JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
 QUICK SEARCH:   [advanced]


     


J Am Coll Cardiol, 1986; 8:675-681
© 1986 by the American College of Cardiology Foundation
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mirvis, D.
Right arrow Articles by Wilson, J.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Mirvis, D.
Right arrow Articles by Wilson, J.

R and S wave changes produced by experimental nontransmural and transmural myocardial infarction

DM Mirvis, LA Ingram, KB Ramanathan, and JL Wilson

Electrocardiographic R and S wave changes occur after transmural myocardial infarction. It was the purpose of this study to define the spatial characteristics of these changes and their pathologic determinants after nontransmural as well as transmural necrosis. Twenty-six dogs were studied after occlusion of the left circumflex coronary artery for 60 to 240 minutes, followed by reperfusion. Electrocardiographic potentials were recorded before and 1 week after infarction using an 84 electrode array to compute maximal and root-mean-square R and S wave voltages. Infarct size was quantitated by computer-aided evaluation of heart slices stained by triphenyltetrazolium chloride. R and S wave amplitudes after infarction varied widely from one torso site to another in a pattern generally consistent with the inferoposterior location of the infarcted zones. Although changes in peak R and S wave potentials did not significantly correlate with infarct size, differences in pre- and postocclusion root-mean-square R and S wave amplitudes did, with correlation coefficients of -0.79 and -0.63, respectively. Root-mean-square values increased for small lesions and decreased for larger ones. These data indicate that nontransmural as well as transmural infarction can produce R and S wave changes that are dependent on overall lesion size and the specific lead studied. Such changes may represent useful methods to quantitate lesion size.





HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
Copyright © 1986 by the American College of Cardiology Foundation.