Myocardial thallium-201 kinetics.

To the Editor: We believe that Grunwald et al.,i in their report of myocardial thallium kinetics in normal and ischemic myocardium, have inaccurately summarized the analysis and interpretation we made of the data we reported in Circulation in 1980.2 We also believe their assertion that the results of our previous studies2' "are in total agreement" with the results of theirs is not true and is based on erroneous impressions of what we actually reported in our paper.2 The principle observation made by Grunwald et al. concerning thallium kinetics in ischemic myocardium was that the intrinsic washout rate of the isotope was prolonged by a reduction in coronary artery perfusion pressure below 60 mm Hg. Data to support this conclusion were acquired with an external nuclear probe suspended 25 cm over the heart. The authors recognized that "systolic expansion of ischemic myocardium" could spuriously alter their myocardial washout curves, but they apparently could not avoid this problem. Although they state that the results of experiments conducted in five animals in whom simultaneous probe measurements and coronary sinus sampling was performed validate the use of the probe technique, this is obviously incorrect. These experiments only prove that when there is an absence of wall motion abnormalities, there is good agreement between the probe and direct sampling techniques. The authors apparently failed to compare the results of the direct sampling method with that of the probe under precisely those conditions with which they were so concerned acute ischemia. It is hard to understand why they would think that the results of comparing the two methods under conditions of normal perfusion (when geometric factors are perhaps less of an issue) validate the probe method for use under conditions in which geometric factors are precisely at issue. It is apparent from their figure 4 and table I that the myocardial halftime (t/2) for thallium was markedly prolonged only at perfusion pressures close to those seen with complete coronary occlusion (i.e., when blood flow probably was severely reduced and when bulging of the anterior wall very likely occurred). With distal coronary pressures > 40 mm Hg, there appears to be no relation between perfusion pressure and myocardial t/2. This is especially evident when t1⁄2/2 data from the five animals listed in table 1 are plotted on their figure 4. Finally, after release of a 15-minute coronary occlusion, a rapid increase in the washout slope (i.e., a more negative slope) was