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Cardiovascular Research 1998 38(3):727-735; doi:10.1016/S0008-6363(98)00056-X
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

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

Oberdan Parodia,*, Renata De Mariaa, Roberto Testaa, Ettore Vitalib, Livia Ruffinic, Giovanna Palearib, Edoardo Grondab, Jonica Campoloa and Alessandro Pellegrinib

aC.N.R. Clinical Physiology Institute, Milan Section, Niguarda Hospital, Milan, Italy
bMedical and Surgical Cardio-Thoracic Department A. De Gasperis, Niguarda Hospital, Milan, Italy
cNuclear Medicine Service, Niguarda Hospital, Milan, Italy

* Corresponding author. Tel.: +39 (2) 6444 2605; Fax: +39 (2) 647 3407; E-mail: ifcnigmi@tin.it

Objective: Although the relationship between delayed Formula 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 Formula retention (4 h redistribution), blood flow (assessed by means of Formula -labelled human albumin microspheres injected during transplantation) and biochemically-assessed fibrosis. Formula activity was expressed as the percent of the activity in the region with highest flow and the least fibrosis. Results: Fibrosis and Formula activity were inversely related (r=–0.62, P=0.0001). In IDC controls, low flows corresponded to uniformly preserved Formula retention. In IHD, 46 segments with flows ≤0.60 ml·min–1·g–1 and 20 segments with flows >0.60 ml·min–1·g1 showed matching delayed Formula retention and flow values; in the remaining 27, there was a disproportionately high tracer accumulation in comparison with flow (flow/Formula mismatch). Despite significantly less fibrosis and lower flows, the mismatch segments showed significantly greater Formula 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 Formula activity and perfusion. Conclusions: This super-normal Formula retention in hibernating myocardium may indicate a mechanism of cell adaptation to chronic hypoperfusion.

KEYWORDS Heart failure; Transplantation; Radioisotopes; Perfusion; Coronary artery disease; Human


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