Show simple item record

The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing

dc.contributor.authorMorady, Freden_US
dc.contributor.authorHalter, Jeffrey B.en_US
dc.contributor.authorDiCarlo, Jr. , Lorenzo A.en_US
dc.contributor.authorBaerman, Jeffrey M.en_US
dc.contributor.authorDe Buitleir, Michaelen_US
dc.date.accessioned2006-04-07T19:57:56Z
dc.date.available2006-04-07T19:57:56Z
dc.date.issued1987-02en_US
dc.identifier.citationMorady, Fred, Halter, Jeffrey B., DiCarlo, Jr., Lorenzo A., Baerman, Jeffrey M., de Buitleir, Michael (1987/02)."The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing." American Heart Journal 113(2, Part 1): 227-233. <http://hdl.handle.net/2027.42/26830>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6W9H-4C548GJ-TX/2/c9d553c8b6977a48a86003ab337075daen_US
dc.identifier.urihttps://hdl.handle.net/2027.42/26830
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3812177&dopt=citationen_US
dc.description.abstractPlasma epinephrine and norepinephrine concentrations were measured before, during, and shortly after induced ventricular tachycardia (VT) in 22 selected patients. Sustained, unimorphic VT was induced by programmed ventricular stimulation and terminated after 45 to 384 seconds by overdrive pacing in all patients. In no patient did VT result in loss of consciousness. The baseline plasma catecholamine concentrations did not correlate with the baseline right ventricular effective refractory period, the cycle length of induced VT, or the number of extrastimuli required to induced VT. Induced VT was not associated with a significant increase in the mean plasma epinephrine concentration. In contrast, the plasma norepinephrine concentration increased from a mean baseline level of 317 +/- 136 pg/ml (mean +/- standard deviation) to 418 +/- 220 pg/ml during VT (p = 0.01) and increased further to 569 +/- 387 pg/ml shortly after VT (p p &lt; 0.05 for each). In eight patients the same configuration of VT was induced on two sequential attempts; in five patients the same number of extrastimull were required for the second induction of VT as for the first, whereas in three patients fewer extrastiuli were required. Plasma cateholamine concentrations were not higher in patients requiring fewer extrastimuli to induce the second episode of VT, either shortly after the first episode of VT or shortly after the second episode of VT. In conclusion, plasma catecholamines do not influence baseline ventricular refractoriness, the cycle length of induced VT, or the VT induction technique. Induced VT, which does not require termination by direct-current countershock, is generally associated with little or no increase in plasma epinephrine and a variable increase in plasma norepinephrine concentration, depending on the severity and duration of hypotension during VT. The plasma catecholamine response to VT does not affect a second induction of VT. Therefore, endogenous catecholamines exert little influence on the results of electrophysiologic testing in patients with sustained VT which does not require termination by direct-current countershock.en_US
dc.format.extent777047 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleThe interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testingen_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.affiliationumDivision of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA; Division of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA.en_US
dc.contributor.affiliationumDivision of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA; Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA.en_US
dc.contributor.affiliationumDivision of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA; Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA.en_US
dc.contributor.affiliationumDivision of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA; Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA.en_US
dc.contributor.affiliationumDivision of Geriatric Medicine, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA; Division of Cardiology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Mich., USA.en_US
dc.identifier.pmid3812177en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/26830/1/0000389.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0002-8703(87)90258-4en_US
dc.identifier.sourceAmerican Heart Journalen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.