skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Assessment of myocardial injury after reperfusion with T1-201, Tc-99m pyrophosphate (PPi) and F-18 deoxyglucose (FDG)

Abstract

The authors previously demonstrated that enhanced glucose utilization assessed by FDG and Positron-CT in reperfused myocardium predicts functional recovery. This study compared segmental uptake of FDG with T1-201 and PPi as conventional indicators of tissue viability in 5 dogs, submitted to a 3 hr LAD occlusion followed by 24 hrs of reperfusion (R). Myocardial blood flow (MBF) was then determined by microspheres and T1-201, PPi and FDG administered i.v. Regional tracer concentrations were determined by well counting of tissue samples and grouped according to MBF (% of control). Severe flow reductions were associated with PPi uptake increase, T1-201 decrease and depressed glucose utilization representing mainly irreversible injury. Moderately reduced MBF areas showed the highest PPi uptake with T1-201 similar to MBF, but preserved FDG uptake not different from control, indicating partially viable tissue. Areas with MBF >60% had significantly increased PPi despite normal T1-201 uptake and enhanced glucose utilization and thus, preserved viability. Thus, assessment of tissue injury by conventional tracers such as T1-201 and PPi is limited. By contrast, quantification of residual glucose metabolism by PCT appears more accurate for evaluating myocardial viability and predicting potential functional recovery.

Authors:
; ; ; ; ; ; ; ;
Publication Date:
Research Org.:
UCLA School of Medicine, Los Angeles, CA
OSTI Identifier:
6518240
Report Number(s):
CONF-840619-
Journal ID: CODEN: JNMEA
Resource Type:
Conference
Resource Relation:
Journal Name: J. Nucl. Med.; (United States); Journal Volume: 25:5; Conference: 31. annual meeting of the Society of Nuclear Medicine, Los Angeles, CA, USA, 5 Jun 1984
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; 62 RADIOLOGY AND NUCLEAR MEDICINE; MYOCARDIUM; DYNAMIC FUNCTION STUDIES; PATHOLOGICAL CHANGES; RADIONUCLIDE KINETICS; RADIOPHARMACEUTICALS; TISSUE DISTRIBUTION; UPTAKE; BIOLOGICAL EFFECTS; BIOLOGICAL RADIATION EFFECTS; BIOLOGICAL RECOVERY; BLOOD CIRCULATION; BLOOD FLOW; DOGS; EVALUATION; FLUORINE 18; FLUORODEOXYGLUCOSE; GLUCOSE; METABOLISM; PYROPHOSPHATES; RADIATION INJURIES; TECHNETIUM 99; TRACER TECHNIQUES; ALDEHYDES; ANIMALS; ANTIMETABOLITES; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BETA-PLUS DECAY RADIOISOTOPES; BODY; CARBOHYDRATES; CARDIOVASCULAR SYSTEM; DISTRIBUTION; DRUGS; FLUORINE ISOTOPES; HEART; HEXOSES; HOURS LIVING RADIOISOTOPES; INJURIES; INTERMEDIATE MASS NUCLEI; ISOMERIC TRANSITION ISOTOPES; ISOTOPE APPLICATIONS; ISOTOPES; LABELLED COMPOUNDS; LIGHT NUCLEI; MAMMALS; MONOSACCHARIDES; MUSCLES; NUCLEI; ODD-EVEN NUCLEI; ODD-ODD NUCLEI; ORGANIC COMPOUNDS; ORGANS; OXYGEN COMPOUNDS; PHOSPHORUS COMPOUNDS; RADIATION EFFECTS; RADIOISOTOPES; RECOVERY; SACCHARIDES; TECHNETIUM ISOTOPES; VERTEBRATES; YEARS LIVING RADIOISOTOPES 551001* -- Physiological Systems-- Tracer Techniques; 550601 -- Medicine-- Unsealed Radionuclides in Diagnostics

Citation Formats

Sochor, H., Schwaiger, M., Hansen, H.W., Parodi, O., Selin, C., Huang, S.C., Ellison, D., Grover, M., and Schelbert, H.R.. Assessment of myocardial injury after reperfusion with T1-201, Tc-99m pyrophosphate (PPi) and F-18 deoxyglucose (FDG). United States: N. p., 1984. Web.
Sochor, H., Schwaiger, M., Hansen, H.W., Parodi, O., Selin, C., Huang, S.C., Ellison, D., Grover, M., & Schelbert, H.R.. Assessment of myocardial injury after reperfusion with T1-201, Tc-99m pyrophosphate (PPi) and F-18 deoxyglucose (FDG). United States.
Sochor, H., Schwaiger, M., Hansen, H.W., Parodi, O., Selin, C., Huang, S.C., Ellison, D., Grover, M., and Schelbert, H.R.. 1984. "Assessment of myocardial injury after reperfusion with T1-201, Tc-99m pyrophosphate (PPi) and F-18 deoxyglucose (FDG)". United States. doi:.
@article{osti_6518240,
title = {Assessment of myocardial injury after reperfusion with T1-201, Tc-99m pyrophosphate (PPi) and F-18 deoxyglucose (FDG)},
author = {Sochor, H. and Schwaiger, M. and Hansen, H.W. and Parodi, O. and Selin, C. and Huang, S.C. and Ellison, D. and Grover, M. and Schelbert, H.R.},
abstractNote = {The authors previously demonstrated that enhanced glucose utilization assessed by FDG and Positron-CT in reperfused myocardium predicts functional recovery. This study compared segmental uptake of FDG with T1-201 and PPi as conventional indicators of tissue viability in 5 dogs, submitted to a 3 hr LAD occlusion followed by 24 hrs of reperfusion (R). Myocardial blood flow (MBF) was then determined by microspheres and T1-201, PPi and FDG administered i.v. Regional tracer concentrations were determined by well counting of tissue samples and grouped according to MBF (% of control). Severe flow reductions were associated with PPi uptake increase, T1-201 decrease and depressed glucose utilization representing mainly irreversible injury. Moderately reduced MBF areas showed the highest PPi uptake with T1-201 similar to MBF, but preserved FDG uptake not different from control, indicating partially viable tissue. Areas with MBF >60% had significantly increased PPi despite normal T1-201 uptake and enhanced glucose utilization and thus, preserved viability. Thus, assessment of tissue injury by conventional tracers such as T1-201 and PPi is limited. By contrast, quantification of residual glucose metabolism by PCT appears more accurate for evaluating myocardial viability and predicting potential functional recovery.},
doi = {},
journal = {J. Nucl. Med.; (United States)},
number = ,
volume = 25:5,
place = {United States},
year = 1984,
month = 1
}

Conference:
Other availability
Please see Document Availability for additional information on obtaining the full-text document. Library patrons may search WorldCat to identify libraries that hold this conference proceeding.

Save / Share:
  • Fourteen patients with transmural acute myocardial infarction (AMI) were treated with intravenous streptokinase a mean of 4 +/- 1 hours after chest pain and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 7 +/- 2 hours after the onset of chest pain. The early Tc-99m-PPi images were obtained to test the hypothesis that an early, strongly abnormal Tc-99m-PPi image suggests reperfusion. Eleven of 14 patients had early peaking (within 16 hours) serum creatine kinase isoenzyme levels (CK-B) at a mean of 11 +/- 3 hours. Ten of 14 patients had 3+ or 4+ acute Tc-99m-PPi images. Eight of 11 patients had patentmore » infarct-related vessels at cardiac catheterization 15 days after AMI. One patient who had both an early positive Tc-99m-PPi image and CK-B peak level had an occluded infarct-related artery at catheterization. Acute left ventricular (LV) ejection fraction (EF) by radionuclide ventriculography was compared with LVEF on day 15, and improved from 0.37 +/- 0.13 to 0.50 +/- 0.16 (p = 0.004) in the 10 patients with strongly positive acute Tc-99m-PPi images. LVEF also improved from 0.37 +/- 0.12 to 0.49 +/- 0.15 (p = 0.003) in the 11 patients with early peaking serum CK-B values. Three patients without evidence of reperfusion failed to improve the LVEF from the initial value to the one obtained at hospital discharge. Six control patients had acute Tc-99m-PPi images 10 +/- 2 hours after chest pain; none had strongly positive acute Tc-99m-PPi images, and the mean time to peak CK-B was 19 +/- 5 hours.(ABSTRACT TRUNCATED AT 250 WORDS)« less
  • To test the hypothesis that scans with technetium-99m pyrophosphate (Tc-99m-PPi) are positive when performed early after successful thrombolytic therapy for acute myocardial infarction (AMI), 16 consecutive patients with AMI who received thrombolytic therapy within 5 hours after the onset of chest pain were studied. Patients were included if chest pain lasted for greater than 30 minutes, was unresponsive to sublingual nitroglycerin and was associated with at least 0.2 mV ST-segment elevation in at least 2 contiguous electrocardiographic leads. All patients received 1.5 million IU of streptokinase intravenously, a mean of 195 +/- 99 minutes after onset of chest pain. Tc-99m-PPimore » scans and coronary cineangiograms were recorded 491 +/- 156 minutes and 518 +/- 202 minutes, respectively, after the onset of symptoms. Effective reperfusion was present in 10 patients, 6 of whom had positive Tc-99m-PPi scans (sensitivity of 60% to detect reperfusion). Of the 6 patients without effective reperfusion, 3 had positive Tc-99m-PPi scans (specificity of 50%, p greater than 0.05). Analysis of the data using various definitions of effective reperfusion or artery patency yielded similar results. Thus, our findings indicate that early AMI scanning with Tc-99m-PPi does not accurately detect the presence or absence of reperfusion in patients with AMI after treatment with intravenous streptokinase. At this time, coronary cineangiography is the only reliable method to detect reperfusion promptly after thrombolytic therapy.« less
  • Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acutemore » positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).« less
  • Ischemic but viable myocardium has been shown to extract more glucose than normal regions in conditions of predominant fatty acids utilization. To investigate the frequency and significance of this ''ischemic'' metabolic abnormality in patients (pts) after myocardial infarction (MI), the authors have studied 25 fasting pt mean age 61 +- 7 years. 17 had an anterior MI, 8 an inferior or lateral MI, 12 had single vessel disease, 9 were studied 5 to 11 days after fibrinolysis. Tomograms were recorded at 3 levels using FDG and a flow tracer (13N H4+ or 38K). The flow and FDG data were normalizedmore » to the region of maximum cation uptake and a FDG over flow ratio calculated (G/F). In normal regions distribution of tracers was homogenous and G/F=1.13 +- 0.07 (n=4). MI regions had either a concurrent flow and FDG reduction (to +- 36% of normal) with a normal G/F ratio (1.08 +- .09)(n=8) or a similar drop in flow with a higher FDG uptake and a decreased G/F ratio (2.05 +- 0.14)(n=12). 8 of the 9 pts submitted to fibrinolysis belonged to the second group. The authors conclude that high FDG uptake disproportionate to flow suggests persistence of viable tissue in the MI area or residual ischemia at a distance. It is more frequent after fibrinolysis and implies potential improvement with time or after complete revascularization.« less
  • Recent studies suggest that polymorphonuclear leukocytes (PMNs) may cause additional myocyte injury during reperfusion of ischemic myocardium. The present study was done to investigate whether PMNs accumulate in myocardium during early reperfusion after reversible or irreversible ischemic injury. Open-chest anesthetized dogs underwent circumflex coronary occlusions for 12 min, 40 min, or 90 min, followed by 1 h of reperfusion. Autologous PMNs were radiolabeled with {sup 111}In and reinjected to quantitate myocardial PMN influx during reflow. {sup 125}I-labeled albumin was injected simultaneously to correct for {sup 111}In associated with plasma proteins in myocardial tissue. The number of PMNs was determined inmore » the inner, middle, and outer one-third of nonischemic and ischemic-reperfused myocardium. In the 12-min group, 40% fewer PMNs were present in the reperfused than in the nonischemic control tissue. In contrast, in both the 40- and 90-min groups, PMN accumulation was two- to six-fold greater in the ischemic-reperfused than nonischemic myocardium, with a transmural gradient of PMN influx increasing from the outer to inner layers. Collateral blood flow, measured with radioactive microspheres, was not significantly different among the three groups. The failure of PMNs to accumulate during reperfusion after 12 min of ischemia does not support the hypothesis that PMNs contribute to postischemic dysfunction of reversibly injured myocytes. Whether PMNs cause cell death during early reperfusion after longer ischemic episodes remains unknown; however, the rapidity of PMN accumulation in the zones of predicted infarction is consistent with this possibility.« less