Korean Circ J.  2011 Sep;41(9):497-502. 10.4070/kcj.2011.41.9.497.

Molecular Imaging of High-Risk Atherosclerotic Plaques: Is It Clinically Translatable?

• Hwang BH
• Kim MH
• Chang K

• KMID: 2094100
• DOI: http://doi.org/10.4070/kcj.2011.41.9.497

Abstract

The explosive epidemics of diabetes and obesity as well as an aging population have led to cardiovascular diseases as the leading cause of world-wide morbidity and mortality beyond cancer. The recent introduction of drug-eluting stents and medications such as statins, dual anti-platelet therapy, and angiotensin converting enzyme inhibitors has dramatically improved clinical outcomes in patients with cardiovascular diseases. However, mortality is still increasing despite state-of-the-art therapeutics, as current diagnostic and therapeutic strategies against cardiovascular disease center on "locking the barn door after the horse has been stolen". Novel diagnostic solutions that identify individuals at risk before the disease is overt are needs. Imaging approaches that visualize molecular targets rather than anatomical structures aim to illuminate vital molecular and cellular aspects of atherosclerosis biology in vivo. Recent technological advances in small animal imaging systems and dedicated targeted/activatable molecular imaging probes have positioned molecular imaging to greatly impact atherosclerosis imaging in the next decade. However, several issues must be addressed before its clinical translation.

Keyword

Molecular imaging; Atherosclerosis; Primary prevention

MeSH Terms

Aging
Angiotensin-Converting Enzyme Inhibitors
Animals
Atherosclerosis
Biology
Cardiovascular Diseases
Drug-Eluting Stents
Horses
Humans
Molecular Imaging
Obesity
Primary Prevention
Angiotensin-Converting Enzyme Inhibitors

Figure

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  Fig. 1 Development of an atherosclerotic lesion and specific imaging targets at different stage of atherogenesis. The main cellular or molecular processes involved in each stage of atherosclerosis are presented. Potential molecular imaging targets at different stages are also listed.8)

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  Fig. 2 Upper right panel (B) shows a dark signal in the wall of an apoE-/- mouse aorta after an injection of silica-coated iron oxide nanoparticles compared with a precontrast MRI (A). Confocal microscopy shows accumulation of iron oxide nanoparticles in the aorta of a 30-week-old apoE-/- mouse. Most nanoparticles are noted in the macrophage-rich plaque area (C and D).

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  Fig. 3 Effect of simvastatin on fluorodeoxyglucose (FDG) uptake into atherosclerotic plaques. Diet alone does not have an effect on FDG uptake into carotid arteries. In contrast, simvastatin significantly attenuated FDG uptake into carotid arteries.9)

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  Fig. 4 High-resolution in vivo fluorescence molecular imaging of intraplaque neoangiogenesis and apoptosis in carotid atheroma of apoE-/- mice. After injecting angiogenesis- and apoptosis-targeting molecular imaging agents, intravital two-photon microscopy of carotid atheromata in a 34 week-old apoE-/- mouse revealed discrete plaque-specific neoangiogenesis (middle) and apoptosis (right).

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  Fig. 5 Discrepancy between structure and inflammation during imaging. Both patients had a similar degree of stenotic plaques in their carotid arteries, but different positron emission tomography (PET) signals suggestive of greater inflammation in one patient (left column) and lower macrophage infiltration (lower panel) in the other patient (right column).

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