Author + information
- Received December 3, 1985
- Revision received February 25, 1986
- Accepted March 19, 1986
- Published online September 1, 1986.
- David M. Mirvis, MD*,1,
- Leslie A. Ingram, MS1,
- Kodangudi B. Ramanathan, MD, FACC1 and
- Jack L. Wilson, PhD1
- ↵*Address for reprints: David M. Mirvis, MD, 956 Court Avenue, Room F208, Memphis, Tennessee 38163.
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 re-perfusion. 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 tri-phenyltetrazolium 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 in-farcted 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.
- Received December 3, 1985.
- Revision received February 25, 1986.
- Accepted March 19, 1986.
- American College of Cardiology Foundation