Attenuation of Microvascular Injury in Preconditioned Ischemic Myocardium: Imaging with Tc-99m Glucaric Acid and In-Ill Human Fibrinogen

摘要

Background: Tc-99m labeled Glucaric Acid (Tc-GA) and In-111 labeled human fibrinogen (In-HF) were used to demonstrate reduction in myocardial infarction and microvascular injury in rabbit preconditioned ischemic hearts.Methods: New Zealand White rabbits were subjected to preconditioning or non-preconditioning ischemic myocardial injury. Reperfusion was established after 45 min of circumflex occlusion and then Tc-GA and In-HF were injected intravenously. Anteroposterior gamma images were acquired for 4 hours. Perfusion defects, histochemical infarct size and radiotracer uptake were determined.Results: In vivo and ex vivo images were consistent with the gamma scintillation counting data. Minimal GA and fibrin depositions were seen in preconditioned ischemic hearts (3.78+ 10.7 and 0 % of total myocardial area respectively) whereas the areas delineated by GA and fibrin deposition in non-ischemic preconditioned hearts were larger (61.9+ 34.5 and 60.0+ 32.7%). Infarct size of preconditioned ischemic hearts was 4.6+1.9 % of the left ventricle, whereas that of non-preconditioned ischemic hearts was 24.1+5.9% (P <0.01) assessed by histochemical technique. Infarct size from imaging was approximately 2.5 times that of the histochemical assessment. The regions of perfusion defect were similar (23.3+4.1 vs 26.5+8.5% respectively). Images of Tc-GA uptake and In-HF deposition were consistent with histochemical and radiotracer uptake data indicating minimal myocardial injury in preconditioned ischemic hearts even though areas of perfusion defect were similar.Conclusion: The data indicates that ischemic precondition not only preserved myocyte viability but also reduced microvascular injury.