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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiolabeled deoxyglucose (FDG) has been advocated as a marker of viability of reperfused myocardium during acute infarction. However, data for such recommendation are few. We investigated cardiac deposition of C-14 deoxyglucose (C-14 DG) and of Thallium -201 (Tl-201) in rabbits subjected to coronary occlusion (15, 30, 60 or greater than 100 min) and reperfusion (75 min and 24 h). Measured myocardial concentrations of C-14 DG and Tl-201 in macroautoradiograms were quantitatively correlated in a 24 h reperfusion group with presence of myocardial necrosis evaluated by light microscopy. The major finding in this investigation was that with 30 min or 60 min of ischemia followed by reperfusion there were myocardial regions with significant hypoperfusion (Tl-201) and histologic necrosis. However, in the same myocardial areas, the deposition of C-14 DG was not correlated with the extent of necrosis (r = 0.27). Also, the deposition of C-14 DG in acute myocardial infarction was higher than that of Tl-201 (P = 0.05 by paired T test and by nonparametric Wilcoxon's test). It was also demonstrated that when the occlusion time was varied (15-130 min) and early reperfusion was provided for 75 min or omitted altogether, the myocardial accumulation of Tl-201 was variable and that myocardial sequestration of C-14 DG was higher than perfusion in central and peripheral portions of the area-at-risk. These observations do not support a role for the use of radiolabeled deoxyglucose for the detection of myocardial viability in recently infarcted cardiac muscle.
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PMID:Discordance between accumulation of C-14 deoxyglucose and Tl-201 in reperfused myocardium. 188 39

To assess the effects of endogenous substrate on glucose utilization after 15 min of ischemia, we perfused isolated working rat hearts from fed and fasted (16 h) animals with glucose and the positron-emitting glucose analogue 2-[18F]fluoro-2-deoxy-D-glucose (2-FDG). Hearts were perfused in a recirculating system with bicarbonate buffer containing glucose (10 mM) and 2-FDG (0.5 microCi/ml). Mechanical performance and 2-FDG uptake were measured on-line, and glucose and lactate metabolic rates were calculated. Fasting raised the glycogen content by 25% and the triglyceride content by 38%. Hearts in both groups recovered preischemic function. Rates of 2-FDG uptake during the preischemic period were the same in both groups. In contrast, during the postischemic period rates of 2-FDG uptake were significantly depressed in hearts of fed animals but were unchanged in hearts of fasted animals. Thus hearts of fasted animals took up more 2-FDG during the postischemic period than hearts of fed animals (P less than 0.005). The lumped constant (range, 0.38-0.40) was the same in both groups before and after ischemia. Glucose utilization was suppressed during the postischemic period in hearts of fed animals, whereas at the same time lactate utilization was significantly increased. We conclude that 1) 2-FDG accurately traces glucose utilization independent of the nutritional state or ischemic insult; 2) reversibly ischemic, viable myocardium exhibits vastly different rates of glucose utilization depending on the nutritional state of the animal before ischemia; 3) lactate derived from glycolysis suppresses utilization of exogenously supplied glucose in the early reperfusion period without affecting postischemic performance.
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PMID:Feeding and fasting determine postischemic glucose utilization in isolated working rat hearts. 199 97

The identification of ischemic and hibernating myocardium facilitates the selection of patients most likely to benefit from revascularization. This study examined the feasibility of metabolic imaging, using post-exercise F-18 deoxyglucose positron emission tomography (FDG-PET) for the diagnosis of both ischemia and hibernation in 27 patients with known coronary anatomy. Normal post-exercise FDG uptake was defined in each patient by reference to normal resting perfusion and normal coronary supply. Abnormal elevation of FDG (ischemia or hibernation) was compared in 13 myocardial segments in each patient, with the results of dipyridamole stress perfusion imaging performed by rubidium-82 positron emission tomography (Rb-PET). Myocardial ischemia was diagnosed by either FDG-PET or Rb-PET in 34 segments subtended by significant local coronary stenoses. Increased FDG uptake was present in 32/34 (94%) and a reversible perfusion defect was identified by Rb-PET in 22/34 (65%, p less than .01). In 3 patients, ischemia was identified by metabolic imaging alone. In 16 patients with previous myocardial infarction, perfusion defects were present at rest in 89 regions, 30 of which (34%) demonstrated increased FDG uptake, consistent with the presence of hibernation. Increased post-exercise FDG uptake appears to be a sensitive indicator of ischemia and myocardial hibernation. This test may be useful in selecting post-infarction patients for revascularization.
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PMID:Identification of ischemic and hibernating myocardium: feasibility of post-exercise F-18 deoxyglucose positron emission tomography. 200 57

Regional myocardial perfusion and metabolism were evaluated in coronary artery disease with positron emission computed tomography (PET). Regional myocardial perfusion was assessed after the intravenous administration of 13N-ammonia at rest and during exercise loading, using a supine ergometer. In some cases, 18F-FDG was administered at rest, and compared with 13N-ammonia. 13N-ammonia revealed hypoperfusion in coronary artery disease, in 73% of cases at rest and in 97%, during exercise study. Increased accumulations of 18F-FDG were observed in the peri-infarcted areas with decreased perfusions, and in the regions with normal perfusions at rest, where the exercise study showed transient ischemia. These results indicate that PET can detect regional myocardial ischemia with superior sensitivity, and that it provides a means of evaluating myocardial metabolism in vivo.
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PMID:[Assessment of regional myocardial blood flow and energy metabolism]. 350 73

A variety of new radiopharmaceutical agents have been introduced to probe myocardial function in vivo. This review will introduce these new techniques which have recently been available in Japan. Tc-99m perfusion imaging agents provide excellent myocardial perfusion images which may enhance diagnostic accuracy in the study of coronary artery disease. In addition, greater photon flux from the tracer permits simultaneous assessment of regional perfusion and function with use of first-pass angiography or ECG-gated acquisition. Positron emission tomography enables metabolic assessment in vivo. Preserved FDG uptake indicates ischemic but viable myocardium which is likely to improve regional dysfunction after revascularization. In addition, FDG-PET seems to be valuable for selecting a high risk subgroup. Recently I-123 BMIPP, a branched fatty acid analog, has been clinically available in Japan. Less uptake of BMIPP than thallium is often observed in the ischemic myocardium. Such perfusion metabolic mismatch which seems to be similarly observed in FDG-PET is identified in the stunned or hibernating myocardium with regional dysfunction. Both of them are likely to recover afterwards. Severe ischemia is identified as reduced BMIPP uptake at rest, suggesting its role as an ischemic memory imaging. I-123 MIBG uptake in the myocardium reflects adrenergic neuronal function in vivo. In the study of coronary artery disease, neuronal denervation is often observed around the infarcted myocardium and post ischemic region as well. More importantly, reduced MIBG uptake in these patients can identify high risk for ventricular arrhythmias and assess severity of congestive heart failure. These new techniques will provide insights into new pathological states in the ischemic heart disease and enable to select optimal treatment in these patients.
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PMID:Recent advances in nuclear cardiology in the study of coronary artery disease. 921 83

In order to clarify the significance of the discrepancy between myocardial blood flow and fatty acid metabolism on 201TlCl/123I-BMIPP SPECT after acute myocardial infarction, we examined 52 patients (278 segments) with their first acute myocardial infarction using two-dimensional echocardiography and FDG-PET. Patients with Tl/BMIPP discrepancy in the acute stage showed higher FDG accumulation than those without Tl/BMIPP discrepancy. In the chronic stage, however, there was no significant difference between both groups. Patients with Tl/BMIPP discrepancy in the chronic stage had lower wall motion scores than those without Tl/BMIPP discrepancy. Significant improvement of the wall motion score was recognized in patients who showed Tl/BMIPP discrepancy in the acute stage. Patients were classified into stenosis and non-stenosis groups by the presence of significant stenosis on coronary angiography in the chronic stage. In the stenosis group, the Tl/BMIPP discrepancy did not show much change from the acute to chronic stage, but there was a significant decrease in the non-stenosis group. It was concluded that 201TlCl/123I-BMIPP myocardial SPECT is useful for predicting future improvement of wall motion and determining the residual ischemia in the chronic stage based on the presence or absence of this discrepancy.
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PMID:[The relationship between discrepant areas on 201TlCl/123I-BMIPP myocardial scintigraphy, local wall motion, and glucose metabolism in patients with myocardial infarction]. 991 2

The rapid development of nuclear medicine instruments and the widespread availability of new radiopharmaceutical agents has created a new era of nuclear cardiology. This review will introduce new techniques beyond perfusion and function that have recently become available in Japan. Tc-99m perfusion imaging agents provide excellent myocardial perfusion images that may enhance diagnostic accuracy in the study of coronary artery disease. In addition, greater photon flux from the tracer permits simultaneous assessment of regional perfusion and function with the use of first-pass angiography or ECG-gated acquisition. In addition, Tc-99m perfusion agents are available for acute patients in emergency departments. When the tracer is administrated at both the acute and subacute phases of myocardial infarction, perfusion SPECT imaging permits accurate estimates of areas at risk and salvaged myocardium. Nuclear cardiology has progressed toward biochemical imaging in vivo. Positron emission tomography (PET) enables metabolic assessment in vivo. Preserved FDG uptake indicates ischemic but viable myocardium that is likely to improve regional dysfunction after revascularization. While FDG-PET is available only in a limited number of facilities, FDG-SPECT using ultrahigh energy collimators and branched fatty acid analog I-123 BMIPP SPECT offer potential for metabolic imaging in routine clinical settings. Less uptake of BMIPP than thallium is often observed in the ischemic myocardium and hypertrophic cardiomyopathy. Such a perfusion-metabolic mismatch as that in FDG-PET seems to be similarly observed in BMIPP SPECT. Severe ischemia is identified as reduced BMIPP uptake at rest despite normal or normalized perfusion, suggesting a significant role of BMIPP in ischemic memory imaging. I-123 MIBG uptake in the myocardium reflects adrenergic neuronal function in vivo. In the study of coronary artery disease, neuronal denervation is often observed around the infarcted myocardium and post-ischemic region as well. More importantly, reduced MIBG uptake in these patients can assess the severity of congestive heart failure. In addition, the improvement in MIBG can be seen in relation to improved patient condition following medical treatment. These new techniques will provide insights into new pathological states in ischemic heart disease and a variety of myocardial disorders. Nuclear cardiology plays an important role in selecting optimal treatments for these patients.
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PMID:[Progress in nuclear cardiology: new imaging beyond perfusion and function]. 1056 67

Dynamic changes in the regional cerebral glucose metabolic rate induced by hypoxia/reoxygenation or ischemia/reperfusion were investigated with a positron autoradiography technique. Fresh rat brain slices were incubated with [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) in oxygenated Krebs-Ringer solution at 36 degrees C, and serial two-dimensional time-resolved images of [18F]FDG uptake in the slices were obtained. In the case of loading hypoxia (oxygen deprivation)/pseudoischemia (oxygen and glucose deprivation) for various periods of time, the net influx constant (K) of [18F]FDG at preloading and after reoxygenation/pseudoreperfusion (post-loading) was quantitatively evaluated by applying the Patlak graphical method to the image data. Regardless of the brain region, with hypoxia lasting > or =20 minutes, the postloading K value was decreased compared with the unloaded control, whereas with pseudoischemia of < or =40 minutes, approximately the same level as the unloaded control was maintained. Next, the neuroprotective effect against hypoxia/pseudoischemia loading induced by the addition of a free radical scavenger or an N-methyl-D-aspartate (NMDA) antagonist was assessed by determining whether a decrease in the postloading K value was prevented. Whereas with 20-minute hypoxia, both agents exhibited a neuroprotective effect, in the case of 50-minute pseudoischemia, only the NMDA antagonist did so, with the free radical scavenger being ineffective. These results demonstrate that hypoxia causes irreversible neuronal damage within a shorter period than ischemia, with both free radicals and glutamate suggested to be involved in tandem in the neurotoxicity induced by hypoxia, whereas glutamate alone is involved in ischemic neurotoxicity.
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PMID:Hypoxic but not ischemic neurotoxicity of free radicals revealed by dynamic changes in glucose metabolism of fresh rat brain slices on positron autoradiography. 1069 73

Fresh rat brain slices were incubated with [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) in oxygenated Krebs-Ringer solution at 36 degrees C, and serial two-dimensional time-resolved images of [18F]FDG uptake in the slices were obtained on imaging plates. The fractional rate constant of [18F]FDG (proportional to the cerebral glucose metabolic rate) from pre-loading of ischemia (O(2) and glucose deprivation)/hypoxia (O(2) deprivation) to the reperfused/reoxygenated post-loading phase was quantitatively evaluated by applying the Gjedde-Patlak graphical method to the image data. Against ischemia an N-methyl-D-aspartate antagonist and hypothermia, but not a free radical scavenger, showed a protective effect when administered during ischemia, whereas no such effect was achieved with any of the above agents when administered after reperfusion. Against hypoxia, there was no protective effect with any of the above agents when administered during hypoxia, although an effect was noted with each when administered after reoxygenation. Excitatory amino acids during ischemia loading were found to be the main factor in the neuronal damage associated with ischemia, while in hypoxia, excitatory amino acids working in tandem with free radicals immediately after reoxygenation were implicated.
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PMID:Neurotoxicity after hypoxia/during ischemia due to glutamate with/without free radicals as revealed by dynamic changes in glucose metabolism. 1082 28

Copper-62 labeled diacetyl-bis(N4-methylthiosemicarbazone) (62Cu-ATSM) has been proposed as a generator produced positron-emitting tracer for hypoxic tissue imaging. To clarify the usefulness of 62Cu-ATSM for myocardial ischemia, 62Cu-ATSM PET was performed in 7 patients with coronary artery disease. Increased myocardial uptake of 62Cu-ATSM was observed (myocardium/blood ratio: 3.09) in one patient with unstable angina, who had increased 18F-fluorodeoxyglucose (18F-FDG) uptake under the fasting condition. The other 6 patients, who were clinically stable, did not have increased 62Cu-ATSM uptake, although abnormal 18F-FDG uptake was seen in 4 patients. This preliminary study suggests that 62Cu-ATSM is a promising PET tracer for hypoxic imaging in acute ischemia.
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PMID:Copper-62 ATSM as a hypoxic tissue tracer in myocardial ischemia. 1154 5


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