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Relevant bibliographies by topics / Drug-induced Arrhythmias

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Academic literature on the topic 'Drug-induced Arrhythmias'

Author: Grafiati

Published: 5 September 2021

Last updated: 1 February 2022

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Journal articles on the topic "Drug-induced Arrhythmias"

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Leonova, M. V. "Drug-induced arrhythmias." Meditsinskiy sovet = Medical Council, no. 21 (January 17, 2021): 26–40. http://dx.doi.org/10.21518/2079-701x-2020-21-26-40.

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The article provides a scientific review based on the proceedings of the 2020 American Heart Association consensus on drugs that may cause arrhythmias on a risk-sensitive basis and a guidance on strategies for monitoring, prevention methods and therapeutic approaches.The risk factors for drug-induced arrhythmias are divided into modifiable and non-modifiable. Among the non-modifiable risk factors are congenital anomalies (changes in the conduction system, ion channel polymorphism) and heart diseases (cavity dilatation, myocardial ischemia). Among the modifiable risk factors are various electro

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Barnes, Brian J., and James M. Hollands. "Drug-induced arrhythmias." Critical Care Medicine 38 (June 2010): S188—S197. http://dx.doi.org/10.1097/ccm.0b013e3181de112a.

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Doig, J. Colin. "Drug-Induced Cardiac Arrhythmias." Drug Safety 17, no. 4 (1997): 265–75. http://dx.doi.org/10.2165/00002018-199717040-00006.

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Abbott, Geoffrey W., and Torsten K. Roepke. "Pharmacogenetics of drug-induced arrhythmias." Expert Review of Clinical Pharmacology 1, no. 1 (2008): 93–104. http://dx.doi.org/10.1586/17512433.1.1.93.

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Roden, D. "Pharmacogenetics and drug-induced arrhythmias." Cardiovascular Research 50, no. 2 (2001): 224–31. http://dx.doi.org/10.1016/s0008-6363(00)00302-3.

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Moreland-Head, Lindsay N., James C. Coons, Amy L. Seybert, Matthew P. Gray, and Sandra L. Kane-Gill. "Use of Disproportionality Analysis to Identify Previously Unknown Drug-Associated Causes of Cardiac Arrhythmias Using the Food and Drug Administration Adverse Event Reporting System (FAERS) Database." Journal of Cardiovascular Pharmacology and Therapeutics 26, no. 4 (2021): 341–48. http://dx.doi.org/10.1177/1074248420984082.

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Introduction: Drug-induced QTc-prolongation is a well-known adverse drug reaction (ADR), however there is limited knowledge of other drug-induced arrhythmias. Purpose: The objective of this study is to determine the drugs reported to be associated with arrhythmias other than QTc-prolongation using the FAERS database, possibly identifying potential drug causes that have not been reported previously. Methods: FAERS reports from 2004 quarter 1 through 2019 quarter 1 were combined to create a dataset of approximately 11.6 million reports. Search terms for arrhythmias of interest were selected from

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&NA;. "An overview of drug-induced arrhythmias." Reactions Weekly &NA;, no. 365 (1991): 2–3. http://dx.doi.org/10.2165/00128415-199103650-00004.

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Chehab, Bassem, and Peter Tadros. "The Electrocardiogram and Drug-Induced Arrhythmias." Kansas Journal of Medicine 4, no. 3 (2011): 84–86. http://dx.doi.org/10.17161/kjm.v4i3.11345.

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Vos, Marc, and Aimée DC Paulussen. "Genetic basis of drug‐induced arrhythmias." Annals of Medicine 36, sup1 (2004): 35–40. http://dx.doi.org/10.1080/17431380410032634.

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Corrias, A., X. Jie, L. Romero, et al. "Arrhythmic risk biomarkers for the assessment of drug cardiotoxicity: from experiments to computer simulations." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1921 (2010): 3001–25. http://dx.doi.org/10.1098/rsta.2010.0083.

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In this paper, we illustrate how advanced computational modelling and simulation can be used to investigate drug-induced effects on cardiac electrophysiology and on specific biomarkers of pro-arrhythmic risk. To do so, we first perform a thorough literature review of proposed arrhythmic risk biomarkers from the ionic to the electrocardiogram levels. The review highlights the variety of proposed biomarkers, the complexity of the mechanisms of drug-induced pro-arrhythmia and the existence of significant animal species differences in drug-induced effects on cardiac electrophysiology. Predicting d

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Dissertations / Theses on the topic "Drug-induced Arrhythmias"

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Hartigan-Go, Kenneth. "Drug induced QT interval prolongation." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389560.

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Philp, Karen L. "Acute actions of 17#beta# on ischaemia- and drug- induced arrhythmias." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250376.

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Opstal, Jurren Marie van. "Drug-induced torsade de pointes arrhythmias and sudden cardiac death in the remodeled canine heart." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2002. http://arno.unimaas.nl/show.cgi?fid=7511.

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Wilchesky, Machelle 1965. "Arrhythmia risk associated with the use of bronchodilators in patients with chronic obstructive pulmonary disease : cohort studies and methodological issues." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115713.

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Whereas first line therapy for chronic obstructive pulmonary disease (COPD) usually includes a short-acting bronchodilator, there are suggestions that these agents may increase the risk of cardiac arrhythmias. In this thesis, we first assessed the risks associated with short-acting beta-agonists (SABA), long-acting beta-agonists (LABA), ipratropium bromide (IB), and methyl xanthines (MX) within a cohort of COPD patients using the health databases of Saskatchewan. In order to confirm these findings and to address some methodological issues we then replicated this analysis within a larger cohort

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Azarbayjani, Faranak. "Common mechanism for teratogenicity of antiepileptic drugs : Drug-induced embryonic arrhythmia and hypoxia-reoxygenation damage." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5065-2/.

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Sköld, Anna-Carin. "Teratogenicity as a consequence of drug-induced embryonic cardiac arrhythmia : Common mechanism for almokalant, sotalol, cisapride, and phenytoin via inhibition of IKr." Doctoral thesis, Uppsala University, Department of Pharmaceutical Biosciences, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-515.

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<p>During the last years, drugs that prolong the repolarisation phase of the myocardial action potential, due to inhibition of the rapid component of the delayed-rectifying potassium channel (I<sub>Kr</sub>) have been in focus. In addition to arrhythmogenic potential, selective Ikr-blockers have also been shown to be embryotoxic and teratogenic in animal studies. The aim of this thesis was to investigate a theory that these developmental toxic results from pharmacologically induced episodes of embryonic cardiac arrhythmias leading to hypoxia related damage in the embryo. Almokalant (ALM) was u

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Silva, José Diogo Ramalho e. "Drug-induced potentially fatal arrhythmias and sudden cardiac death: a clinical perspective of long QT, short QT and Brugada syndromes." Dissertação, 2017. https://hdl.handle.net/10216/104358.

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Silva, José Diogo Ramalho e. "Drug-induced potentially fatal arrhythmias and sudden cardiac death: a clinical perspective of long QT, short QT and Brugada syndromes." Master's thesis, 2017. https://hdl.handle.net/10216/104358.

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Fernandes, Diogo Filipe de Almeida Ferreira. "Adequation of the therapeutic profile, co-morbidities and personal habits of Brugada patients with ICD and its link to dysrhythmic events." Master's thesis, 2018. http://hdl.handle.net/10316/82021.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina<br>Introdução: A síndrome de Brugada é uma doença hereditária associada a um aumento do risco de morte súbita com possível necessidade de colocação de cardioversor-desfibrilhador implantável (CDI) de forma a interromper os eventos disrítmicos. Os nossos objetivos foram identificar possíveis desencadeadores de terapias apropriadas do CDI em doentes com síndrome de Brugada e avaliar se o perfil terapêutico passado e atual é adequado à doença.Métodos: Um total de 30 doentes com síndrome de Brugada submetidos a im

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Books on the topic "Drug-induced Arrhythmias"

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Wijdicks, Eelco F. M., and Sarah L. Clark. Antihypertensives and Antiarrhythmics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0013.

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Acute brain injury can precipitate a hypertensive response, which for the most part is the result of stress-induced, increased sympathetic activity. Acute stroke with hypertension may not be a response but more often a prior, untreated hypertension or a patient with no access to medication. This hypertensive response may wane quickly, and aggressive treatment of these temporary surges in blood pressure could have unwanted consequences. Important characteristics of most antihypertensive drugs used in the neurosciences intensive care unit are cost, having a rapid onset with a short duration of a

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Azarbayjani, Faranak. Common Mechanism for Teratogenicity of Antiepileptic Drugs: Drug-Induced Embryonic Arrhythmia and Hypoxia-Reoxygenation Damage (Comprehensive Summaries ... from the Faculty of Pharmacy, 253). Uppsala Universitet, 2001.

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Book chapters on the topic "Drug-induced Arrhythmias"

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Ovsyshcher, I. E., and N. Gulko. "Drug-Induced Bradycardia:When Is a Pacemaker Warranted?" In Cardiac Arrhythmias 2003. Springer Milan, 2004. http://dx.doi.org/10.1007/978-88-470-2137-2_91.

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El-Sherif, N., and G. Turitto. "Drug-Induced Torsade de Pointes. Role of Genetic Factors." In Cardiac Arrhythmias 2003. Springer Milan, 2004. http://dx.doi.org/10.1007/978-88-470-2137-2_50.

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Seifert, Roland. "Drug-Induced Arrhythmias and Drugs for the Treatment of Arrhythmias." In Basic Knowledge of Pharmacology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18899-3_17.

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Virginia Soldovieri, Maria, and Maurizio Taglialatela. "Cellular Mechanisms, Molecular Targets, and Structure-Function Relationships in Drug-Induced Arrhythmias: Antihistamines, Psychoactive Drugs, and Antimicrobial Agents." In Cardiotoxicity of Non-Cardiovascular Drugs. John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470660379.ch3.

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"Chapter 25: Ventricular Arrhythmias." In Drug-Induced Diseases. American Society of Health-System Pharmacists, 2018. http://dx.doi.org/10.37573/9781585285310.025.

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"Chapter 26: Supraventricular Arrhythmias." In Drug-Induced Diseases. American Society of Health-System Pharmacists, 2018. http://dx.doi.org/10.37573/9781585285310.026.

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Ouali, Sana, Omar Guermazi, Fatma Guermazi, et al. "Drug Abuse-Induced Cardiac Arrhythmias: Mechanisms and Management." In Cardiac Arrhythmias. InTech, 2018. http://dx.doi.org/10.5772/intechopen.76022.

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"The Mechanisms Underlying Drug-Induced Arrhythmias." In Cardiac Drug Safety. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814317467_0005.

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Bazan, Victor, Enrique Rodriguez-Font, and Francis E. Marchlinski. "Sustained and non-sustained ventricular tachycardia and no associated heart disease (idiopathic ventricular tachycardia)." In ESC CardioMed, edited by Brian Olshansky. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0540_update_001.

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Around 10% of ventricular arrhythmias (VA) occur in the absence of underlying structural heart disease. These so-called ‘idiopathic’ VAs usually have a benign clinical course. Only rarely do these “benign” arrhythmias trigger polymorphic ventricular tachycardia (PVT) and idiopathic ventricular fibrillation (VF). Due to their focal origin and to the absence of underlying myocardial scar, the 12-lead ECG very precisely establishes the right (RV) or left (LV) ventricular site of origin of the arrhythmia and can help regionalizing the origin of VT for ablation. A 12-lead ECG obtained during the baseline rhythm and 24-hour ECG Holter monitoring are indicated in order to identify structural or electrical disorders leading to PVT/VF and to determine the VA burden. The most frequent origin of idiopathic VAs is the RV outflow tract (OT). Other origins include the LVOT, the LV fascicles (fascicular VTs), the LV and RV papillary muscles, the crux cordis, the mitral and tricuspid annuli and the RV moderator band. Recognizing the typical anatomic sites of origin combined with a 12 lead ECG assessment facilitates localization. Antiarrhythmic drug therapy (including use of beta-blockers) or catheter ablation may be indicated to suppress or eliminate idiopathic VAs, particularly upon severe arrhythmia-related symptoms or if the arrhythmia burden is high and ‘tachycardia’-induced cardiomyopathy is suspected. Catheter ablation is frequently preferred to prevent lifelong drug therapy in young patients.

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"CHAPTER 7. Drug-Induced Cardiac Arrhythmias and Sudden Cardiac Death." In Iatrogenicity. Rutgers University Press, 2019. http://dx.doi.org/10.36019/9780813586434-009.

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Conference papers on the topic "Drug-induced Arrhythmias"

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Mirin, Arthur A., David F. Richards, James N. Glosli, et al. "Toward real-time modeling of human heart ventricles at cellular resolution: Simulation of drug-induced arrhythmias." In 2012 SC - International Conference for High Performance Computing, Networking, Storage and Analysis. IEEE, 2012. http://dx.doi.org/10.1109/sc.2012.108.

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Couderc, J. P., S. Kaab, M. Hinterseer, et al. "Investigating the role of ventricular repolarization morphology in surface ECGs for identifying patients with a history of drug-induced arrhythmias." In 2007 34th Annual Computers in Cardiology Conference. IEEE, 2007. http://dx.doi.org/10.1109/cic.2007.4745490.

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