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Myocardial uptake of 99TC-noet in dogs with reperfused acute myocardial infarction: Comparison to TL-201
Journal of Nuclear Cardiology Volume 4, Number I, Part 2
Abstracts Monday morning, April 7, 1997
$21
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14.5
MYOCARDIAL UPTAKE OF 99TC-NOET IN DOGS WITH REPERFUSED ACUTE MYOCARDIAL INFARCTION: COMPARISON TO TL-201 G. Vanzetto, DA.Calnon, M. Ruiz, DD. Watson, GA. Beller, DK. GIover. University of Virginia, Charlottesville, USA NOET is a new neutral lipophilic myocardial perfusion agent that redistributes in canine models of short term hibernation. We sought to determine the ability of NOET to assess viability in acutely infarcted reperfused myocardium. Accordingly, T1 and NOET were co-injected in 6 dogs after 1 hr of reperfusion (Rep) following 3 hrs of total LAD occlusion (Occ). Serial NOET images were acquired for 2 hrs. Regional myocardial blood flow (MBF) and Tl and NOET activities were determined by gamma-welt counting. Infarct size averaged 39+7% of the risk area by TTC staining, Mean infarct-to-normal MBF ratio was 0.13+_0.04 during Occ, and 0.93+_0.23 after Rep. Infarct-to-normal T1 activity ratio was 0.32+0.07 reflecting the extent of the necrosis. In contrast, NOET activity ratio was 0.74_+0.12 (p<0.01 vs TI), more reflective of Rep flow. Similarly, the LAD/LCX count ratios on NOET images were 0.71+_0.10 and 0.82__.0.I2 at 5 and 120 min after injection. Thus, in the setting of acutely infarcted, Rep myocardium, NOET uptake is a good marker of Rep flow, whereas TI uptake appears to be a better marker of viability.
KINETICS OF 1, 3, 4, 6-TETRA-ACETYL-2-[F-18]-2-DEOXY-DGLUCOSE (A-FDG) IN THE ISOLATED RAT HEART. N. Nguyen, M. Herz, S. Egert, S. Ziegler, G. St6cklin, M. Schwaiger. Technische Universit&tM0nchen, Germany. It has been suggested that the glucose transporter dependent cellular uptake of FDG is rate-limiting in exogenous glucose utilization in the heart. Thus, the purpose of this study was t o evaluate the kinetics of A-FDG, which in £ontrast to FDG is taken up independentlyof transport. However, it is hydrolyzed and phosphorylated within the cells similarly to FDG. Hearts were perfused according to Langendorff with Krebs-Hensleit bicarbonate buffer containing A-FDG andl0mM glucose. After baseline measurements, insulin was added. Rate of tracer accumulation (ml/g/min) was calculated. At baseline, A-FDG accumulated (0.16_+0.01) approximately 7 times faster than FDG (0.02±0.01)in the same model. After insulin, there was an initial clearance of A-FDG (-0.029+0.001) in contrast to FDG, which showed an approximately 6-fold increase in uptake compared to baseline (0.11±0.06). Approximately 10 minutes after insulin, however, A-FDG was again taken up at a reduced rate (0.02+0.01). Thus, the faster accumulation of A-FDG compared to FDG provides further evidence that transport is rate-limiting for glucose utilization at baseline. The initial clearance of A-FDG after insulin suggests that the increase in glucose transport stimulated by insulin increases cellular glucose concentration, which competes with FDG for hexokinase activity, causing a net efflux of the tracer. After approximately 10 minutes, glucose transport again appears to be rate-limiting; hence, the positive myocardial accumulation of A-FDG. The presented dual tracer technique may provide new insights into the roles of transport and phosphorylation in the regulation of exogenous glucose utilization.
14.4
15.1
BMS-194796 UPTAKE IN A SWINE MODEL OF
NITROGLYCERINE ENHANCED Tc-gPm SESTAMIBI IS COMPARABLE TO TI-201 FOR THE DETECTION OF VIABLE MYOCARDIUM IN CONGESTIVE HEART FAILURE R. Senior, S. Kaul, U. Raval, A. Lahiri. Deparmlentof Cardiology, Northwick Park Hospital, Harrow, UK.
DEMAND ISCHEMIA.
Lynne L. Johnson, Lorraine Schofieid, Patricia Mastrofrancesco, Tammy Donahay. Rhode Island Hospital, Brown University, Providence, RI. USA To evaluate the uptake of Tc-99m labeled nitroheterocycle BMS 194796 in a demand myocardial ischemia model 8 swine underwent the following experimental protocol: 1) catheter placement of stenosis into the LAD, 2) baseline blood flow (BF) measurement (microspheres) and anterior interventricular vein (AIV) lactate sampling, 3) rapid atrial pacing x 4-6 mins, pacing BF measurement, AIV sampling, followed by i.v. injection of BMS-194796, 5) serial planar imaging x 2 hrs followed by SPECT imaging in the last 3 animals, 6) recovery BF measurement, 7) sacrifice, heart sliced, TTC stained and imaged on detector. None of the animals had infarcts in risk region (RR) by TIC. HR % lactate endo endo extraction BF RR BF nl control 104+21 6.2+23.2 0.85+.4 1.73+.3 pacing 191+14 -64.2+53.7 0.33+.3 1.37+.6 recovery 113+13 0.68+.2 1.62+.6 Positive scans: 1/8 planar, 3/4 SPECT, 8/8 ex-vivo. Cts in the RR/normal = 2.29-2_1.8 and the uptake of BMS in the RR = 0.25+0.10% of injected dose. Blood pool clearance was biexponential; early T 1/2 = 1.0, late = 62.2 mins. These data suggest that in this model, BMS-194796 is taken up in RR but that due to high background activity SPECT imaging is necessary.
Tc-99m sestamibi imaging (MIBI) is widely used to assess coronary artery disease (CAD) but its value for the detection of myocardial viability remains controversial. We prospectively evaluated 52 consecutive patients with congestive heart failure(CHF) (NYHA II-IV) due to CAD with LVEF_< 35%. Both T1-201 and MIBI SPECT imagingwere performed at rest following 0.5rag of sublingual nitroglycerine (NTG). Systolic wall thickening was assessed by echocardiography. Tracer uptake was scored semiquantitatively(0 = nomaal; 4 = absent) and viability was present when 50% tracer uptake was in a severely dysfunctional segment. The mean tracer uptake was also calculated in the dysfunctional segments using the semiquantitativescore for both MIBI and T1-201. Of a total of 624 segments (12 segment model) 459 (74%) showed severe dysfunction; of these, MIBI showed viability in 318(65%) and TI-201 in 298(61%) segments (p=NS). Concordance between TI-201 and MIBI was 81% (kappa = 0.60). The mean score of TI-201 and MIB1 were 1.89+0.74 and 1.99+0.66 (p=NS). Thus, NTG M1BI is comparable to T1-201 for the detection of viability in severelydysfunctional,nyocardium.
Abstracts Monday morning, April 7, 1997
$21
14.3
14.5
MYOCARDIAL UPTAKE OF 99TC-NOET IN DOGS WITH REPERFUSED ACUTE MYOCARDIAL INFARCTION: COMPARISON TO TL-201 G. Vanzetto, DA.Calnon, M. Ruiz, DD. Watson, GA. Beller, DK. GIover. University of Virginia, Charlottesville, USA NOET is a new neutral lipophilic myocardial perfusion agent that redistributes in canine models of short term hibernation. We sought to determine the ability of NOET to assess viability in acutely infarcted reperfused myocardium. Accordingly, T1 and NOET were co-injected in 6 dogs after 1 hr of reperfusion (Rep) following 3 hrs of total LAD occlusion (Occ). Serial NOET images were acquired for 2 hrs. Regional myocardial blood flow (MBF) and Tl and NOET activities were determined by gamma-welt counting. Infarct size averaged 39+7% of the risk area by TTC staining, Mean infarct-to-normal MBF ratio was 0.13+_0.04 during Occ, and 0.93+_0.23 after Rep. Infarct-to-normal T1 activity ratio was 0.32+0.07 reflecting the extent of the necrosis. In contrast, NOET activity ratio was 0.74_+0.12 (p<0.01 vs TI), more reflective of Rep flow. Similarly, the LAD/LCX count ratios on NOET images were 0.71+_0.10 and 0.82__.0.I2 at 5 and 120 min after injection. Thus, in the setting of acutely infarcted, Rep myocardium, NOET uptake is a good marker of Rep flow, whereas TI uptake appears to be a better marker of viability.
KINETICS OF 1, 3, 4, 6-TETRA-ACETYL-2-[F-18]-2-DEOXY-DGLUCOSE (A-FDG) IN THE ISOLATED RAT HEART. N. Nguyen, M. Herz, S. Egert, S. Ziegler, G. St6cklin, M. Schwaiger. Technische Universit&tM0nchen, Germany. It has been suggested that the glucose transporter dependent cellular uptake of FDG is rate-limiting in exogenous glucose utilization in the heart. Thus, the purpose of this study was t o evaluate the kinetics of A-FDG, which in £ontrast to FDG is taken up independentlyof transport. However, it is hydrolyzed and phosphorylated within the cells similarly to FDG. Hearts were perfused according to Langendorff with Krebs-Hensleit bicarbonate buffer containing A-FDG andl0mM glucose. After baseline measurements, insulin was added. Rate of tracer accumulation (ml/g/min) was calculated. At baseline, A-FDG accumulated (0.16_+0.01) approximately 7 times faster than FDG (0.02±0.01)in the same model. After insulin, there was an initial clearance of A-FDG (-0.029+0.001) in contrast to FDG, which showed an approximately 6-fold increase in uptake compared to baseline (0.11±0.06). Approximately 10 minutes after insulin, however, A-FDG was again taken up at a reduced rate (0.02+0.01). Thus, the faster accumulation of A-FDG compared to FDG provides further evidence that transport is rate-limiting for glucose utilization at baseline. The initial clearance of A-FDG after insulin suggests that the increase in glucose transport stimulated by insulin increases cellular glucose concentration, which competes with FDG for hexokinase activity, causing a net efflux of the tracer. After approximately 10 minutes, glucose transport again appears to be rate-limiting; hence, the positive myocardial accumulation of A-FDG. The presented dual tracer technique may provide new insights into the roles of transport and phosphorylation in the regulation of exogenous glucose utilization.
14.4
15.1
BMS-194796 UPTAKE IN A SWINE MODEL OF
NITROGLYCERINE ENHANCED Tc-gPm SESTAMIBI IS COMPARABLE TO TI-201 FOR THE DETECTION OF VIABLE MYOCARDIUM IN CONGESTIVE HEART FAILURE R. Senior, S. Kaul, U. Raval, A. Lahiri. Deparmlentof Cardiology, Northwick Park Hospital, Harrow, UK.
DEMAND ISCHEMIA.
Lynne L. Johnson, Lorraine Schofieid, Patricia Mastrofrancesco, Tammy Donahay. Rhode Island Hospital, Brown University, Providence, RI. USA To evaluate the uptake of Tc-99m labeled nitroheterocycle BMS 194796 in a demand myocardial ischemia model 8 swine underwent the following experimental protocol: 1) catheter placement of stenosis into the LAD, 2) baseline blood flow (BF) measurement (microspheres) and anterior interventricular vein (AIV) lactate sampling, 3) rapid atrial pacing x 4-6 mins, pacing BF measurement, AIV sampling, followed by i.v. injection of BMS-194796, 5) serial planar imaging x 2 hrs followed by SPECT imaging in the last 3 animals, 6) recovery BF measurement, 7) sacrifice, heart sliced, TTC stained and imaged on detector. None of the animals had infarcts in risk region (RR) by TIC. HR % lactate endo endo extraction BF RR BF nl control 104+21 6.2+23.2 0.85+.4 1.73+.3 pacing 191+14 -64.2+53.7 0.33+.3 1.37+.6 recovery 113+13 0.68+.2 1.62+.6 Positive scans: 1/8 planar, 3/4 SPECT, 8/8 ex-vivo. Cts in the RR/normal = 2.29-2_1.8 and the uptake of BMS in the RR = 0.25+0.10% of injected dose. Blood pool clearance was biexponential; early T 1/2 = 1.0, late = 62.2 mins. These data suggest that in this model, BMS-194796 is taken up in RR but that due to high background activity SPECT imaging is necessary.
Tc-99m sestamibi imaging (MIBI) is widely used to assess coronary artery disease (CAD) but its value for the detection of myocardial viability remains controversial. We prospectively evaluated 52 consecutive patients with congestive heart failure(CHF) (NYHA II-IV) due to CAD with LVEF_< 35%. Both T1-201 and MIBI SPECT imagingwere performed at rest following 0.5rag of sublingual nitroglycerine (NTG). Systolic wall thickening was assessed by echocardiography. Tracer uptake was scored semiquantitatively(0 = nomaal; 4 = absent) and viability was present when 50% tracer uptake was in a severely dysfunctional segment. The mean tracer uptake was also calculated in the dysfunctional segments using the semiquantitativescore for both MIBI and T1-201. Of a total of 624 segments (12 segment model) 459 (74%) showed severe dysfunction; of these, MIBI showed viability in 318(65%) and TI-201 in 298(61%) segments (p=NS). Concordance between TI-201 and MIBI was 81% (kappa = 0.60). The mean score of TI-201 and MIB1 were 1.89+0.74 and 1.99+0.66 (p=NS). Thus, NTG M1BI is comparable to T1-201 for the detection of viability in severelydysfunctional,nyocardium.