Evaluation of equivalence of upslope method-derived myocardial perfusion index and transfer constant based on two-compartment tracer kinetic model

The isolated arterially perfused rabbit interventricular septum was used to determine the feasibility of using the glucose analogue 18F-2-deoxy-2-fluoro-d-glucose (DG) with a tracer kinetic model to estimate the rate of exogenous glucose utilization. FDG was delivered to the septum by constant infusion, and tissue 18F radioactivity was measured as a function of time by external coincidence counting. The following four conditions were studied: flow rates of 0.5, 1.0, and 1.5 ml/min with a heart rate of 72 beats/min and flow at 1.5 ml/min with 96 beats/min. The rate constants for FDG forward and reverse transport between the vascular and extravascular compartments (k*1, k*2, respectively), phosphorylation of FDG (k*3), and dephosphorylation of FDG-6-phosphate (FDG-6-P) (k*4) were determined from the tissue curves using a tracer kinetic model. The lumped constant (LC) of the deoxyglucose model calculated using Fick-derived myocardial metabolic rates of glucose (MMRGlc), was 0.60 +/- 0.10 and was stable over the range of conditions studied. Average k*'s and LC were used to calculate MMRGlc's employing the model and were not significantly (P greater than 0.05) different from those determined by the Fick method. Tissue analyses using high-pressure liquid chromatography documented that tissue 18F radioactivity wa due to FDG and FDG-6-P, and their relative fractions agreed well with the values predicted from the tracer kinetic model. Only FDG was detected in the effluent. These studies also indicate the presence of a myocardial enzyme that can hydrolyze FDG-6-P to FDG. Thus our results support the use of the FDG method with positron-computed tomography for the in vivo determination of the myocardial rate of exogenous glucose utilization.

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Magnetic Resonance Imaging in Cardiac Syndrome X

JMS SKIMS ◽

10.33883/jms.v14i2.82 ◽

2011 ◽

Vol 14 (2) ◽

pp. 46-51

Author(s):

Syed Maqbool Ahmad ◽

Hilal Rather ◽

Khurshid Iqbal ◽

Nisar A Tramboo ◽

Vicar Jan ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Chest Pain ◽

Magnetic Resonance ◽

Myocardial Perfusion ◽

Perfusion Index ◽

Syndrome X ◽

Resonance Imaging ◽

Cardiac Syndrome X ◽

Subendocardial Ischemia ◽

Cardiac Syndrome

BACKGROUND: Cardiac syndrome X is a subject with yet unsettled etiology and management. Conventional investigations have not been able to establish that chest pain is due to myocardial ischemia. Magnetic resonance imaging has higher resolution and is more accurate for detecting ischemia. AIMS AND OBJECTIVES: To establish subendocardial ischemia as the cause of chest pain in cardiac syndrome X by virtue of stress perfusion cardiac MRI. METHODS: Contrast enhanced cardiac MRI was performed in 15 cases and 7 matched controls both at rest and during a six minute infusion of adenosine. Both visual and quantitive analysis were performed. In quantitative analysis both myocardial perfusion index and myocardial perfusion reserve index was measured. RESULTS: There was a significant increase in myocardial perfusion in both subendocardium as well as in subepicardium in both cases as well as in controls upon stress with adenosine. In controls the subendocardial perfusion index rose from 0.13 0.3 to 0.18 .03 and in the subepicardium from 0.12 .02 to 0.18 .03. In patients with cardiac syndrome X subendocardial perfusion index rose from 0.14 .03 to 0.19 .03 and subepicardial perfusion index rose from 0.13+.03 to 0.19 .03. Visual analysis showed short lasting subendocardial dark rim artificats in both cases and controls which lasted for only 3 to 5 beats. CONCLUSION: Our cardiovascular MR study of patients with cardiac syndrome X demonstrated significant and almost similar magnitude adenosine induced increase in both subendocardial and subepicardial myocardial perfusion indices in both study as well as control group. We found no evidence of subendocardial ischemia in patients with cardiac syndrome X. JMS 2011;14(2):46-51

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Study of Perfusion Kinetics in Human Brain Tumor Using Leaky Tracer Kinetic Model of DCE-MRI Data and CFD

Communications in Computer and Information Science - Advanced Computational Methods in Life System Modeling and Simulation ◽

10.1007/978-981-10-6370-1_7 ◽

2017 ◽

pp. 63-73 ◽

Cited By ~ 1

Author(s):

A. Bhandari ◽

A. Bansal ◽

A. Singh ◽

N. Sinha

Keyword(s):

Brain Tumor ◽

Kinetic Model ◽

Human Brain ◽

Human Brain Tumor ◽

Dce Mri ◽

Tracer Kinetic

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TRACER KINETIC MODEL ANALYSIS OF POTASSIUM UPTAKE BY DISSOCIATED NERVE CELL CULTURES: GLIAL-NEURONAL INTERRELATIONSHIP

Journal of Neurochemistry ◽

10.1111/j.1471-4159.1974.tb06934.x ◽

1974 ◽

Vol 23 (1) ◽

pp. 193-200 ◽

Cited By ~ 25

Author(s):

L. Latzkovits ◽

M. Sensenbrenner ◽

P. Mandel

Keyword(s):

Kinetic Model ◽

Nerve Cell ◽

Cell Cultures ◽

Model Analysis ◽

Potassium Uptake ◽

Tracer Kinetic

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Is bone equally responsive to calcium and vitamin D intake from food vs. supplements? Use of 41calcium tracer kinetic model

Bone Reports ◽

10.1016/j.bonr.2016.05.001 ◽

2016 ◽

Vol 5 ◽

pp. 117-123 ◽

Cited By ~ 4

Author(s):

Tara S. Rogers ◽

Marjorie G. Garrod ◽

Janet M. Peerson ◽

Darren J. Hillegonds ◽

Bruce A. Buchholz ◽

...

Keyword(s):

Vitamin D ◽

Kinetic Model ◽

Vitamin D Intake ◽

Tracer Kinetic

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Tracer kinetic model–driven registration for dynamic contrast-enhanced MRI time-series data

Magnetic Resonance in Medicine ◽

10.1002/mrm.21405 ◽

2007 ◽

Vol 58 (5) ◽

pp. 1010-1019 ◽

Cited By ~ 52

Author(s):

Giovanni A. Buonaccorsi ◽

James P.B. O'Connor ◽

Angela Caunce ◽

Caleb Roberts ◽

Sue Cheung ◽

...

Keyword(s):

Time Series ◽

Kinetic Model ◽

Time Series Data ◽

Series Data ◽

Dynamic Contrast Enhanced Mri ◽

Model Driven ◽

Dynamic Contrast Enhanced ◽

Contrast Enhanced ◽

Tracer Kinetic ◽

Contrast Enhanced Mri

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Quantitative Myocardial Perfusion with Dynamic Contrast-Enhanced Imaging in MRI and CT: Theoretical Models and Current Implementation

BioMed Research International ◽

10.1155/2016/1734190 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 12

Author(s):

G. J. Pelgrim ◽

A. Handayani ◽

H. Dijkstra ◽

N. H. J. Prakken ◽

R. H. J. A. Slart ◽

...

Keyword(s):

Myocardial Perfusion ◽

Theoretical Models ◽

Positron Emission ◽

Technological Advances ◽

Quantitative Myocardial Perfusion ◽

Tracer Kinetic ◽

Artery Disease ◽

Perfusion Quantification ◽

Magnetic Resonance Imaging Mri ◽

Similar Accuracy

Technological advances in magnetic resonance imaging (MRI) and computed tomography (CT), including higher spatial and temporal resolution, have made the prospect of performing absolute myocardial perfusion quantification possible, previously only achievable with positron emission tomography (PET). This could facilitate integration of myocardial perfusion biomarkers into the current workup for coronary artery disease (CAD), as MRI and CT systems are more widely available than PET scanners. Cardiac PET scanning remains expensive and is restricted by the requirement of a nearby cyclotron. Clinical evidence is needed to demonstrate that MRI and CT have similar accuracy for myocardial perfusion quantification as PET. However, lack of standardization of acquisition protocols and tracer kinetic model selection complicates comparison between different studies and modalities. The aim of this overview is to provide insight into the different tracer kinetic models for quantitative myocardial perfusion analysis and to address typical implementation issues in MRI and CT. We compare different models based on their theoretical derivations and present the respective consequences for MRI and CT acquisition parameters, highlighting the interplay between tracer kinetic modeling and acquisition settings.

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