Endothelial Cells Are Sex Dimorphic in Their Proliferative Potential. Implications for Plexiform Arteriopathy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6080.

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"DIABETES COMPLICATIONS - Development of a New Tool for Obliterating Arteriopathy of the Lower Limbs Detection." In International Conference on Biomedical Electronics and Devices. SciTePress - Science and and Technology Publications, 2012. http://dx.doi.org/10.5220/0003703700930098.

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Nouh, Claire Delpirou, Noor Mahmoud, Juliane Chainakul, Robert Hamilton, and Evgeny Sidorov. "A Rare Mutation Associated with Cerebral Arteriopathy with Subcortical Infarct and Leukoencephalopathy (CADASIL) (P2-5.002)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202715.

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Dhillon, NK, A. O'Brien Ladner, and S. Buch. "Diffuse Pulmonary Arteriopathy, Increased IL-18 and Associated Right Ventricular Hypertrophy in a HIV Transgenic Rat Model." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2289.

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Dhillon, NK, S. Buch, and A. O'Brien-Ladner. "Loss of Tight Junction Proteins within Pulmonary Arteriopathy in Lungs of Intravenous Drug Users with and without HIV Infection." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2290.

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Lu, B., C. Toolis, D. Thompson, and V. Ganesan. "G151 Characteristics and outcomes in children with sickle cell disease and severe occlusive cerebral arteriopathy referred for neurological evaluation." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.147.

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