Linked Life Data

1848871

Source:http://linkedlifedata.com/resource/pubmed/id/1848871

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-5-1
pubmed:abstractText
Sodium channel blocking antiarrhythmic drugs have preferential effects on diseased, slowly conducting myocardium, and slowing of tachycardia caused by these drugs may result primarily from further prolongation of conduction time in slowly conducting tissue. In patients with sustained ventricular tachycardia, late potentials detected by signal-averaged electrocardiography (ECG) are thought to arise from slowly conducting ventricular myocardium. This study tested the hypothesis that sodium channel blocking drugs selectively prolong the late potential, or terminal low amplitude signal, portion of the signal-averaged QRS complex and that prolongation of the late potential would correlate with slowing of ventricular tachycardia. Fifty-six drug trials in 32 patients with spontaneous and inducible ventricular arrhythmias were studied. Prolongation of the late potential (11 +/- 15 ms) was significantly greater than prolongation of the initial portion of the QRS complex (4 +/- 9 ms) (p = 0.01). Selective prolongation of the late potential by drugs resulted in significantly greater QRS prolongation detectable by signal-averaged ECG than by standard ECG (p less than 0.0001). In 40 trials in which ventricular tachycardia remained inducible during drug therapy, the increase in induced tachycardia cycle length correlated strongly with the increase in late potential duration (p = 0.005) but not with change in the initial portion of the QRS complex. These data suggest that in patients with ventricular tachycardia, sodium channel blocking antiarrhythmic drugs have preferential effects on slowly conducting tissue and that drug effect on slowly conducting tissue contributes to prolongation of ventricular tachycardia cycle length.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0735-1097
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1017-25
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Selective prolongation of QRS late potentials by sodium channel blocking antiarrhythmic drugs: relation to slowing of ventricular tachycardia. Electrophysiologic Study Versus Electrocardiographic Monitoring Trial (ESVEM) Investigators.
pubmed:affiliation
Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City.
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Multicenter Study