Thallium redistribution in dogs with severe coronary artery stenosis of fixed caliber
Patients with severe coronary artery disease may have defects on initial rest myocardial thallium-201 (Tl-201) images which fill in over time. To study the time course and mechanism for this defect disappearance, a canine model of persistent reduction in regional myocardial blood flow was created using partial left anterior descending coronary occlusion with a balloon cuff. Radiolabeled microspheres to determine regional myocardial blood flow and Tl-201 were administered 20-30 minutes after contriction, and one group of dogs (n = 7) was killed 10 minutes, another group (n = 7) 2 hours, and a third group (n = 6) 4 hours after Tl-201 administration. Microspheres also were given immediately prior to death in the 2- and 4-hour groups and demonstrated no significant change in regional myocardial blood flow compared to 10 minutes. In the regions with 20-100% of normal flow, a linear correlation was demonstrated between 10-minute blood flow and Tl-201 activity at 10 minutes (r = 0.91; P<0.001), 2 hours (r = 0.79; P<0.001), and 4 hours (r = 0.66; P<0.01) after Tl-201 administration. The slopes of the regression lines (Tl-201 vs. flow) became progressively lower between 10 minutes, 2 hours, and 4 hours, with a Tl-201 excess relative to flow in the ischemic flow zone. This was consistent with a relative increase in Tl-201 activity in the ischemic zone compared to the nonischemic zone and resolution of Tl-201 defects observed clinically. To determine the change in absolute myocardial activity of Tl-201, dogs in the 4-hour group also had transmural myocardial drill biopsies of both ischemic anterior and nonischemic posterior wall at 10 minutes after Tl-201 administration and immediately prior to death. These biopsies demonstrated that development of the Tl-201 excess relative to flow was significantly related to both release of Tl-201 from the nonischemic zone and accumulation of Tl-201 in the ischemic zone. These data show that the deficit of Tl-201 in an underperfused zone distal to a persistent severe coronary stenosis slowly resolves over time and that this resolution does not require restoration of normal blood flow. Both accumulation of Tl-201 in the ischemic zone and release from the nonischemic zone account for resolution of an initial Tl-201 deficit.