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dc.contributor.authorDonahue, J. Kevin
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:40:06Z
dc.date.available2022-08-23T15:40:06Z
dc.date.issued2016-01-01
dc.date.submitted2018-05-02
dc.identifier.citation<p>J Cardiovasc Pharmacol. 2016 Jan;67(1):19-25. doi: 10.1097/FJC.0000000000000293. <a href="https://doi.org/10.1097/FJC.0000000000000293">Link to article on publisher's site</a></p>
dc.identifier.issn0160-2446 (Linking)
dc.identifier.doi10.1097/FJC.0000000000000293
dc.identifier.pmid26222989
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26323
dc.description.abstractAtrial fibrillation is a prominent cause of morbidity and mortality in developed countries. Treatment strategies center on controlling atrial rhythm or ventricular rate. The need for anticoagulation is an independent decision from the rate versus rhythm control debate. This review discusses novel biological strategies that have potential utility in the management of atrial fibrillation. Rate controlling strategies predominately rely on G-protein gene transfer to enhance cholinergic or suppress adrenergic signaling pathways in the atrioventricular node. Calcium channel blocking gene therapy and fibrosis enhancing cell therapy have also been reported. Rhythm controlling strategies focus on disrupting reentry by enhancing conduction or suppressing repolarization. Efforts to suppress inflammation and apoptosis are also under study. Resistance to blood clot formation has been shown with thrombomodulin. These strategies are in various stages of preclinical development.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26222989&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879872/
dc.subjectatrial fibrillation
dc.subjectgene therapy
dc.subjectcell therapy
dc.subjectatrioventricular node
dc.subjectconduction
dc.subjectrepolarization
dc.subjectBiological Factors
dc.subjectCardiology
dc.subjectCardiovascular Diseases
dc.subjectGenetic Phenomena
dc.subjectGenetics and Genomics
dc.subjectPharmacology
dc.subjectTherapeutics
dc.titleBiological Therapies for Atrial Fibrillation: Ready for Prime Time
dc.typeJournal Article
dc.source.journaltitleJournal of cardiovascular pharmacology
dc.source.volume67
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cardio_pp/100
dc.identifier.contextkey12057207
html.description.abstract<p>Atrial fibrillation is a prominent cause of morbidity and mortality in developed countries. Treatment strategies center on controlling atrial rhythm or ventricular rate. The need for anticoagulation is an independent decision from the rate versus rhythm control debate. This review discusses novel biological strategies that have potential utility in the management of atrial fibrillation. Rate controlling strategies predominately rely on G-protein gene transfer to enhance cholinergic or suppress adrenergic signaling pathways in the atrioventricular node. Calcium channel blocking gene therapy and fibrosis enhancing cell therapy have also been reported. Rhythm controlling strategies focus on disrupting reentry by enhancing conduction or suppressing repolarization. Efforts to suppress inflammation and apoptosis are also under study. Resistance to blood clot formation has been shown with thrombomodulin. These strategies are in various stages of preclinical development.</p>
dc.identifier.submissionpathcardio_pp/100
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine
dc.source.pages19-25


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