Thallium redistribution in dogs with severe coronary artery stenosis of fixed caliber.

Abstract

Patients with severe coronary artery disease may have defects on initial rest myocardial 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 min after constriction, and 1 group of dogs (7) was killed 10 min, another group (7) 2 h, and a 3rd group (6) 4 h after Tl-201 administration. Microspheres were given immediately prior to death in the 2- and 4-h groups and demonstrated no significant change in regional myocardial blood flow compared to 10 min. In the regions with 20-100% of normal flow, a linear correlation was demonstrated between 10 min blood flow and Tl-201 activity at 10 min (r = 0.91; P < 0.001), 2 h (r = 0.79; P < 0.001) and 4 h (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 min, 2 h and 4 h, 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 and resolution of Tl-201 defects observed clinically. To determine the change in absolute myocardial activity of Tl-201, dogs in the 4-h group had transmural myocardial drill biopsies of ischemic anterior and nonischemic posterior wall at 10 min 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 release of Tl-201 from the nonischemic zone and accumulation of Tl-201 in the ischemic zone. The deficit of Tl-201 in an underperfused zone distal to a persistent severe coronary artery stenosis apparently slowly resolves over time; this resolution does not require restoration of normal blood flow. Accumulation of Tl-201 in the ischemic zone and release from the nonischemic zone account for resolution of an initial Tl-201 deficit.