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 distributi on and blood flow in acutely ischemic and infarcted myocardium has bee n widely explored in the experimental setting, its behaviour in chroni cally hypoperfused dysfunctioning human myocardium has not yet been ev aluated. Methods: In tissue samples of excised failing hearts taken fr om ischemic (IHD) patients and idiopathic dilated cardiomyopathy (IDC) controls, we evaluated the relationship between delayed Tl-201 retent ion (4 h redistribution), blood flow (assessed by means of Tc-99m-labe lled human albumin microspheres injected during transplantation) and b iochemically-assessed fibrosis. Tl-201 activity was expressed as the p ercent of the activity in the region with highest flow and the least f ibrosis. Results: Fibrosis and Tl-201 activity were inversely related (r = -0.62, P = 0.0001). In IDC controls, low flows corresponded to un iformly preserved Tl-201 retention. In IHD, 46 segments with flows les s than or equal to 0.60 ml . min(-1) . g(-1) and 20 segments with flow s > 0.60 ml . min(-1) . g(1) showed matching delayed Tl-201 retention and flow values; in the remaining 27, there was a disproportionately h igh tracer accumulation in comparison with flow (flow/Tl-201 mismatch) . Despite significantly less fibrosis and lower flows, the mismatch se gments showed significantly greater Tl-201 activity than the segments with concordantly high tracer retention and flow values. Conversely, a t equivalent flow rates, the mismatch regions had less fibrosis than t he areas with concordantly depressed Tl-201 activity and perfusion. Co nclusions: This super-normal Tl-201 retention in hibernating myocardiu m may indicate a mechanism of cell adaptation to chronic hypoperfusion . (C) 1998 Elsevier Science B.V. All rights reserved.