Fluorodeoxyglucose uptake in dysfunctional myocardium subtended by an occluded coronary artery View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-06

AUTHORS

Klaus F. Kofoed, Steen Carstensen, Birger Hesse, Jens D. Hove, Søren Holm, Mikael Jensen, Stig Haunsø, Henning Kelb\sgmaelig;k

ABSTRACT

BACKGROUND: Myocardial segments with impaired function may have the potential for functional recovery. Augmented exogenous glucose uptake in relation to blood flow estimated by [2-18F]2-fluorodeoxyglucose (FDG) and positron emission tomography (PET) frequently indicates functional reversibility. The spectrum of FDG uptake levels in relation to Sestamibi uptake and dobutamine contraction reserve in areas with impaired function subtended by an occluded coronary artery has never been reported. METHODS AND RESULTS: Seventeen patients with stable angina pectoris and dysfunctional myocardium subtended by an occluded coronary artery were studied with FDG-PET, low-dose dobutamine echocardiography and Sestamibi-Single Photon Emission Computerized Tomography. In a 16 segment model dysfunctional myocardial segments showed a normally distributed FDG uptake ranging from 34% to 150% when normalized to peak segmental Sestamibi uptake. Low FDG uptake was associated with both lack of dobutamine induced contractile reserve and low Sestamibi uptake (in 73% of the segments) whereas high FDG uptake displayed both contractile reserve and Sestamibi uptake (57%). Segments with intermediate FDG uptake had either contractile reserve or a preserved Sestamibi uptake (62%). CONCLUSION: Dysfunctional myocardium subtended by an occluded coronary artery represents a continuum of metabolic states with a high degree of heterogeneity with regard to contractile reserve and Sestamibi uptake. More... »

PAGES

97-104

Identifiers

URI

http://scigraph.springernature.com/pub.10.1023/a:1005913113840

DOI

http://dx.doi.org/10.1023/a:1005913113840

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031507245

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9617639


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