PET detection of viable tissue in myocardial segments with persistent defects at T1-201 SPECT.

Brunken, Richard C.; Kottou, Sofia; Nienaber, C.A.; Schwaiger, M; Ratib, Osman; Phelps, M.E.; Schelbert, H R

doi:10.1148/radiology.172.1.2787037

Cited by 125 publications

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“…PET analysis was based on the eight-segment heart phantom map, which is based on the segmental division described by Brunken and colleagues (9,10) dividing the myocardium into anterobasilar, anteroseptal, anterior, lateral, posteroseptal, apical, posterobasilar, and inferior segments. The feasibility of this analysis has been tested in previous studies (26,34).…”

Section: Determination Of the Nonischemic And Nonstenotic Region In Mmentioning

confidence: 99%

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

Lautamäki¹,

Borra²,

Iozzo³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

141

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Nuutila. Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes. Am J Physiol Endocrinol Metab 291: E282-E290, 2006. First published February 14, 2006 doi:10.1152/ajpendo.00604.2005.-Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [15 O]H2O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[ 18 F]fluoro-D-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 Ϯ 2.0%) and high (17.4 Ϯ 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level (P ϭ 0.012) and muscle (P ϭ 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake (P ϭ 0.040) and glucose extraction rate (P ϭ 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 (P Ͻ 0.05) and lower coronary flow reserve (P ϭ 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function. hepatic steatosis; coronary disease; positron emission tomography; magnetic resonance spectroscopy INSULIN RESISTANCE characterizes over 80% of patients with type 2 diabetes (T2DM) (44). Impaired glucose uptake in several tissues and endothelial dysfunction are usual findings. Increased hepatic fat content has been found to affect ϳ50% of type 2 diabetic patients in the United States (6); thus nonalcoholic fatty liver (NAFL) often coexists with metabolic syndrome and insulin resistance. Futhermore, Hamaguchi et al. Fatty liver has been closely linked to insulin resistance at the whole body level irrespective of body weight, BMI, fat distribution, and glucose tolerance (35). Coronary risk factors tend to cluster in patients with high liver fat content, and patients with NAFL show more advanced carotid atherosclerosis compared with healthy controls (3,8,52). Recently, in a prospective study, it was shown that T2DM patients with NAFL had more cardiovascular related events during follo...

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Section: Determination Of the Nonischemic And Nonstenotic Region In Mmentioning

confidence: 99%

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

Lautamäki¹,

Borra²,

Iozzo³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

141

View full text Add to dashboard Cite

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“…For the PET analysis, the data from the SPECT, coronary angiography, and echocardiography studies were combined, and the ischemic and the nonischemic regions of the myocardium were identified in all subjects. PET analysis used an eight-segment heart phantom map, which is based on the segmental division described by Brunken and colleagues (15,16) dividing the myocardium into anterobasilar, anteroseptal, anterior, lateral, posteroseptal, apical, posterobasilar, and inferior segments. The feasibility of this analysis has been tested in previous studies (17,18).…”

Section: Spect Perfusion Imagingmentioning

confidence: 99%

Insulin Improves Myocardial Blood Flow in Patients With Type 2 Diabetes and Coronary Artery Disease

et al. 2006

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Insulin infusion improves myocardial blood flow (MBF) in healthy subjects. Until now, the effect of insulin on myocardial perfusion in type 2 diabetic subjects with coronary artery disease (CAD) has been unknown. We studied the effects of insulin on MBF in ischemic regions evaluated by single-photon emission-computed tomography and coronary angiography and in nonischemic regions in 43 subjects (ages 63 ؎ 7 years) with type 2 diabetes (HbA 1c 7.1 ؎ 0.9%). MBF was measured at fasting and during a euglycemic-hyperinsulinemic clamp at rest (n ‫؍‬ 43) and during adenosine-induced (140 g ⅐ kg ؊1 ⅐ min ؊1 for 7 min) hyperemia (n ‫؍‬ 26) using positron emission tomography and 15 O-labeled water. MBF was significantly attenuated in ischemic regions as compared with in nonischemic regions (P < 0.0001) and was increased by insulin as compared with in the fasting state (P < 0.0001). At rest, insulin infusion increased MBF by 13% in ischemic regions (P ‫؍‬ 0.043) and 22% in nonischemic regions (P ‫؍‬ 0.003). During adenosine infusion, insulin enhanced MBF by 20% (P ‫؍‬ 0.018) in ischemic regions and 18% (P ‫؍‬ 0.045) in nonischemic regions. In conclusion, insulin infusion improved MBF similarly in ischemic and nonischemic regions in type 2 diabetic subjects with CAD. Consequently, in addition to its metabolic effects, insulin infusion may improve endothelial function and thus increase the threshold for ischemia and partly contribute to the beneficial effects found in clinical trials in these subjects. Diabetes 55:511-516, 2006

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“…As an alternative to`01T1 scintigraphy, metabolic imaging using positron emission tomography (PET) also may be used for the detection of viable myocardium. 3,[15][16][17][18][19] In particular, the identification of viable myocardium from PET studies is based on the presence of either normal '8fluorodeoxyglucose (FDG) uptake or FDG: blood flow mismatch,15 whereas the identification of viable myocardium from`01T1 scintigraphy is based on the presence of either normal`'TI uptake or reversiblè "Tl defects (after either redistribution or reinjection). "1 The accuracy of these criteria to predict an improvement in regional function after revascularization has been evaluated, for both PET and`'Tl scintigraphy with rest-reinjection, in a relatively small number of patients.3,1'"'2 '19 The results of these studies indicate that the current PET and 2"T1 criteria used to identify viable myocardium are quite accurate but not perfect, as they may underestimate viability in up to 22% of the myocardial segments classified as nonviable.…”

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confidence: 99%

Regional left ventricular wall thickening. Relation to regional uptake of 18fluorodeoxyglucose and 201Tl in patients with chronic coronary artery disease and left ventricular dysfunction.

et al. 1992

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BACKGROUND In previous studies comparing regional 201Tl (201Tl) and 18fluorodeoxyglucose (FDG) activity in patients with chronic coronary artery disease and left ventricular dysfunction, we hypothesized that regions with mild-to-moderate reduction in FDG activity and regions with mild-to-moderate irreversible 201Tl defects after 3- to 4-hour redistribution represent viable myocardium. In the present study, regional FDG and 201Tl activities were compared with regional systolic wall thickening by gated magnetic resonance imaging (MRI) to confirm the presence of viable myocardium in these territories. METHODS AND RESULTS Twenty-five patients with chronic stable coronary artery disease and left ventricular dysfunction (ejection fraction, 28 +/- 10) underwent exercise 201Tl tomographic imaging (SPECT), using a reinjection protocol, positron emission tomography (PET) with FDG and H2(15)O, and gated MRI. Matched SPECT, PET, and MRI tomograms were analyzed. From the PET data, 105 regions had matched reduction in FDG and blood flow, of which 69 regions had moderately reduced FDG uptake (50-79% uptake relative to a normal reference region) and 36 had severely reduced FDG uptake (less than 50% of normal activity). Regions with moderately reduced as compared with severely reduced FDG activity had greater end-diastolic wall thickness (9.4 +/- 2.6 versus 8.0 +/- 3.7 mm; p less than 0.05) and regional systolic wall thickening (1.7 +/- 2.7 versus -0.7 +/- 2.1 mm; p less than 0.01). From the SPECT data, 169 irreversible 201Tl defects after 3-4 hour redistribution were identified, of which 70 were mild (greater than 65 to less than 85% of maximal 201Tl activity), 52 were moderate (50-65% of maximal activity), and 47 were severe (less than 50% of maximal activity). Regional systolic wall thickening was greater in regions with normal 201Tl uptake (3.3 +/- 2.3 mm) as compared with all other regions. Regions showing only mild or moderate irreversible defects at redistribution, however, showed wall thickening (2.4 +/- 2.4 and 2.2 +/- 2.5 mm, respectively), which was similar to that observed in regions with reversible 201Tl defects (2.1 +/- 2.2 mm). Only regions with severe irreversible defects at redistribution showed absence of thickening (-0.1 +/- 2.9 mm, p less than 0.01 versus all other groups). After 201Tl reinjection, 12 of 47 (26%) regions with severe irreversible defects showed enhanced 201Tl uptake. The impairment in regional systolic wall thickening was not significantly different between 201Tl defects with and without enhanced 201Tl uptake after reinjection. FDG activity, however, was present in all 12 regions (100%) with enhanced 201Tl uptake after reinjection as compared with only five of 35 (14%) that were unchanged after reinjection (p less than 0.01). CONCLUSIONS Therefore, preserved wall thickness and systolic wall thickening in regions with moderate reduction in blood flow and FDG activity, and in irreversible 201Tl defects that are only mild-to-moderate, provide additional evidence that such regions represent viable myocardium. Moreover, the finding of metabolic activity and 201Tl uptake in regions with reduced blood flow and absent wall thickening provides clinical evidence of hibernating myocardium in humans.

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PET detection of viable tissue in myocardial segments with persistent defects at T1-201 SPECT.

Cited by 125 publications

References 0 publications

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

Insulin Improves Myocardial Blood Flow in Patients With Type 2 Diabetes and Coronary Artery Disease

Regional left ventricular wall thickening. Relation to regional uptake of 18fluorodeoxyglucose and 201Tl in patients with chronic coronary artery disease and left ventricular dysfunction.

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