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Articles by S. G Nekolla
Total Records ( 5 ) for S. G Nekolla
  R Lautamaki , K. H Schuleri , T Sasano , M. S Javadi , A Youssef , J Merrill , S. G Nekolla , M. R Abraham , A. C Lardo and F. M. Bengel

Background— Hybrid positron emission tomography/computed tomography (PET-CT) allows for combination of PET perfusion/metabolism imaging with infarct detection by CT delayed contrast enhancement. We used this technique to obtain biomorphological insights into the interrelation between tissue damage, inflammation, and microvascular obstruction early after myocardial infarction.

Methods and Results— A porcine model of left anterior descending coronary artery occlusion/reperfusion was studied. Seven animals underwent PET-CT within 3 days of infarction, and a control group of 3 animals was scanned at >4 weeks. Perfusion and glucose uptake were assessed by [13N]-ammonia/[18F]-deoxyglucose (FDG), and 64-slice CT delayed contrast enhancement was measured. In the acute infarct model, CT revealed a no-reflow phenomenon suggesting microvascular obstruction in 80% of all infarct segments. PET showed increased FDG uptake in 68% of the CT-defined infarct segments. Ex vivo staining and histology showed active inflammation in the acute infarct area as an explanation for increased glucose uptake. In chronic infarction, CT showed no microvascular obstruction and agreed well with matched perfusion/metabolism defects on PET.

Conclusions— Perfusion/metabolism PET and delayed enhancement CT can be combined within a single hybrid PET-CT session. Increased regional FDG uptake in the acute infarct area is frequently observed. In contrast to the chronic infarct setting, this indicates tissue inflammation that is commonly associated with microvascular obstruction as identified by no reflow on CT. The consequences of these pathophysiological findings for subsequent ventricular remodeling should be explored in further studies.

  I Laitinen , A Saraste , E Weidl , T Poethko , A. W Weber , S. G Nekolla , P Leppanen , S Yla Herttuala , G Holzlwimmer , A Walch , I Esposito , H. J Wester , J Knuuti and M. Schwaiger

Background— 18F-Galacto-RGD is a positron emission tomography (PET) tracer binding to vβ3 integrin that is expressed by macrophages and endothelial cells in atherosclerotic lesions. Therefore, we evaluated 18F-galacto-RGD for imaging vascular inflammation by studying its uptake into atherosclerotic lesions of hypercholesterolemic mice in comparison to deoxyglucose.

Methods and results— Hypercholesterolemic LDLR–/–ApoB100/100 mice on a Western diet and normally fed adult C57BL/6 control mice were injected with 18F-galacto-RGD and 3H-deoxyglucose followed by imaging with a small animal PET/CT scanner. The aorta was dissected 2 hours after tracer injection for biodistribution studies, autoradiography, and histology. Biodistribution of 18F-galacto-RGD was higher in the atherosclerotic than in the normal aorta. Autoradiography demonstrated focal 18F-galacto-RGD uptake in the atherosclerotic plaques when compared with the adjacent normal vessel wall or adventitia. Plaque-to-normal vessel wall ratios were comparable to those of deoxyglucose. Although angiogenesis was not detected, 18F-galacto-RGD uptake was associated with macrophage density and deoxyglucose accumulation in the plaques. Binding to atherosclerotic lesions was efficiently blocked in competition experiments. In vivo imaging visualized 18F-galacto-RGD uptake colocalizing with calcified lesions of the aortic arch as seen in CT angiography.

Conclusions— 18F-Galacto-RGD demonstrates specific uptake in atherosclerotic lesions of mouse aorta. In this model, its uptake was associated with macrophage density. 18F-Galacto-RGD is a potential tracer for noninvasive imaging of inflammation in atherosclerotic lesions.

  I Matsunari , H Aoki , Y Nomura , N Takeda , W. P Chen , J Taki , K Nakajima , S. G Nekolla , S Kinuya and K. Kajinami

Although both 123I-metaiodobenzylguanidine (123I-MIBG) imaging and 11C-hydroxyephedrine (11C-HED) positron emission tomography (PET) are used for assessing cardiac sympathetic innervation, their relationship remains unknown. The aims were to determine whether 123I-MIBG parameters such as heart-to-mediastinum ratio (H/M) are associated with quantitative measures by 11C-HED PET and to compare image quality, defect size, and location between 123I-MIBG single-photon emission computed tomography (SPECT) and 11C-HED PET.

Methods and Results—

Twenty-one patients (mean left ventricular ejection fraction, 39±15%) underwent 123I-MIBG imaging and 11C-HED PET. Early (15-minute), late (3-hour) H/M, and washout rate (WR) were calculated for 123I-MIBG. Myocardial retention and WR was calculated for 11C-HED. Using a polar map approach, defect was defined as the area with relative activity <60% of the maximum. Both the early (r=0.76) and late (r=0.84) 123I-MIBG H/M were correlated with 11C-HED retention. 123I-MIBG WR was correlated with 11C-HED WR (r=0.57). Defect size could not be measured in 3 patients because of poor quality 123I-MIBG SPECT, whereas 11C-HED defect was measurable in all patients. Although defect size measured by early or late 123I-MIBG SPECT was closely correlated with that by 11C-HED PET (early: r=0.94; late: r=0.88), the late 123I-MIBG overestimated defect size particularly in the inferior and septal regions.


123I-MIBG H/M gives a reliable estimate of cardiac sympathetic innervation as measured by 11C-HED PET. Furthermore, despite the close correlation in defect size, 11C-HED PET appears to be more suitable for assessing regional abnormalities than does 123I-MIBG SPECT.

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