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Electrophysiologic effects of sotalol and amiodarone in patients with sustained monomorphic ventricular tachycardia

dc.contributor.authorMan, K. Chingen_US
dc.contributor.authorWilliamson, Brian D.en_US
dc.contributor.authorNiebauer, Mark J.en_US
dc.contributor.authorDaoud, Emile G.en_US
dc.contributor.authorBakr, Omaren_US
dc.contributor.authorStrickberger, S. Adamen_US
dc.contributor.authorHummel, John D.en_US
dc.contributor.authorKou, William H.en_US
dc.contributor.authorMorady, Freden_US
dc.date.accessioned2006-04-10T17:44:23Z
dc.date.available2006-04-10T17:44:23Z
dc.date.issued1994-12-01en_US
dc.identifier.citationMan, K. Ching, Williamson, Brian D., Niebauer, Mark, Daoud, Emile, Bakr, Omar, Strickberger, S. Adam, Hummel, John D., Kou, William, Morady, Fred (1994/12/01)."Electrophysiologic effects of sotalol and amiodarone in patients with sustained monomorphic ventricular tachycardia." The American Journal of Cardiology 74(11): 1119-1123. <http://hdl.handle.net/2027.42/31172>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6T10-4C7VJGW-147/2/3b884ce2b957c0a86009e0fcba6c520ben_US
dc.identifier.urihttps://hdl.handle.net/2027.42/31172
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7977070&dopt=citationen_US
dc.description.abstractNo prospective studies have compared sotalol and amiodarone during electropharmacologic testing. The purpose of this prospective, randomized study was to compare the electrophysiologic effects of sotalol and amiodarone in patients with coronary artery disease and sustained monomorphic ventricular tachycardia (VT). Patients with coronary artery disease and sustained monomorphic VT inducible by programmed stimulation were randomly assigned to receive either sotalol (n = 17) or amiodarone (n = 17). The sotalol dose was titrated to 240 mg twice daily over 7 days. Amiodarone dosing consisted of 600 mg 3 times daily for 10 days. An electrophysiologic test was performed in the baseline state and at the end of the loading regimen. An adequate response was defined as the inability to induce VT or the ability to induce only relatively slow hemodynamically stable VT. During the follow-up electrophysiologic test, 24% of patients taking sotalol and 41% of those taking amiodarone had an adequate response to therapy (p = 0.30). Amiodarone lengthened the mean VT cycle length to a greater degree than sotalol (28% vs 12%, p &lt; 0.01). There were no significant differences in the effects of sotalol and amiodarone on the ventricular effective refractory period. In patients with coronary artery disease, amiodarone and sotalol are similar in efficacy in the treatment of VT as assessed by electropharmacologic testing. The effects of the 2 drugs on ventricular refractoriness are similar, but amiodarone slows VT to a greater extent than sotalol.en_US
dc.format.extent794072 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleElectrophysiologic effects of sotalol and amiodarone in patients with sustained monomorphic ventricular tachycardiaen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Cardiology, The University of Michigan Medical Center, Ann Arbor, Michigan, USAen_US
dc.identifier.pmid7977070en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/31172/1/0000073.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0002-9149(94)90463-4en_US
dc.identifier.sourceThe American Journal of Cardiologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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