Quantitative planar imaging of glucose metabolic activity in myocardial segments with exercise thallium-201 perfusion defects in patients with myocardial infarction: comparison with late (24-hour) redistribution thallium imaging for detection of reversible ischemia.

Exercise thallium-201 24-hour redistribution imaging and myocardial glucose metabolism with F-18-deoxyglucose were used to identify reversible ischemia in 30 patients with previous myocardial infarction. Metabolic images were obtained using a planar gamma camera fitted with a rotating tungsten collimator. Of 184 exercise thallium perfusion defects, late redistribution occurred in 88. Metabolic evidence for reversibility (metabolism-perfusion mismatch) was identified in 91% of these 24-hour reversible segments. However, 72% of the segments with fixed perfusion defects also had residual ischemia by F-18-deoxyglucose. Out of 26 fixed severe thallium defects, 69% had F-18-deoxyglucose evidence for residual ischemia. A subset of 14 patients underwent serial exercise thallium scintigraphy or gated equilibrium radionuclide angiography after revascularization or medical therapy. Out of 46 fixed thallium defects in these patients, 30 demonstrated serial scintigraphic improvement. F-18-deoxyglucose-thallium mismatch was present in 81% of these segments, but was absent in the majority of the unimproved segments. Thus quantitative planar imaging of myocardial glucose metabolism with F-18-deoxyglucose using a well-collimated gamma camera can detect clinically important reversible ischemia in segments with fixed thallium defects at late redistribution imaging.

Accumulation of indium-111-labeled human low density lipoprotein in the rabbit aorta: Implications for nuclear imaging of vascular lesions.

Nuclear imaging of atheromata must distinguish lesions from both blood pool and normal arterial tissue. We have examined spatial and temporal variations of indium-111-labeled human low density lipoprotein (LDL) accumulation in rabbit aortas. LDL-derived In-111 activity was time-independent in lesion-resistant regions of aortas from normal and hypercholesterolemic animals (mean 2.9 × 10(-6) percent injected activity per milligram tissue [%IA/mg]) and in lesion-prone regions of normal aortas (mean 7.1 × 10(-6) %IA/mg). In contrast, activity in sudanophilic lesions of hypercholesterolemic rabbit aortas reached a peak of 31 × 10(-6) %IA/mg at 92 hours postinjection. The mean ratio between activity in lesions versus lesion-resistant regions described a broad convex curve with minima of 4:1 at 14 hours and 136 hours and a peak of 14:1 measured at 72 hours postinjection. The mean ratio between In-111 in lesions and blood followed a sigmoid curve, rising exponentially from 1:25 at 14 hours to 1:3 by 72 hours postinjection. We conclude that optimal signal-to-noise ratios for monitoring atheroma-associated LDL-derived radioactivity occur late, not before about 3 days postinjection. Therefore, LDL labeled with In-111 or even longer-lived radionuclides holds the greatest promise for effective clinical nuclear imaging of atherosclerosis.

Nuclear imaging analysis of human low-density lipoprotein biodistribution in rabbits and monkeys.

We have evaluated the biodistribution of human low-density lipoprotein (LDL) radiolabeled with 99mTc or with 123I-tyramine cellobiose in rabbits and in rhesus monkeys. Biodistribution was assessed after intravenous injection of radiolabeled LDL by quantitative analysis of scintigrams, counting of excreta, and counting of tissues at necropsy. Both rabbits and monkeys showed lower renal uptake (123I:99mTc approximately 1:3, as regional percent injected activity corrected for physical decay) and excretion (1:2 to 1:4), but higher hepatic (1.5:1 to 2:1) and cardiac (1.7:1 to 4:1) uptake of 123I than of 99mTc. Adrenals were visualized in normolipemic animals with 123I-tyramine cellobiose-LDL but not with 99mTc-LDL. Hyperlipemic animals showed increased cardiac (up to six-fold) and decreased hepatic activity (by 50%-60%) of both radionuclides. We conclude that 123I-tyramine cellobiose-LDL is better suited than 99mTc-LDL for dynamic studies of LDL metabolism in vivo.