The relation of localized myocardial warming to changes in cardiac surface electrograms in dogs.

We studied the relationship of the size and severity of alteration of recovery properties in localized areas to changes in cardiac surface electrograms in experiments on six open-chest dogs. Alterations in recovery properties were induced thermally because size and severity of the affected area could be controlled on the basis of physical principles which were modeled. We recorded unipolar electrograms from 75 cardiac surface sites simultaneously during stimulation of atria and pulmonary conus in control periods and in the presence of warmed areas of varying sizes and intensities. Size of the areas was controlled by the diameter of an aperture through which a light source was directed. Intensity was controlled by the light source excitation voltage. Myocardial temperature was monitored with a thermistor. The QRS, STT, and QRST deflection areas were determined by computer processing and displayed as isoarea maps. Difference maps also were determined by subtracting control QRST isoarea maps from those obtained in the presence of warmed areas. QRST area difference maps were related closely to the size and severity of the thermally induced changes in recovery properties. With areas of the same size and increasing myocardial temperatures, the magnitude of the change in QRST area increased, and the gradient of contour lines between the affected and unaffected areas increased. When myocardial temperature at the center of the warmed area was kept constant and the size of the warmed area was increased, the affected cardiac surface area increased, but the number of isoarea contours remained approximately the same. These findings suggest that the change in QRST isoarea maps may be a useful indicator of lesion size when combined with an index of lesion severity such as the QRST area change in the electrogram with the maximum change. QRST areas during both activation orders were similar, suggesting that the QRST area is independent of changes in activation sequence.