FDG–PET imaging of atherosclerosis: Do we know what we see?
Received 7 October 2009; received in revised form 10 December 2009; accepted 4 January 2010. published online 04 March 2010. Corrected Proof
Abstract
Imaging atherosclerosis may help to identify subjects harboring rupture-prone atherosclerotic plaques who may benefit from preventive interventions. Potential of plaques to rupture depends on their structural changes and metabolic activation, which are difficult to assess using anatomic imaging modalities. Recent studies suggested that functional imaging with positron emission tomography (PET) utilizing fluorine-18-labeled 2-deoxy-d-glucose (FDG) has the potential to assess plaque metabolism and add to prediction of vascular risk. Aortic, iliac, and carotid plaques can be detected with FDG–PET, even though not all plaques exhibit high FDG uptake. Detection of coronary artery plaques is more cumbersome due to technical limitations of PET and fast movement of these vessels during cardiac and respiratory cycles. Studies on substrate accumulating FDG in plaques are contradictory and mostly do not extend beyond correlation analyses. Vascular FDG uptake has an excellent short-term stability, but larger fluctuations of uptake long-term, which may complicate interpretation of such changes in therapeutic trials. FDG uptake in major arteries correlates with some cardiovascular risk factors and atherosclerosis markers, but clinical utility of such correlations is unclear. What is more important is that recently reported studies in cancer patients showed correlation between higher baseline FDG uptake and subsequent cardiovascular mortality. Anti-atherogenic therapy and therapeutic lifestyle changes seem to decrease vascular FDG uptake but it is not clear whether the latter predicts subsequent lower morbidity and mortality. These initial findings suggest that vascular FDG–PET may in the future find some utility in management of patients with atherosclerosis, but a number of important issues need to be addressed first. We need to: (1) determine optimal standard ways of performing imaging and quantifying vascular FDG uptake; (2) understand molecular mechanisms governing FDG accumulation in plaques; (3) perform studies prospectively linking vascular FDG uptake to cardiovascular events in non-cancer patients. As of today, vascular FDG–PET is not ready for its prime time in clinical practice.
aNoninvasive Cardiovascular Imaging Program, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
bExperimental Cardiovascular Research Unit, Center for Molecular Medicine, Department of Medicine at Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden
cDepartment of Internal Medicine, Division of Cardiology, University of Nebraska Medical Center, Omaha, NE, USA
dJoint Program in Nuclear Medicine, Harvard Medical School, Boston, MA, USA
Corresponding author at: Experimental Cardiovascular Research Unit, Karolinska Institutet, Center for Molecular Medicine L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden. Tel.: +46 8 51776424; fax: +46 8 313147.