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Suivi à long terme de 190 patients après Tilt-testJacq, Hugues Probst, Vincent January 2005 (has links) (PDF)
Thèse d'exercice : Médecine. Pathologie cardiovasculaire : Université de Nantes : 2005. / Bibliogr. f. 46-59 [59 réf.].
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Cardioinhibitory carotid sinus hypersensitivity and unexplained falls in older subjectsParry, Steve W. January 2002 (has links)
No description available.
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A preliminary exploration into the factors that influence fainting behaviorKnott, Diane M. January 1981 (has links)
Thesis (M.S.)--University of Wisconsin--Madison, 1981. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 64-65).
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Physical manoeuvres to prevent vasovagal syncope and initial orthostatic hypotensionKrediet, Constantijn Thomas Paul. January 2007 (has links)
Academisch Proefschrift--Universiteit van Amsterdam, 2007. / Includes bibliographical references (p. 91-108).
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Vasovagal SyncopeKress, Magdalena 17 April 2014 (has links)
No description available.
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Prevalence of venous thromboembolism in admissions and readmissions with and without syncope: A nationwide cohort studyKadri, Amer N., Zawit, Misam, Al-Adham, Raed, Hader, Ismail, Nusairat, Leen, Almahmoud, Mohamed F., Senussi, Mourad, Altibi, Ahmed, Barakat, Amr, Hernandez, Adrian V., Masri, Ahmad 01 January 2021 (has links)
Aims: The Pulmonary Embolism in Syncope Italian Trial reported 17.3% prevalence of pulmonary embolism (PE) in patients admitted with syncope. We investigated the prevalence of venous thromboembolism [VTE, including PE and deep vein thrombosis (DVT)] in syncope vs. non-syncope admissions and readmissions, and if syncope is an independent predictor of VTE. Methods and results: We conducted an observational study of index admissions of the 2013-14 Nationwide Readmission Database. / National Institutes of Health / Revisión por pares
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Benefits of cardiac pacing in carotid sinus hypersensitivity and fallsRichardson, David Andrew January 2001 (has links)
No description available.
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Causes and predictors of 30‐day readmission in patients with syncope/collapse: a nationwide cohort studyKadri, Amer N., Abuamsha, Hasan, Nusairat, Leen, Kadri, Nazih, Abuissa, Hussam, Masri, Ahmad, Hernandez, Adrian V. 09 1900 (has links)
Background Syncope accounts for 0.6% to 1.5% of hospitalizations in the United States. We sought to determine the causes and predictors of 30‐day readmission in patients with syncope. Methods and Results We identified 323 250 encounters with a primary diagnosis of syncope/collapse in the 2013-2014 Nationwide Readmissions Database. We excluded patients younger than 18 years, those discharged in December, those who died during hospitalization, hospital transfers, and those whose length of stay was missing. We used multivariable logistic regression analysis to evaluate the association between baseline characteristics and 30‐day readmission. A total of 282 311 syncope admissions were included. The median age was 72 years (interquartile range, 58-83), 53.9% were women, and 9.3% had 30‐day readmission. The most common cause of 30‐day readmissions was syncope/collapse, followed by cardiac, neurological, and infectious causes. Characteristics associated with 30‐day readmissions were age 65 years and older (odds ratio [OR], 0.7; 95% confidence interval [CI], 0.6-0.7), female sex (OR, 0.9; 95% CI, 0.8-0.9), congestive heart failure (OR, 1.5; 95% CI, 1.2-1.9), atrial fibrillation/flutter (OR, 1.3; 95% CI, 1.3-1.4), diabetes mellitus (OR, 1.2; 95% CI, 1.2-1.3), coronary artery disease (OR, 1.2; 95% CI, 1.2-1.3), anemia (OR, 1.4; 95% CI, 1.4-1.5), chronic obstructive pulmonary disease (OR, 1.4; 95% CI, 1.3-1.4), home with home healthcare disposition (OR, 1.5; 95% CI, 1.5-1.6), leaving against medical advice (OR, 1.7; 95% CI, 1.6-1.9), length of stay of 3 to 5 days (OR, 1.5; 95% CI, 1.4-1.6) or >5 days (OR, 2; 95% CI, 1.8-2), and having private insurance (OR, 0.6; 95% CI, 0.6-0.7). Conclusions The 30‐day readmission rate after syncope/collapse was 9.3%. We identified causes and risk factors associated with readmission. Future prospective studies are needed to derive risk‐stratification models to reduce the high burden of readmissions. / Revisión por pares
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Pre-Donation Fluid Loading Attenuates Negative Reactions in First-Time Blood DonorsHanson, Sarah A. 20 July 2004 (has links)
No description available.
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Contribution à l'étude du système adénosinergique en pathologie cardiovasculaireFranceschi, Frédéric 22 February 2013 (has links)
L'adénosine est un nucléoside ubiquitaire issu de la déphosphorylation de l'ATP qui est libéré par les cellules endothéliales et les myocytes lors de l'hypoxie, de l'ischémie ou du stress oxydatif. Elle exerce un contrôle puissant sur les systèmes nerveux, immunitaire et cardiovasculaire par l'intermédiaire de quatre récepteurs membranaires : A1R, A2AR, A2BR et A3R. La compréhension de l'implication du système adénosinergique dans le système cardiovasculaire implique la possibilité technique d'un dosage de l'adénosine endogène et la quantification de l'expression de ses récepteurs. L'adénosine ayant globalement une action hypotensive (via les récepteurs A2AR) et chronotrope négative (via les récepteurs A1R), nous nous sommes intéressés à son implication chez les patients présentant des syncopes neurocardiogéniques, la bradycardie et l'hypotension étant 2 signes cardinaux dans ce syndrome. Les manifestations cliniques de cette affection peuvent être reproduites par le test d'inclinaison (HUT) et/ou le test à l'ATP. Dans un premier temps nous avons réalisé des dosages d'adénosine plasmatiques chez ces patients au moment d'un test d'inclinaison. Les concentrations en adénosine étaient élevées chez les patients présentant un test positif. Par la suite, nous avons comparé les concentrations en adénosine plasmatiques et l'expression des récepteurs A2A en fonction du résultat du test d'inclinaison et du test à l'ATP. / Adenosine is a ubiquitous nucleoside that comes from the dephosphorylation of ATP and which is released during hypoxia or oxidative stress, by endothelial cells and myocytes. Adenosine interacts on its cell surface receptors, namely A1R, A2AR, A2BR and A3R, to exert physiological effects on target tissues. Our knowledge about the adenosinergic system was improved because of our ability to measure adenosine plasma levels and to quantify its receptors expression. Because adenosine, via A1 or A2A receptor activation leads to bradycardia and hypotension, we first tried to understand the implication of the adenosinergic system in patients with neurocardiogenic syncope (NMS for neutrally mediated syncope). Indeed, this syndrome is characterized by relative or absolute bradycardia associated with a drop in blood pressure and a loss of consciousness. The symptomatology can be reproduced by the tilt test (HUT) or by the intravenous administration of ATP (ATP test). First, we measured adenosine plasma levels in patients with NMS just before and during HUT. We found that adenosine plasma levels were higher in patients with a positive HUT. Then, we compared adenosine plasma levels and the expression of A2A receptors in patients with NMS depending on the result of HUT and ATP-test. We found that elevated adenosine plasma levels and A2A receptors overexpression were associated with positive HUT. On the opposite, low adenosine plasma levels and normal expression of A2A receptor were associated with positive ATP test.
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