Influence of high and low plasma insulin levels on the uptake of fluorine-18 fluorodeoxyglucose in myocardium and femoral muscle, assessed by planar imaging.

The aim of this study was to optimize the metabolic conditions for planar myocardial fluorine-18 fluorodeoxyglucose (FDG) imaging. The effects of high and low insulin levels during euglycaemic clamping on myocardial and femoral muscle FDG uptake were compared since insulin plays a major role in glucose metabolism. FDG uptake in 11 patients was studied using planar scintigraphy. Patients were studied twice: in the low-dose insulin protocol (LDI), insulin was infused at a rate of 20 mU/kg per hour, starting 1 h before FDG administration, while in the high-dose insulin protocol (HDI) it was infused at a rate of 100 mU/kg per hour. Glucose infusion rate was adjusted according to frequently determined blood glucose levels. Somatostatin was infused to block endogenous insulin release. Planar images were obtained from the thorax region and femoral muscles. Regions of interest were drawn over normal and abnormal myocardial areas (based on angiographic and thallium-201 data) and over lung, liver and muscle areas. After clamping, insulin levels during LDI and HDI at t = 60 were 30.6 +/- 13.3 and 129.6 +/- 30.5 mU/l respectively (P < 0.0001). Femoral muscle uptake was significantly higher during HDI (P < 0.001). Uptake in normal and abnormal myocardial areas did not differ between the two protocols. Heart/lung ratios (NS) and heart/liver ratios (P < 0.05) increased during HDI. It may be concluded that planar FDG imaging is influenced by plasma insulin levels. The euglycaemic hyperinsulinaemic clamp technique, although more demanding, gives an adjustable metabolic steady state without significantly altering the FDG uptake patterns in normal and abnormal myocardial regions. The image quality of planar FDG images improves due to lower background uptake of FDG during clamping with high plasma insulin levels.

Feasibility of planar fluorine-18-FDG imaging after recent myocardial infarction to assess myocardial viability.

UNLABELLED: The aim of this study was to define the clinical feasibility of planar myocardial 18F-fluorodeoxyglucose (FDG) imaging and to assess the relation between 201Tl, FDG and left ventricular function early after myocardial infarction. METHODS: Fifty-one patients were studied 5 +/- 2 days after infarction. Scintigraphic images were visually and quantitatively analyzed using a circumferential profiles technique. FDG uptake was normalized to the area with maximal 201Tl uptake. Scintigraphic data were compared with left ventricular wall motion as assessed by ventriculography in 22 patients. Relative regional 201Tl uptake was categorized as normal (> or = 75% of peak activity), moderately reduced (50%-75%) or severely reduced (< 50%). These tracer defects were considered viable if FDG uptake exceeded 201Tl uptake by > or = 20% and/or if FDG uptake was normal (> or = 75%). All regions with FDG uptake 20% less than 201Tl uptake were considered nonviable. RESULTS: Four hundred forty-one myocardial regions were analyzed; 200 showed normal 201Tl uptake, 241 had reduced uptake, 191 had moderately reduced 201Tl uptake and 50 regions had severely reduced uptake. Viability for moderately and severely reduced regions was observed in 62% and 48%, respectively. A concordance between flow and metabolism was observed in 38% and 52%, respectively. CONCLUSION: Myocardial FDG imaging is feasible with standard gamma camera systems and enables the identification of regions with preserved glucose metabolism in patients shortly after infarction.

Feasibility of assessing regional myocardial uptake of 18F-fluorodeoxyglucose using single photon emission computed tomography.

Differentiation between viable myocardium and scar tissue in segments with abnormal contraction has important consequences in the clinical management of patients with coronary artery disease. Positron emission tomography (PET) can identify viable tissue using 18F-fluorodeoxyglucose (FDG). However, application of PET for daily routine is limited. In this study, FDG uptake was visualized with single photon emission computed tomography (SPECT) and compared with regional perfusion assessed with thallium-201 (201Tl) SPECT. The scintigraphic findings were related to regional wall motion determined with two-dimensional echocardiography. Patients (n = 9) with wall motion abnormalities underwent FDG SPECT and resting 201Tl SPECT. To control the metabolic status patients were studied with a hyperinsulinaemic euglycemic clamp during FDG SPECT. Analysis of reconstructed data was performed visually and semiquantitatively using circumferential profiles. High-quality images were obtained. Eight 201Tl defects showed concordantly decreased FDG uptake (metabolism-perfusion matches) indicating scarred tissue, whereas six regions of hypoperfusion demonstrated a relatively increased FDG uptake (mismatches), suggesting viable myocardium. Semiquantitative analysis confirmed visual findings. Mean 201Tl and FDG activities were not significantly different in matching defects. In mismatches the mean FDG activity was 81 +/- 11% vs 64 +/- 9% mean 201Tl activity (P < 0.0001). In four of six segments with increased FDG uptake, two-dimensional echo revealed hypokinesia. Seven of eight regions with a matching defect in contrast were akinetic. Thus, in the areas with a mismatch contractility was preserved. We conclude that FDG uptake can be visualized with SPECT. Furthermore, our preliminary observations suggest that this approach can identify viable tissue.

Stunning does not change the relation between calcium and force in skinned rat trabeculae.

To test the hypothesis that stunning is due to a decreased sensitivity of the myofibrils for calcium, we compared the isometric force-Ca2+ relation in skinned trabeculae from stunned and control hearts. Hearts were made ischemic for 40 min followed by 30 min reperfusion. In one group (Group 1) changes in left ventricular systolic and diastolic pressure were monitored. From another group (Group 2), trabeculae were isolated to determine the relation between force and Ca2+ concentration. Trabeculae isolated from hearts (Group 3) perfused aerobically for 90 min served as controls. Left ventricular developed pressure and end diastolic pressure were 5.9 +/- 0.7 kPa and 5.8 +/- 0.7 kPa, respectively in stunned hearts as compared to 9.9 +/- 1.2 kPa and 1.2 +/- 0.1 kPa prior to ischemia. The nucleotide content decreased from 24.9 +/- 3.4 mumol.g-1(dw) in control hearts to 9.3 +/- 0.8 mumol.g-1(dw) after ischemia and reperfusion while the creatine kinase levels were about the same. Force-Ca2+ relations obtained from trabeculae from control and stunned hearts were fitted to the Hill equation. Maximal isometric force, the midpoint and the steepness of the curves estimated for the two groups were not significantly different. We conclude that the maximum isometric force and the sensitivity of the contractile apparatus of skinned myocardium of stunned hearts do not differ from that of control hearts. This suggests that structural changes of the contractile proteins leading to a decreased sensitivity of the myofibrils to calcium are not involved in the mechanism responsible for stunning.