Relevant bibliographies by topics / Embolie pulmonaire Thrombose Veines

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

Academic literature on the topic 'Embolie pulmonaire Thrombose Veines'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Embolie pulmonaire Thrombose Veines"

1

Pernod, G. "Risque de récidive après thrombose veineuse profonde et embolie pulmonaire." Journal des Maladies Vasculaires 40, no. 2 (March 2015): 81. http://dx.doi.org/10.1016/j.jmv.2014.12.087.

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Cordeanu, Elena-Mihaela, J. Di Cesare, C. Mirea, A. M. Faller, A. Delatte, W. Younes, H. Lambach, et al. "Embolie pulmonaire et thrombose veineuse profonde concomitante : une association délétère ?" JMV-Journal de Médecine Vasculaire 44, no. 2 (March 2019): 156. http://dx.doi.org/10.1016/j.jdmv.2018.12.149.

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Soya, Esaï, F. Koffi, J. J. N’djessan, A. Ekou, A. Ahoua, E. Monney, S. Kouamé, and C. Konin. "Thrombose veineuse profonde et embolie pulmonaire sont-elles si identiques ?" JMV-Journal de Médecine Vasculaire 44, no. 2 (March 2019): 159. http://dx.doi.org/10.1016/j.jdmv.2018.12.156.

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Bressollette, L., and G. Le Gal. "Une embolie pulmonaire est plus grave qu’une thrombose veineuse profonde proximale." Journal des Maladies Vasculaires 37, no. 2 (March 2012): 57. http://dx.doi.org/10.1016/j.jmv.2011.12.110.

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Zuily, S. "Embolie pulmonaire et thrombose veineuse profonde : même maladie oui, mais même malades ?" Journal des Maladies Vasculaires 38, no. 2 (March 2013): 91. http://dx.doi.org/10.1016/j.jmv.2012.12.147.

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Vignat, N. "Prise en charge d’une thrombose veineuse profonde et/ou une embolie pulmonaire." Archives des Maladies du Coeur et des Vaisseaux - Pratique 2014, no. 231 (October 2014): 9–20. http://dx.doi.org/10.1016/s1261-694x(14)70673-x.

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Meneveau, N., and J. P. Bassand. "Quand suspecter une embolie pulmonaire chez un malade ayant une thrombose veineuse profonde ?" Annales de Cardiologie et d'Angéiologie 51, no. 3 (2002): 139–45. http://dx.doi.org/10.1016/s0003-3928(02)00086-0.

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8

Ly, K. H., E. Liozon, G. Gondran, H. Bezanahary, S. Palat, F. X. Lapébie, A. Cypierre, S. Nadalon, and A. Fauchais. "Thrombose veineuse profonde et embolie pulmonaire au cours de l’artérite à cellules géantes." La Revue de Médecine Interne 35 (December 2014): A46—A47. http://dx.doi.org/10.1016/j.revmed.2014.10.070.

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Fiori, S., S. Accassat, J. Catella-Chatron, L. Bertoletti, V. Chambefort, C. Duvillard, and B. Seffert. "Impact pronostique d’une thrombose veineuse profonde asymptomatique chez les patients pris en charge pour embolie pulmonaire." JMV-Journal de Médecine Vasculaire 43, no. 2 (March 2018): 118. http://dx.doi.org/10.1016/j.jdmv.2017.12.096.

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Minvielle, F. "Durée du traitement anticoagulant après une embolie pulmonaire ou une thrombose veineuse proximale des membres inférieurs." Archives des Maladies du Coeur et des Vaisseaux - Pratique 2021, no. 300 (September 2021): 35–38. http://dx.doi.org/10.1016/j.amcp.2021.06.011.

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Dissertations / Theses on the topic "Embolie pulmonaire Thrombose Veines"

1

Broch, Hélène Kouri Dominique El. "Evaluation de la prise en charge de la maladie veineuse thromboembolique dans le service de Médecine Polyvalente du CHU de Nantes étude prospective sur 56 patients hospitalisés de novembre 2006 à juillet 2007 /." [S.l.] : [s.n.], 2007. http://castore.univ-nantes.fr/castore/GetOAIRef?idDoc=23186.

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MICHON, MARIE-LAURE. "Etude de la maladie thromboembolique pendant une annee dans six services hospitaliers dijonnais." Dijon, 1994. http://www.theses.fr/1994DIJOM035.

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ROTOMONDO, CHRISTINE. "Embolie pulmonaire et thrombose veineuse : a propos de 86 cas angiographies et phlebographies." Nice, 1990. http://www.theses.fr/1990NICE6802.

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BRUNNER, FREDERIQUE. "Evaluation du risque d'embolie pulmonaire lie au traitement thrombolytique in situ des thromboses veineuses profondes." Lyon 1, 1992. http://www.theses.fr/1992LYO1M139.

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5

Frappé, Paul. "Epidémiologie en soins primaires de la thrombose veineuse superficielle des membres inférieurs." Thesis, Saint-Etienne, 2015. http://www.theses.fr/2015STET004T/document.

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La sévérité potentielle de la thrombose veineuse superficielle (TVS) des membres inférieurs a récemment été documentée par des études réalisées en soins secondaires et tertiaires. Son épidémiologie reste cependant inconnue en soins primaires. Le premier objectif de ce travail était de mesurer la prévalence de la TVS en soins primaires, ainsi que le taux d'évènements thromboemboliques concomitants au moment du diagnostic. Pour y répondre, un réseau de recherche collaborative entre médecins généralistes et médecins vasculaires de la région stéphanoise a été mis en place. Une étude transversale descriptive a été réalisée au sein de ce réseau pendant un an. La prévalence annuelle de la TVS a été mesurée à 0,64 pour mille habitants. Au moment du diagnostic, 24,6% des TVS étaient associées à une thrombose veineuse profonde symptomatique et 4,7% à une embolie pulmonaire symptomatique. Une seconde étude a recherché une variation saisonnière de la fréquence de la TVS en analysant les données individuelles de trois études aux designs différents ; l'étude STENOX, l'étude POST et l'étude STEPH. Une variation significative n'a été retrouvée que dans l'étude POST, et les peak-to-low ratios étaient inférieurs à 1,2 dans les trois études. Ainsi, si une variation existe, celle-ci parait être de faible envergure, sans conséquence sur la pratique et la recherche
The potential severity of superficial vein thrombosis (SVT) of the lower limbs has recently been shown by studies perfomed in secondary and tertiary care. The epidemiology of SVT remains unknown in primary care. The first objective of this study was to measure the prevalence of SVT in primary care, and the rate of concomitant thromboembolic events at diagnosis. A collaborative research network between general practitioners and vascular physicians from Saint-Etienne has been set up. A cross-sectional study has been conducted within this network during one year. The annual prevalence of SVT was measured to 0.64 per thousand inhabitants. At diagnosis, 24.6% of SVT were associated with symptomatic deep vein thrombosis and 4.7% with symptomatic pulmonary embolism. A second study was looking for a seasonal variation of SVT frequency by analyzing individual data from three studies with different designs; the STENOX study, the POST study and the STEPH study. A significant variation was found only in the POST study, and peak-to-low ratios were below 1.2 in the three studies. Thus, if other more powerful and exhaustive studies could find a seasonal variation, that variation would probably be of low magnitude and without clinical significance
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DELORME, FREDERIC. "Prevention des accidents thrombo-emboliques chez l'adulte jeune en traumatologie courante : a propos de 19 cas." Nantes, 1988. http://www.theses.fr/1988NANT038M.

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EL, ALAMI PAYELLE NATHALIE. "Dosage des d. Dimeres en urgence : interet dans le diagnostic de la maladie veineuse thrombo-embolique." Rennes 1, 1992. http://www.theses.fr/1992REN1M033.

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Bertoletti, Laurent. "Prise en charge diagnostique et thérapeutique des patients suspects d'embolie pulmonaire : problématique particulière en cas de Broncho-Pneumopathie Chronique Obstructive." Phd thesis, Université Jean Monnet - Saint-Etienne, 2011. http://tel.archives-ouvertes.fr/tel-00694010.

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La simplification des algorithmes diagnostiques a entrainé une augmentation de la suspicion d'une embolie pulmonaire (EP). Sa prévalence est passée de 50% à moins de 20%. L'évocation du diagnostic peut être gênée par la coexistence d'une Broncho Pneumopathie Chronique Obstructive (BPCO). La 1ère étape de prise en charge d'un patient suspect d'EP est l'évaluation de la probabilité clinique, par exemple par le score de Genève. Nous montrons qu'en revenant au résultat de ce score, le clinicien prédit le risque de décès et de ré-hospitalisation dans les 3 mois que le patient ait - ou n'ait pas- d'EP. Ces résultats devraient permettre d'aider à décider d'un traitement ambulatoire ou d'une hospitalisation. De plus, nous montrons que l'existence d'une BPCO est associée à une modification de la présentation clinique de la Maladie Veineuse Thrombo-Embolique (MVTE): alors que ratio dans la population sans BPCO est de 2 Thromboses Veineuses Profondes (TVP) pour une 1 EP, ce rapport s'inverse dans la population de patients souffrant de BPCO. Ce point est critique car nous montrons par ailleurs que les patients BPCO avec MVTE présentent une moins bonne évolution que les patients sans BPCO, avec une augmentation du nombre de décès et de complication hémorragique pendant les 3 mois de suivi. En se concentrant sur les patients avec BPCO, il apparait que ceux se présentant initialement avec une EP sont plus à risque de mourir et de saigner dans les 3 mois de suivi par rapport aux patients BPCO avec TVP. Il est donc indispensable de trouver un traitement protégeant efficacement les patients BPCO avec EP d'une récidive embolique, mais sans augmenter le risque hémorragique
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FLAJOLLET, JEAN-GABRIEL. "Suivi a court et long terme des thromboses veineuses profondes et/ou embolies pulmonaires fibrinolysees." Lille 2, 1992. http://www.theses.fr/1992LIL2M207.

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DELAHAYE, DOMINIQUE. "Maladie thrombo-embolique et deficit en proteines de la coagulation : a propos de 87 observations." Lille 2, 1988. http://www.theses.fr/1988LIL2M306.

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Books on the topic "Embolie pulmonaire Thrombose Veines"

1

Griffin, Jane. Deep vein thrombosis and pulmonary embolism. London: Office of Health Economics, 1996.

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2

Patenaude, Jean-Victor. Les maladies thrombo-emboliques veineuses: Module d'auto-apprentissage : les thrombophlébites superficielles et profondes, les embolies pulmonaires. 2nd ed. Montréal: Presses de l'Université de Montréal, 1998.

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3

Sheares, Karen, and Joanna Pepke-Zaba. Venous thrombosis and pulmonary embolism. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0101.

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Venous thromboembolism (VTE) is a condition in which thrombus forms in a vein, commonly in the deep veins of the leg, termed deep-vein thrombosis (DVT). The thrombus may dislodge from the site of origin and be carried into the pulmonary vasculature, causing a pulmonary embolism (PE). Deep vein thrombosis and pulmonary embolism share similar predisposing factors; however, mortality is greater in those who present with PE than in those who present with DVT. Thrombi may form in other parts of the vasculature.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0066.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_001.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_002.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_003.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Singer, Mervyn. Pathophysiology and causes of pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0170.

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Pulmonary embolus is predominantly due to thrombus breaking off from deep veins or from within the right heart, lodging within large or small vessels within the pulmonary vasculature, causing a variable degree of clinical features ranging from asymptomatic through to shock and cardiac arrest. Non-thrombotic causes include air or fat embolism. Outcome is predicated by the degree of right ventricular dysfunction. There are multiple risk factors including surgery, arrhythmias, prolonged immobility, venous stasis, pregnancy and an underlying pro-thrombotic tendency, either congenital or acquired. Numerous risk stratification scores have been developed derived from clinical features, imaging findings and biochemical markers of right ventricular strain and myocardial damage.
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Irani, Zubin, and Sara Zhao. Dual and Balloon-Assisted AngioJet Thrombectomy for Iliofemoral Deep Venous Thrombosis. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0038.

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Lower extremity deep venous thrombosis (DVT) may be complicated by pulmonary embolism, post-thrombotic syndrome, and phlegmasia cerulea dolens. Due to these complications, the American Venous Forum now recommends thrombus removal for large or symptomatic thrombus burden. The AngioJet Solent Proxy and Omni thrombectomy sets are indicated for use in iliofemoral and lower extremity veins with a diameter ≥3 mm. The device has quickly become a preferred device among the available mechanical thrombectomy options. The AngioJet system has been demonstrated as both efficacious and safe as a method of thrombectomy in lower extremity DVT. This chapter discusses two techniques to utilize the AngioJet device in iliofemoral DVT.
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Watson, Max, Caroline Lucas, Andrew Hoy, and Jo Wells. Palliative haematological aspects. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199234356.003.0023.

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This chapter on palliative haematological aspects covers anaemia in chronic disorders, blood transfusion, erythropoietin, bleeding and haemorrhage, blood products, bleeding directly related to cancer, haemoptysis, haematemesis, rectal bleeding, haematuria, massive terminal haemorrhage, thromboembolism, deep vein thrombosis (DVT), pulmonary embolism (PE), chronic venous thrombosis, warfarin in patients with cancer, and developing a good relation with haematology colleagues.
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Book chapters on the topic "Embolie pulmonaire Thrombose Veines"

1

Bashal, Fozya. "Thrombosis in Rheumatological Diseases." In Skills in Rheumatology, 263–89. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8323-0_12.

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AbstractVenous thromboembolism (VTE) is a disease of blood coagulation that occurs in the veins, most often in the calf veins first, from where it may extend and cause deep vein thrombosis (DVT) or pulmonary embolism (PE). The first described case of venous thrombosis that we know of dates back to the thirteenth century, when deep vein thrombosis was reported in the right leg of a 20-year-old man [1].
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Currier, Paul F., and Charles A. Hales. "Pulmonary Embolism and Deep Vein Thrombosis." In Textbook of Pulmonary Vascular Disease, 1231–38. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-87429-6_86.

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Goldhaber, Samuel Z., and Joseph F. Polak. "Deep Vein Thrombosis, Pulmonary Embolism, and Primary Pulmonary Hypertension." In Atlas of Vascular Disease, 205–27. London: Current Medicine Group, 2003. http://dx.doi.org/10.1007/978-1-4757-4564-1_10.

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Gary, Thomas, and Marianne Brodmann. "Venous Thromboembolism: Deep Vein Thrombosis and Pulmonary Embolism." In Interdisciplinary Concepts in Cardiovascular Health, 147–59. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01074-8_7.

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Hull, R. D., G. F. Pineo, and R. F. Brant. "A randomized trial of the effect of low molecular weight heparin vs. warfarin on mortality in the long-term treatment of proximal vein thrombosis." In Acute Pulmonary Embolism, 161–74. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-51190-5_15.

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Carlsson, Anders. "Drug Treatment in Deep Vein Thrombosis and Pulmonary Embolism." In Essential Guide to Blood Coagulation, 75–90. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444314465.ch8.

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Kawasaki, Tomio, Jun-Ichi Kambayashi, and Yoshio Uemura. "Genetic Predisposition to Pulmonary Embolism Following Deep Vein Thrombosis." In Modern Vascular Surgery, 549–57. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2632-1_59.

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Moroz, Leslie, and Vivek Kumar Moitra. "Management and Prevention of Thrombotic and Embolic Phenomena During Pregnancy: Deep Vein Thrombosis, Pulmonary Embolism, and Amniotic Fluid Embolism." In Principles and Practice of Maternal Critical Care, 87–97. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43477-9_8.

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Muck, Patrick. "Deep Vein Thrombosis and Pulmonary Embolus Thrombolysis and Endovascular Treatment." In Vascular Reconstructions, 531–42. New York, NY: Springer New York, 2021. http://dx.doi.org/10.1007/978-1-0716-1089-3_33.

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da Silva, Raisa Cristina Teodoro, Lucas Ferreira Botelho, Raquel Ferreira Nogueira, and Francesco Evangelista Botelho. "Risk Factors and Prophylaxis of Deep Vein Thrombosis and Pulmonary Embolism." In Vascular Diseases for the Non-Specialist, 125–33. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46059-8_11.

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Conference papers on the topic "Embolie pulmonaire Thrombose Veines"

1

Huisman, M. V., H. R. Buller, J. W. ten Cate, E. A. van Royen, and J. Vreeken. "SILENT PULMONARY EMBOLISM IN PATIENTS WITH DEEP VEIN THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642890.

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In patients presenting with clinically suspected deep vein thrombosis symptomatic pulmonary embolism is rarely apparent. To assess the prevalence of asymptomatic pulmonary embolism in outpatients with proven deep vein thrombosis, perfusion ventilation lungscans were performed in 101 consecutive patients at the first day of treatment and after one week of therapy. Fifty-one percent of these patients had a high probability lung-scan at the start of treatment. In control patients (n=44) without deep venous thrombosis but referred through the same filter, the prevalence of high-proba-bility scans was only 5%. After one week of anticoagulant treatment complete to partial improvement was observed in 55% of the patients while in another 24% of the patients the scan remained normal.It is concluded that lungscan detected asymptomatic pulmonary embolism occurs frequently in patients presenting with symptomatic deep venous thrombosis and that the majority of these emboli resolve within one week of anticoagulant treatment.
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2

Lowe, O. DG. "RHEOLOGY AND VENOUS THROMBOEMBOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643990.

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Changes in the composition of the blood, venous stasis, and interaction of the blood with the vessel wall (Virchow's triad) all have rheological aspects which may promote venous thrombogenesis.Blood composition and rheology. Increasing levels of venous haematocrit and fibrinogen increase bulk blood viscosity, especially at low shear rates such as are encountered in veins, when red cell aggregation occurs. Static blood requires a minimum shear stress for flow (yield stress), which is also strongly dependent on haematocrit and fibrinogen levels. Increases in haematocrit and fibrinogen also promote platelet adhesion and aggregation. Polycythaemia carries an increased risk of venous thromboembolism, which can be reduced by lowering the haematocrit; conversely, anaemic patients (renal failure, pernicious anaemia) have a subnormal prevalence of pulmonary embolism at autopsy. Increased preoperative levels of haematocrit, fibrinogen and blood viscosity predicted postoperative deep vein thrombosis in some studies, but not in others: they have complex relationships to other risk factors and illnesses. Postoperative changes in haematocrit, fibrinogen and blood viscosity may also be relevant to thrombogenesis, as may haemoconcentration in leg veins.Venous flow disturbance and rheology. The flow behaviour of particles and cells in venous valve pockets has been studied by Karino: particles and cells were observed to leave mainstream flow and circulate in paired vortices in low-shear areas within the valve pockets. A cell-poor hypoxic area at the apex of the valve pocket may favour thrombogenesis. Valve pockets might therefore act as in vivo aggregometers, with optimal conditions for activated cells or coagulation products to promote platelet and red cell aggregation, which might be facilitated by increases in haematocrit or fibrinogen. Sevitt has observed cellular aggregates in valve pockets at autopsy, which might act as a nidus for thrombus initiation. Successive layers of thrombus will disturb flow steamlines, as well as generating procoagulant activity: hence a series of "aggregometers" might result in successive bursts of thrombosis and the layered structure of venous thrombi observed by Sevitt. Variations in haematocrit, fibrinogen and red cell aggregation may influence stasis of blood following venous occlusion by thrombus, and hence affect thrombotic extension; they may also influence residual lung perfusion following pulmonary embolism.Therapeutic aspects of rheology. Leg stockings and other physical methods of preventing deep vein thrombosis may improve flow disturbance in valve pockets, as well as in axial veins. The efficacy of perioperative dextran in prevention of venous thromboembolism may partly reflect haemodilution and its rheological consequences. Likewise, postoperative defibrination with ancrod reduced the incidence and extent of deep vein thrombosis after hip surgery, which may partly reflect reductions in plasma viscosity and red cell aggregation. Defibrination with ancrod reduced the haemodynamic disturbance, and the mortality, of experimental pulmonary embolism in dogs, possibly by increasing residual perfusion.. Similarly, improved perfusion after thrombolytic therapy of pulmonary embolism in man may reflect the rheological consequences of fibrinogen depletion, as well as thrombolysis.
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Singer, Michael A., William D. Henshaw, and Stephen L. Wang. "Towards the Optimal Placement of Inferior Vena Cava Filters: Modeling the Impact of Renal Inflow." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204802.

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The endovascular deployment of inferior vena cava (IVC) filters is a clinical treatment for the prevention of pulmonary embolism due to deep vein thrombosis. In addition, IVC filters are used routinely for prophylactic purposes in patients who are at high risk of developing pulmonary embolism, e.g., trauma patients. There are approximately eight IVC filters available in the U.S., each with a unique design.
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Slaboch, Constance L., and Timothy Ovaert. "Mechanical Characterization and Simulation of Murine Thrombi." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53190.

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Deep vein thrombosis (DVT) is the formation of a thrombus, or blood clot, in one of the extremities, often in the vein of a leg. Approximately 2 million incidences of DVT occur annually. Roughly 300,000 people die due to the development of a pulmonary embolism (PE), which occurs when the thrombus from a DVT relocates to the pulmonary artery. Abdominal aortic aneurysm (AAA) is another life-threatening disease involving thrombi, resulting in 15,000 deaths annually. Together, these diseases impact over 2.5 million people each year. The effects of mechanical properties on thrombi dissociation and aortic rupture are not well characterized, and this lack of knowledge has hampered significant treatment and management of many blood-related diseases, as well as the development of optimal drug therapies. Determining these mechanical properties (i.e., elastic modulus and viscosity) is valuable information, as it can be used as inputs to simulations of thrombi disorders to more accurately determine thrombus dissociation or aortic rupture. The goal of this research is to determine the mechanical properties of murine (rat) thrombi under physiologic conditions via nanoindentation, for use as inputs data to numerical flow simulations.
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Slaboch, Constance L., and Timothy C. Ovaert. "Mechano-Rheological Properties of the Murine Thrombus Determined via Nanoindentation and Finite Element Modeling." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206520.

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Deep vein thrombosis (DVT) is the formation of a thrombus, or blood clot, in one of the extremities, often in the vein of a leg. Approximately 2 million incidences of DVT occur annually [1]. Roughly 300,000 people die due to the development of a pulmonary embolism (PE), which occurs when the thrombus from a DVT relocates to the pulmonary artery. Abdominal aortic aneurysm (AAA) is another life-threatening disease involving thrombi, resulting in 15,000 deaths annually. Increased life expectancy raises significant concern for AAA, as it generally affects people age 55 and older. Together, these diseases impinge over 2.5 million people each year. Determining the mechanical properties of thrombi, which can be platelet- and/or fiber-rich, and understanding how they dissociate or fail mechanically under fluid flow conditions, can help diagnose these diseases at an earlier stage in their progression, thereby providing time to initiate treatments. In addition, increased knowledge of thrombi properties can lead to the development of preventative drug therapies. Both of these outcomes have the potential to decrease the number of deaths from the aforementioned diseases.
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Hach-Wunderle, V., R. Walter-Fincke, H. K. Beck, and I. Scharrer. "FAMILY STUDIES OF PATIENTS WITH RECURRENT VENOUS THROMBOSES AND INHERITED DISORDERS OF BLOOD COAGULATION OR FIBRINOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643045.

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Several defects of the coagulation and/or fibrinolytic system have been found to be associated with venous thromboembolism. In young patients with recurrent thromboses or a positive family history, an inherited disorder should be excluded535 young patients with venous thromboses, phlebitis and/or pulmonary embolism were investigated from 1980 until 1986. The first thrombotic event had occurred at an age of less than 45 years.An inborn disorder of the blood coagulation or fibrinolytic system was found in 18 families. Most of them (n=13/18) had a positive family history. In all families either thromboses had occurred in at least one member (n=12/18) and/or the defect could be detected in one of them (n=12/18)Most often we found a deficiency of antithfombin III (n=6). A deficiency of protein C (type I) was detected in 3 and a deficiency of protein S in 5 families. In one patient a combined deficiency of anti thrombin III, protein C and protein S was found. Extensive family studies revealed a deficiency of antithrombin III in the grandmother of the patient, who suffered from arterial thrombosis. A deficiency of plasminogen and an abnormal plasminogen molecule were detected in 2 other families. Defective release of t-PA could be demonstrated in 3 members of one investigated family up to nowSeme family members with either defects of protein C, protein S or plasminogen as well as a defective release of t-PA lack thrombotic events. Furthermore thromboses of mesenteric veins occurred in 2 of 6 patients with anti thrombin III deficiency and in 1 of 5 patients with protein S deficiency. Superficial vein thromboses were mainly found in patients with protein C- or protein S-deficiency
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Powers, P. J., M. Gent, R. Jay, J. Hirsh, M. Levine, and G. Turpie. "DEEP VEIN THROMBOSIS PROPHYLAXIS IN SURGICALLY TREATED FRACTURED HIP PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643692.

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Deep vein thrombosis is a major complication in'patients treated surgically for fractured hip. Methods employed toreduce the risk of thrombosis include dextran, ASA, warfarin, low or adjusted dose heparin and calf compression, but none has widespread acceptance.A randomized trial wascarried out to assess the effectiveness of sodium warfarinand acetyl salicylic acid(aspirin) compared to placebo inthe prevention of venous thrombosis in fractured hip patients. One hundred and ninty four patients were randomizedto receive warfarin (65 patients), ASA (66 patients) or placebo (63 patients).Prophylaxis commenced post operatively and continued for 21 days or until discharge, if earlier.Warfarin patients received 10 mg sodium warfarin orally as soon as possible after surgery. Warfarin was then given daily according to the prothrombin time (PT), to obtain a PT of 16 seconds on the 5th post operative day. The PT was maintain at 16 to 18 seconds until the end of treatment.ASA and placebo patients received enteric coated tablets, 650 mg twice daily, in a double blind fashion beginning as soon as possible post operatively and continuingto the end of treatment. Surveillance testing and I-fibrinogen leg scanning and impedance plethysmography was performed and venography was done if either test suggested thrombus at the popliteal vein or above. Otherwise venography was performed at day 21 or prior to discharge, if earlier. Venous thrombosis occurred in 13 patients (20%) in the warfarin group, 27 patients (^0.9%) in the ASA group, and 29 patients (46%) in the placebo group (P=0.005). Proximal vein thrombosis or pulmonary embolism occurred in 6patients (9.2%) in the warfarin group,7 patients (10.6%) in the ASA and 19 patients (30.2%) in the placebo group (P=0.002). Two major hemorrhages occurred in the warfarin group, none in the ASA group, and 2 in the placebo group.The results of this study show sodium warfarin to be safeand effective in reducing thromboembolic complications infractured hip patients and ASA to be effective in reducing thrombosis involving the proximal deep veins of the lower limbs in these patients.
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Lowe, G. D. O. "EPIDEMIOLOGY AND RISK PREDICTION OF VENOUS THROMBOEMBOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642965.

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Uses of epidemiology. Venous thromboembolism continues to be an important cause of death and disability in Western Countries. Its epidemiology may provide clues to etiology, e.g. the increased incidence in oral contraceptive users, and the low prevalence at autopsy in Central Africa or Japan compared to the U.S.A. A second use is the monitoring of time-trends: the diagnosis of pulmonary embolism increased during the 1970s, although the case fatality decreased. A third use is the identification and quantification of risk factors: these could be modified in the hope of prevention, or else used to select high risk groups for selective prophylaxis, e.g. during acute illness. Prevention is the only feasible approach to reducing the burden of venous thromboembolism, since most cases are not diagnosed, and since the value of current treatment is debatable.Case definition. Presents problems: clinical diagnosis is unreliable, and should if possible be supported by objective methods. Autopsy studies are performed on selected populations, at a decreasing rate; the frequency of thromboembolism depends on technique; and pathologists cannot be blinded and are open to bias. It can also be difficult to judge whether a patient dying with pulmonary embolism died from pulmonary embolism. 125I-fibrinogen scans indicate minimal disease, and now present ethical problems in screening due to risks of viral transmission. Venography is invasive and is not readily repeatable, which limits its use as a screening method. Plethysmography merits wider evaluation, since it is non-invasive, and sensitive to major thrombosis.Community epidemiology. Data on the community epidemiology are limited. The risk increases with age. When age is taken into account, there is little sex difference. Overweight in women, use of oral contraceptives and blood group A increase the risk: smoking, varicose veins, blood pressure, cholesterol and glucose do not, on current evidence. Long-term follow-up of patients with proven thromboembolism shows an increased risk of malignancy, hence occult cancer may also be a risk factor. Polycythaemia and certain congenital deficiencies (e.g. antithrombin III) are also well-recognised risk factors, although uncommon.Hospital epidemiology. Data on hospital epidemiology are derived largely from autopsy prevalence, and from short-term incidence of minimal thrombosis detected by 125I—fibrinogen scanning. Old, immobile and traumatised patients are most at risk. Previous thromboembolism, polycythaemia, antithrombin III deficiency, hip and leg fractures, elective hip and leg surgery, hemiplegia, paraplegia, and heart failure carry high risks, and merit consideration for routine prophylaxis. The risk in elective surgery precedes the operation, and increases with age, overweight, malignancy, varicose veins, non-smoking, and operative factors (duration, approach, general anaesthesia, intravenous fluids). Diabetics appear to have no extra risk. Combinations of clinical variables can be used to predict high risk groups for selective prophylaxis, but combination indices require further study. Laboratory variables may increase the predictability of deep vein thrombosis, but the results of published studies are conflicting, and the cost-effectiveness of laboratory prediction should be evaluated.
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Azam, Hamad, Nader Mahmood, Sukhchain Singh, Vincent A. DeBari, Muhammad I. Ali, Maria Alfakir, and M. A. Khan. "Elevated Trigylceride Levels In Patient With Pulmonary Embolism And Deep Vein Thrombosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2679.

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Pecqueur, J., S. Joseph, A. Slater, and A. Babiker. "G422(P) Deep vein thrombosis and silent pulmonary emboli: diagnostic dilemmas and lessons learnt." 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.407.

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Reports on the topic "Embolie pulmonaire Thrombose Veines"

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Saldanha, Ian J., Wangnan Cao, Justin M. Broyles, Gaelen P. Adam, Monika Reddy Bhuma, Shivani Mehta, Laura S. Dominici, Andrea L. Pusic, and Ethan M. Balk. Breast Reconstruction After Mastectomy: A Systematic Review and Meta-Analysis. Agency for Healthcare Research and Quality (AHRQ), July 2021. http://dx.doi.org/10.23970/ahrqepccer245.

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Objectives. This systematic review evaluates breast reconstruction options for women after mastectomy for breast cancer (or breast cancer prophylaxis). We addressed six Key Questions (KQs): (1) implant-based reconstruction (IBR) versus autologous reconstruction (AR), (2) timing of IBR and AR in relation to chemotherapy and radiation therapy, (3) comparisons of implant materials, (4) comparisons of anatomic planes for IBR, (5) use versus nonuse of human acellular dermal matrices (ADMs) during IBR, and (6) comparisons of AR flap types. Data sources and review methods. We searched Medline®, Embase®, Cochrane CENTRAL, CINAHL®, and ClinicalTrials.gov from inception to March 23, 2021, to identify comparative and single group studies. We extracted study data into the Systematic Review Data Repository Plus (SRDR+). We assessed the risk of bias and evaluated the strength of evidence (SoE) using standard methods. The protocol was registered in PROSPERO (registration number CRD42020193183). Results. We found 8 randomized controlled trials, 83 nonrandomized comparative studies, and 69 single group studies. Risk of bias was moderate to high for most studies. KQ1: Compared with IBR, AR is probably associated with clinically better patient satisfaction with breasts and sexual well-being but comparable general quality of life and psychosocial well-being (moderate SoE, all outcomes). AR probably poses a greater risk of deep vein thrombosis or pulmonary embolism (moderate SoE), but IBR probably poses a greater risk of reconstructive failure in the long term (1.5 to 4 years) (moderate SoE) and may pose a greater risk of breast seroma (low SoE). KQ 2: Conducting IBR either before or after radiation therapy may result in comparable physical well-being, psychosocial well-being, sexual well-being, and patient satisfaction with breasts (all low SoE), and probably results in comparable risks of implant failure/loss or need for explant surgery (moderate SoE). We found no evidence addressing timing of IBR or AR in relation to chemotherapy or timing of AR in relation to radiation therapy. KQ 3: Silicone and saline implants may result in clinically comparable patient satisfaction with breasts (low SoE). There is insufficient evidence regarding double lumen implants. KQ 4: Whether the implant is placed in the prepectoral or total submuscular plane may not be associated with risk of infections that are not explicitly implant related (low SoE). There is insufficient evidence addressing the comparisons between prepectoral and partial submuscular and between partial and total submuscular planes. KQ 5: The evidence is inconsistent regarding whether human ADM use during IBR impacts physical well-being, psychosocial well-being, or satisfaction with breasts. However, ADM use probably increases the risk of implant failure/loss or need for explant surgery (moderate SoE) and may increase the risk of infections not explicitly implant related (low SoE). Whether or not ADM is used probably is associated with comparable risks of seroma and unplanned repeat surgeries for revision (moderate SoE for both), and possibly necrosis (low SoE). KQ 6: AR with either transverse rectus abdominis (TRAM) or deep inferior epigastric perforator (DIEP) flaps may result in comparable patient satisfaction with breasts (low SoE), but TRAM flaps probably increase the risk of harms to the area of flap harvest (moderate SoE). AR with either DIEP or latissimus dorsi flaps may result in comparable patient satisfaction with breasts (low SoE), but there is insufficient evidence regarding thromboembolic events and no evidence regarding other surgical complications. Conclusion. Evidence regarding surgical breast reconstruction options is largely insufficient or of only low or moderate SoE. New high-quality research is needed, especially for timing of IBR and AR in relation to chemotherapy and radiation therapy, for comparisons of implant materials, and for comparisons of anatomic planes of implant placement.
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