Super-normal Tl-201 retention in hibernating myocardium: an ex-vivo study using the failing human heart

Objective: Although the relationship between delayed Tl-201 distribution and blood flow in acutely ischemic and infarcted myocardium has been widely explored in the experimental setting, its behaviour in chronically hypoperfused dysfunctioning human myocardium has not yet been evaluated. Methods: In tissue samples of excised failing hearts taken from ischemic (IHD) patients and idiopathic dilated cardiomyopathy (IDC) controls, we evaluated the relationship between delayed Tl-201 retention (4 h redistribution), blood flow (assessed by means of Tc-99m-labelled human albumin microspheres injected during transplantation) and biochemically-assessed fibrosis. Tl-201 activity was expressed as the percent of the activity in the region with highest flow and the least fibrosis. Results: Fibrosis and Tl-201 activity were inversely related (r = -0.62, P = 0.0001). In IDC controls, low flows corresponded to uniformly preserved Tl-201 retention. In IHD, 46 segments with flows less than or equal to 0.60 ml . min(-1) . g(-1) and 20 segments with flows > 0.60 ml . min(-1) . g(1) showed matching delayed Tl-201 retention and flow values; in the remaining 27, there was a disproportionately high tracer accumulation in comparison with flow (flow/Tl-201 mismatch). Despite significantly less fibrosis and lower flows, the mismatch segments showed significantly greater Tl-201 activity than the segments with concordantly high tracer retention and flow values. Conversely, at equivalent flow rates, the mismatch regions had less fibrosis than the areas with concordantly depressed Tl-201 activity and perfusion. Conclusions: This super-normal Tl-201 retention in hibernating myocardium may indicate a mechanism of cell adaptation to chronic hypoperfusion. (C) 1998 Elsevier Science B.V. All rights reserved.